Oral Health in America: . A Report of the Surgeon General Department of Health and Human Services U.S. PUBLIC HEALTH SERVICE National Institute of Dental and Craniofacial Research Suggested Citation U.S. Department of Health and Human Services. Oral Health in America: A Report of the Surgeon General. Rockville, MD: U.S. Department of Heal&ad Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health, ZOO& __-. i Message from Donna E. Shalala Secretary of Health and Human Services The intent of this first-ever Surgeon General's Report on Oral Health is to alert Americans to the full meaning of oral health and its importance to general health and well-being. Great progress has been made in reducing the extent and severity of common oral diseases. Successful prevention measures adopted by communities, individuals, and oral health professionals have resulted in marked improvements in the nation's oral and dental health. The terms oral health and general health should not be interpreted as separate entities. Oral health is integral to general health; this report provides important reminders that oral health means more than healthy teeth and that you cannot be healthy without oral health. Further, the report outlines existing safe and effective disease prevention measures that everyone can adopt to improve oral health and prevent disease. However, not everyone is experiencing the same degree of improvement. This Surgeon General's report addresses the inequities and disparities that affect those least able to muster the resources to achieve optimal oral health. For whatever the reason, ignoring oral health problems can lead to needless pain and suffering, causing devastating complications to an individual's well- being, with financial and social costs that significantly diminish quality of life and burden American society For a third decade, the nation has developed a plan for the prevention of disease and the pro- motion of health, including oral health, embodied in the U.S. Department of Health and Human Services document, Healthy People 2010. This Surgeon Generals Report on Oral Health empha- sizes the importance of achieving the Healthy People goals to increase quality of life and eliminate disparities. As a nation, we hope to address the determinants of health-individual and environ- mental factors -in order to improve access to quality care, and to support policies and programs that make a difference for our health. We hope to prevent oral diseases and disorders, cancer, birth defects, AIDS and other devastating infections, mental illness and suicide, and the chronic diseases of aging. We trust that this Surgeon Generals report will ensure that health promotion and disease pre- vention programs are enhanced for all Americans. This report proposes solutions that entail part- nerships-government agencies and officials, private industry, foundations, consumer groups, health professionals, educators, and researchers-to coordinate and facilitate actions based on a National Oral Health Plan. Together, we can effect the changes we need to maintain and improve oral health for all Americans. ORAL HWLTH IN AMERICA: A REPORT OF THE SURGEON GENERAL . . . III Foreword The growth of biomedical research since World War II has wrought extraordinary advances in the health and well-being of the American people. The story is particularly remarkable in the case of oral health, where we have gone from a nation plagued by the pains of toothache and tooth loss to a nation where most people can smile about their oral health. The impetus for change-to take on the challenge of addressing oral diseases as well as the many other health problems that shorten lives and diminish well-being-led to the postwar growth of the National Institutes of Health. In 1948 the National Institute of Dental Research-now the National Institute of Dental and Craniofacial Research-joined the National Cancer Institute and the National Heart, Lung, and Blood Institute as the third of the National Institutes of Health. The Institute's research initially focused on dental caries and studies demonstrating the effec- tiveness of fluoride in preventing dental caries, research that ushered in a new era of health promo- tion and disease prevention. The discovery of fluoride was soon complemented by research that showed that both dental caries and periodontal diseases were bacterial infections that could be pre- vented by a combination of individual, community, and professional actions. These and other appli- cations of research discoveries have resulted in continuing improvements in the oral, dental, and craniofacial health of Americans. Today, armed with the high-powered tools, automated equipment, and imaging techniques of genetics and molecular and cell biology, scientists have set their sights on resolving the full array of craniofacial diseases and disorders, from common birth defects such as cleft lip and palate to the debilitating,chronic oral-facial pain conditions and oral cancers that occur later in life. The National Institute of Dental and Craniofacial Research has served as the lead agency for the development of this Surgeon Generals Report on Oral Health. As part of the National Institutes of Health, the Institute has had ready access to ongoing federal research and the good fortune to work collaboratively with many other agencies and individuals, both within and outside government. The establishment of a Federal Coordinating Committee provided a formal mechanism for the exchange of ideas and information from other departments, including the U.S. Department of Agriculture, Department of Education, Department of Justice, Department of Defense, Department of Veterans Affairs, and Department of Energy Active participation in the preparation and review of the report came from hundreds of individuals who graciously gave of their expertise and time. It has been a pleasure to have had this opportunity to prepare the report, and we thank Surgeon General David Satcher for inviting us to participate. Despite the advances in oral health that have been made over the last half century, there is still much work to be done. This past year we have seen the release of Healthy People 2010, which emphasizes the broad aims of improving quality of life and eliminating health disparities. The recently released U.S. General Accounting Office report on the oral health of low-income popula- tions further highlights the oral health problems of disadvantaged populations and the effects on their well-being that result from lack of access to care. Agencies and voluntary and professional organizations have already begun to lay the groundwork for research and service programs that directly and comprehensively address health disparities. The National Institutes of Health has joined these efforts and is completing an agencywide action plan for research to reduce health dis- parities. Getting a healthy start in life is critical in these efforts, and toward that end, a Surgeon OR4L HE4LTH IN AMERICA: A REPORT OF THE SL'RGEON GENERAL Foreword General's Conference on Children and Oral Health, The Face of a Child, is scheduled for June 2000. Many other departmental and agency activities are under way The report concludes with a framework for action to enable further progress in oral health. It emphasizes the importance of building partnerships to facilitate collaborations to enhance educa- tion, service, and research and eliminate barriers to care. By working together, we can truly make a difference in our nation's health-a difference that will benefit the health and well-being of all our citizens. Ruth L Kirsckstein MD Acting Director National Institutes of Health Harold C. Shvhin DDS Director National Institute of Dental and Craniofacial Research Vi ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Preface from the Surgeon Gened U.S. public Health Service AS we begin the twenty-first century, we can be proud of the strides we have made in improving the oral health of the American people. At the turn of the last century, most Americans could expect to lose their teeth by middle age. That situation began to change with the discovery of the properties of fluoride, and the observation that people who lived in communities with naturally fluoridated drinking water had far less dental caries (tooth decay) than people in comparable com- munities without fluoride in their water supply Community water fluoridation remains one of the great achievements of public health in the twentieth century-an inexpensive means of improving oral health that benefits all residents of a community, young and old, rich and poor alike. We are fortunate that additional disease prevention and health promotion measures exist for dental caries and for many other oral diseases and disorders- measures that can be used by individuals, health care providers, and communities. Yet as we take stock of how far we have come in enhancing oral health, this report makes it abundantly clear that there are profound and consequential disparities in the oral health of our citi- zens. Indeed, what amounts to a "silent epidemic" of dental and oral diseases is affecting some pop- ulation groups. This burden of disease restricts activities in school, work, and home, and often sig- nificantly diminishes the quality of life. Those who suffer the worst oral health are found among the poor of all ages, with poor children and poor older Americans particularly vulnerable. Members of racial and ethnic minority groups also experience a disproportionate level of oral health prob- lems. Individuals who are medically compromised or who have disabilities are at greater risk for oral diseases, and, in turn, oral diseases further jeopardize their health. The reasons for disparities in oral health are complex. In many instances, socioeconomic fac- tors are the explanation. In other cases,, disparities are exacerbated by the lack of community pro- grams such as fluoridated water supplies. People may lack transportation to a clinic and flexibility in getting time off from work to attend to health needs. Physical disability or other illness may also limit access to services. Lack of resources to pay for care, either out-of-pocket or through private or public dental insurance, is clearly another barrier. Fewer people have dental insurance than have medical insurance, and it is often lost when individuals retire. Public dental insurance programs are often inadequate. Another major barrier to seeking and obtaining professional oral health care relates to a lack of public understanding and awareness of the importance of oral health. We know that the mouth reflects general health and well-being. This report reiterates that gen- eral health risk factors common to many diseases, such as tobacco use and poor dietary practices, also affect oral and craniofacial health. The evidence for an association between tobacco use and oral diseases has been clearly delineated in every Surgeon General's report on tobacco since 1964, and the oral effects of nutrition and diet are presented in the Surgeon Generals report on nutrition ( 1988). Recently, research findings have pointed to possible associations between chronic oral infections and diabetes, heart and lung diseases, stroke, and low-birth-weight, premature births. This report assesses these emerging associations and explores factors that may underlie these oral- systemic disease connections. To improve quality of life and eliminate health disparities demands the understanding, compas- sion, and will of the American people. There are opportunities for all health professions, individu- als. and communities to work together to improve health. But more needs to be done if we are to make further improvements in America's oral health. We hope that this Surgeon Generals report ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL vii Preface will inform the American people about the opportunities to improve oral health and provide a plat- form from which the science base for craniofacial research can be expanded. The report should also serve to strengthen the translation of proven health promotion and disease prevention approaches into policy development, health care practice, and personal lifestyle behaviors. A framework for action that integrates oral health into overall health is critical if we are to see further gains. David Satcher MD, PhD Surgeon General . . . VIII ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments This report was prepared by the Department of Health and Human Set-vices under the direction of the National Institutes of Health, National Institute of Dental and Craniofacial Research. Ruth L. Kirschstein MD Acting Director, National Institutes of Health, DHHS, Bethesda, MD Harold C. Slavkin DDS Director, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD David Satcher MD, PhD Assistant Secretary for Health and Surgeon General, Office of Public Health and Science, Office of the Secretary, Washington, DC Nicole Lurie MD, MSPH Prmcipal Deputy Assistant Secretary for Health, Office of Public Health and Science, Office of the Secretary \Vashington, DC Beverly L. Malone PhD, RN, FAAN Deputy Assistant Secretary for Health, Office of Public Health and Science, Office of the Secretary, Washington, DC r\rthur Lawrence PhD rissistant Surgeon General, USPHS, Deputy Assistant Secretary for Health (Operations), Office of Public Health and Science, Office of the Secretary, W'ashington, DC Kenneth Moritsugu MD, MPH Deputy Surgeon General, LJSPHS, Office of the Surgeon General, Office of the Secretary, LVashington, DC .-\l!an S. Noonan MD, dMPH Captain, USPHS, Office of the Surgeon General, Office of the Secretary, Washington, DC *Indicates Coordinating Author PROJECT TEAM Caswell A. Evans DDS, MPH Project Director and Executive Editor Assistant Director, Los Angeles County Department of Health Services, Los Angeles, CA Dushanka V Kleinman DDS, MScD Co-Executive Editor Assistant Surgeon General, USPHS Deputy Director, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD William R. Maas DDS, MPH, MS Assistant Surgeon General, Chief Dental Officer, USPHS Director, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Joan S. Wilentz MA Science Writer and Editor, Bethesda, MD Roseanne Price ELS Editor, Silver Spring, MD Marla Fogelman Editor, Silver Spring, MD CONTRIBUTORS Margo Adesanya DDS Staff Scientist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Alfred0 Aguirre DDS, MS Director and Associate Professor, Advanced Oral and Maxillofacial Pathology, State University of New York at Buffalo School of Dental Medicine, Buffalo, NY *Ronald Andersen PhD, MA Wasserman Professor of Health Services and Professor of Sociology, University of California Los Angeles School of Public Health, Los Angeles, CA ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL iX Acknowledgments Jay R. Anderson DMD, MHSA Chief Dental Officer, Division of Community and Migrant Health, Bureau of Primary Health Care, Health Resources and Services Admmistration, DHHS, Rockville, MD Kenneth J. Anusavice PhD, DMD Associate Dean for Research, Chair. Department of Dental Biomaterials, University of Florida College of Dentistry, Gainesville. FL +Kathryn A. Atchison DDS, MPH Professor and Associate Dean for Research, University of California Los Angeles School of Dentistry, Los Angeles, CA James Bader DDS, MPH Professor, University of North Carolina School of Dentistry, Chapel Hill, NC Charles Bertolami DDS, D.Med.Sc. Dean. University of California San Francisco School of Dentistry, San Francisco, CA Aljernon Bolden DMD, MPH Director, Community Health Programs and Co- Director, Division of Dental Public Health, Boston University Goldman School of Dental Medicine, Boston. MA L. Jackson Brown DDS, PhD Associate Executive Director, American Dental Association, Chicago, IL Janet A. Bnmelle MS Statistician (retired), National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS. Bethesda, MD Brian A. Burt BDS, MPH, PhD Professor of Dental Public Health, Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor. MI Nita Chainani-Wu DMD, MPH University of California San Francisco School of Dentistry. San Francisco, CA David W. Chen MD, MPH Commander, USPHS, Deputy Director, Division of Associated, Dental, and Public Health Professions. Bureau of Health Professions, Health Resources and Services Administration, DHHS, Rockville, MD Joseph Ciardi PhD Consultant, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Betty DeBerry-Summer DDS, MPH Captain. USPHS, Chief Dental Officer, Bureau of Primary Health Care, Health Resources and Services Administration, DHHS, Bethesda, MD Teresa A. Dolan DDS, MPH Professor and Associate Dean, University of Florida College of Dentistry, Gainesville, FL *Chester W. Douglass DMD, PhD Professor and Chair, Department of Oral Health Policy and Epidemiology, Harvard School of Dental Medicine. Boston, MA M. Ann Drum DDS, MPH Captain, USPHS, Acting Director, Division of Research, Education and Training, Maternal and Child Health Bureau, Health Resources and Services Administration, DHHS, Rockville, MD Thomas E Drury PhD Senior Scientist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Burton L. Edelstein DDS, MPH , Director, Children's Dental Health Project, American Academy of Pediatrics, Washington, DC Frederick C. Eichmiller DDS Director, Paffenbarger Research Center, American Dental Association Health Foundation, National Institute of Standards and Technology, Gaithersburg, MD Mary P Faine MS, RD, CD Associate Professor and Director of Nutrition Education, University of Washington School of Dentistry, Seattle, WA Denise J. Fedele DMD, MS Chief Professional Development and Research in Dental Care Clinical Research, Veterans Administration Medical Health Care System, Department of Veterans Affairs, Perrypoint, MD Christopher H. Fox DMD, DMSc Director of Professional Relations, Europe, Colgate- Palmolive Co., New Jersey Philip C. Fox DDS Director, Research and Development Affiliation, Amarillo Biosciences, Inc., Amarillo, TX Lawrence J. Furman DDS, MPH Captain, USPHS, Head, Department of Health Services, U.S. Merchant Marine Academy, Kings Point, NY Isabel Garcia DDS, MPH Captain, USPHS, Special Assistant for Science Transfer, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD *Robert J. Genco DDS, PhD Distinguished Professor and Chair, Department of Oral Biology, State University of New York at Buffalo School of Dental Medicine, Buffalo, NY Gretchen Gibson DDS, MPH Director, Special Care Dental Clinics, Veterans Administration North Texas Healthcare Systems, Department of Veterans Affairs, Dallas, TX X ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Sharon M. Gordon DDS, MPH Director, Office of Education, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD &therine Hayes DMD, DMSc ;\ssistant Professor, Department of Oral Health Policy and Epidemiology, Harvard School of Dental Medicine, Boston, MA .-\lice M. Horowitz PhD Senior Scientist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS. Bethesda, MD Herschel Horowitz DDS, MPH Consultant, Dental Research and Public Health, Bethesda, MD lcffrev Hpman DDS, PhD Epidemiologist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD .\mld I. lsmail BDS, MPH, DrPH Professor, University of Michigan School of Dentistry, &in Arbor, MI . Marjorie Jeffcoat DMD Rosen Professor and Chair, Department of Periodontics, University of Alabama School of Dentistry, Birmingham, AL Clrndace Jones RDH, MPH Captain, USPHS, Director, Dental Diseases Prevention Program, Indian Health Service, DHHS, Rockville, MD David Jones DDS, MPH Captain, USPHS (retired), Rockville, MD Judith A. Jones DDS, MPH Scmor Research Associate, Veterans Administration Center for Health Quality, Outcomes and Economic Research, Department of Veterans Affairs and, Associate Professor, Boston University Goldman School of Dental Medicine, Bedford, MA Kaumudi J. Joshipura BDS, DSc Assistant Professor, Harvard School of Dental Medicine, Boston, MA l-in& M. Kaste DDS, PhD .Associate Professor and Division Director, Division of Dental Public Health and Oral Epidemiology, Medical University of South Carolina College of Dental bledicine, Charleston, SC W'illiam Kohn DDS, MS Captain, USPHS, Associate Director for Science, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Man Sue Lancaster RN, MA Health Education Specialist, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Acknowledgments Linda LeResche ScD Research Professor, University of Washington School of Dentistry, Seattle, WA James Lipton DDS, PhD Captain, USPHS, Assistant Director for Training and Career Development, National Institute of Dental and Craniofacial Research, DHHS, Bethesda, MD Reginald Louie DDS, MPH Captain, USPHS, Regional Dental Consultant, Health Resources and Services Administration, DHHS, San Francisco, CA *Irwin D. Mandel DDS Professor Emeritus, Columbia University School of Dental and Oral Surgery, New York, NY Stephen E. Marcus PhD . Epidemiologist, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD Frank Martin DDS, MPH Captain, USPHS, Assistant Chief, Dental Services Branch (retired), Indian Health Service, DHHS, Rockville, MD Wendy E. Mouradian MD Director, Children's Hospital and Regional Medical Center, Departments of Pediatrics, Pediatric Dentistry, Medical History and Ethics, University of Washington, Seattle, WA *Linda Niessen DMD, MPH, MPP Professor, Baylor University College of Dentistry and Vice President, DENTSPLY International, York, PA Ruth E. Nowjack-Raymer RDH, MPH Public Health Researcher, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Steven Offenbacher DDS, PhD, MMSc Professor and Director, Center for Oral and Systemic Diseases, University of North Carolina, Chapel Hill, NC H. Whitney Payne, Jr. DDS, MPH Captain, USPHS, Chief of Dental Services, Federal Correctional Institution, Federal Bureau of Prisons, Department of Justice, Seogoville, TX Edward Peters DMD Instructor in Oral Health and Epidemiology, Department of Oral Health Policy and Epidemiology, Harvard School of Dental Medicine, Boston, MA Douglas E. Peterson DMD, PhD Professor and Head, Department of Oral Diagnosis, University of Connecticut School of Dental Medicine, Farmington, CT Maryann Redford DDS, MPH Health Scientist Administrator, National lnstitute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xi *Susan Reisine PhD Professor, University of Connecticut School of Dental Medicine, Hartford, CT John Rossetti DDS. MPH Captain, USPHS, Chief Dental Officer, Health Resources and Services Administration, DHHS, Rockville, MD #R. Gary Rozier DDS, MPH Professor, Department of Health Policy Administration, University of North Carolina School of Public Health, Chapel Hill, NC Susan Runner DDS, MA Captain, USPHS, Branch Chief Dental Devices, Center for Devices and Radiological Health, Food and Drug Administration, Rockville, MD John S. Rutkauskas DDS, MS Executive Director, American Association of Pediatric Dentistry, Chicago, IL Margaret Scarlett DMD Captain, USPHS, Office of the Secretary, Office of Public Health and Science, DHHS, Washington, DC Don Schneider DDS, MPH Captain, USPHS, Chief Dental Officer, Health Care Financing Administration, Center for Medicaid and State Operations, DHHS, Baltimore, MD Stephen T. Schultz DDS, MS. MPH Lieutenant Commander. U.S. Navy National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Robert H. Selwitz DDS, MPH Captain, USPHS, Senior Dental Epidemiologist, National Institute of Dental and Crariiofacial Research, National Institutes of Health, DHHS. Bethesda, MD Gerald Shklar DDS, MS Charles A. Brackett Professor of Oral Pathology, Harvard School of Dental Medicine, Boston, MA Charles Shuler DMD, PhD Director, Center for Craniofacial Molecular Biology, George and Mary Lou Boone Professor of Craniofacial Molecular Biology, University of Southern California School of Dentistr): Los Angeles, CA Gary Slade BDSc, DDPH, PhD Assistant Professor, University of North Carolina School of Dentistry Chapel Hill, NC Ronald F! Strauss DMD, PhD Professor, School of Dentistry and School of Medicine, University of North Carolina, Chapel Hill, NC Lawrence Tabak DDS, PhD Senior Associate Dean for Research, University of Rochester School of Medicine and Dentistry, Rochester, NY George W. Taylor DMD, DrPH Assistant Professor of Dentistry, University of Michigan School of Dentistry Ann Arbor. MI Amardeep Singh Thind MD, PhD Assistant Professor, University of California LOS Angeles School of Public Health, Los Angeles, CA Scott L. Tomar DMD, DrPH Epidemiologist/Dental Officer, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Benedict I. Truman MD, MPH Senior Scientist and Epidemiology Program Officer, Centers for Disease Control and Prevention, DHHS, Atlanta, GA William Wathen DMD Associate Dean, Center for Professional Development, Baylor College of Dentistry, pallas, TX *Jane A. Weintraub DDS, MPH Lee Hysan Professor and Chair, Division of Oral Epidemiology and Dental Public Health, University of California San Francisco School of Dentistry, San Francisco, CA *B. Alex White DDS, DrPH Assistant Program Director, Economic, Social, and Health Services Research, Kaiser Permanente Center for Health Research, Portland, OR Deborah Winn PhD Senior Investigator, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Athanasios I. Zavras DMD, MS, DMSc Assistant Professor, Department of Health Policy and Epidemiology Harvard School of Dental Medicine, Boston, MA SENIOR REVIEWERS Clifton Dummett Sr. DDS Distinguished Professor Emeritus, University of Southern California School of Dentistry, Los Angeles, CA Helen C. Rodriguez-Trias MD, FAAP Past-President, American Public Health Association, Brookdale, CA John Stamm DDS, DDPH, MScD Dean, University of North Carolina School of Dentistry, Chapel Hill, NC REVIEWERS Michael C. Alfano DMD, PhD Dean, New York University College of Dentistry, New York, NY Myron Allukian Jr. DDS, MPH Director, Oral Health, Boston Public Health Commission, Boston, MA xii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL ;ilcs,a +,ntczak-Bouckoms DMD, ScD, MPH, MS ..lssistant Professor of Medicine, Tufts University School of Medicine, Medford, MA 11oward L. Bailit DMD, PhD H&h Policy and Primary Care Research Center, L.niversitv of Connecticut Health Center, Fimnington. CT D.ivtd Barmes BDSc, DDSc, MPH spccial Expert for International Health, National Institute of Dental and Craniofacial Research, National Institutes of Health. DHHS, Bethesda, MD Brticc J. Baum DMD, PhD C1,icf of Gene Therapy and Therapeutic Branch, \;,tional Institute of Dental and Craniofacial Research, x,tttonal Institutes of Health, DHHS, Bethesda, MD \tq>ticn C. Bayne MS, PhD Professor. University of North Carolina School of Dcntistr): Chapel Hill, NC j~11lc5 D. Beck PhD Kcnan Professor, University of North Carolina School of Dentistr): Chapel Hill, NC I iigcnio Bcltran DMD, MPH, MS, BrPH \cnior Research Fellow, Division of Oral Health, (`cntcrs for Disease Control and Prevention, DHHS, :\rl.m~a. GA I It.iining Birkedal-Hansen DDS, PhD scientific Director, National Institute of Dental and (:raniofacial Research, National Institutes of Health, DI 11~s. Bethesda. MD li.~r~nn Boehm MPH (`h~cf, Health Promotion Branch, National Institute of Dental and Craniofacial Research, National Institutes 01 1 Icalth. DHHS, Bethesda, MD ~~`11l~m H. Bowen BDS. PhD Wclscher Professor of Dentistry, School of Dentistry, t:niversity of Rochester Medical Center, Rochester, NY \orman S. Braveman PhD .-\ssociate Director for Clinical, Behavioral and Health Promotion Research, National Institute of Dental and Craniofacial Research, National Institutes of Health, I)IIH.S. Bethesda, MD Bruce B. Brehm DMD, MPH Lieutenant Colonel, U.S. Army, T&Service Center for Oral Health Studies, Uniformed Services University of the Health Sciences, Department of Defense, Bethesda. MD Patricia S. Byant PhD Director. Behavioral and Health Promotion Research, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD \laria Teresa Canto MS, DDS, MPH Pubhc Health Research Specialist, National Institute of Dental and Craniofacial Research, National Institutes of Health. DHHS. Bethesda. MD Acknowledgments Eli Capilouto DMD, MPH, ScD Dean, School of Public Health, University of Alabama at Birmingham, Birmingham, AL Victoria A. Cargill MD, MSCE Medical Officer, Office of AIDS Research, National Institutes of Health, DHHS, Bethesda, MD D. Walter Cohen DDS Chancellor Emeritus, Medical College of Pennsylvania, Hahneman University, Philadelphia, PA Lois K. Cohen PhD Director, Office of International Health, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Robert J. Collins DMD, MPH , Deputy Executive Director, International and American Associations for Dental Research, Alexandria, VA Stephen B. Corbin DDS, MPH Director of Health and Research Initiatives, Special Olympics, Inc., Washington, DC James G. Corrigan PhD Evaluation Officer, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD James J. Crall DDS, ScD Chairman, Department of Pediatric Dentistry, University of Connecticut School of Dental Medicine, Farmington, CT Ananda E Dasanayake BDS, MPH, PhD Associate Professor, Department of Oral Biology University of Alabama School of Dentistry, Birmingham, AL Dominick I? DePaola DDS, PhD President and CEO, The Forsyth Institute, Boston, MA Richard D'Eustachio DDS Private Practice, Cherry Hill, NJ Ray Dionne DDS, PhD Captain, USPHS, Clinical Director, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Marylin Dodd RN, PhD Professor. University of California San Francisco School of Nursing, San Francisco, CA Scott Dubowsky DMD, FAGD Private Practice, Bayonne, NJ Robert Dumbaugh DDS, MPH Dental Executive Director, Palm Beach County Health Department, Palm Beach, FL Joel Epstein DMD, MSD Research Associate Professor, Department of Oral Medicine, University of Washington School of Dentistry, Seattle, WA ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL . . . XIII Acknowledgments Ronald Ettinger BDS, MDS, DDSc Professor, Department of Prosthodontics and Dows Institute for Dental Research, University of Iowa, Iowa City, IA Raymond Fonseca DMD Dean, University of Pennsylvania School of Dental Medicine, Philadelphia, PA Allan J. Formicola DDS Dean, School of Dental and Oral Surgev, Columbia University, New York, NY Jane L. Forrest Ed.D., RDH Assistant Dean, Dental Hygiene Research and Instructional Technology, Director, National Center for Dental Hygiene Research, University of Southern California School of Dentistry, Los Angeles, CA Robert T. Frame DMD, MS, CHE Assistant Under Secretary for Health for Dentistry, Department of Veterans Affairs, Washington, DC Raul I. Garcia DMD Professor and Chair, Department of Health Policy, Boston University Goldman School of Dental Medicine, Boston, MA Jay Alan Gershen DDS, PhD Executive Vice Chancellor, University of Colorado Health Sciences Center, Denver, CO Michael Glick DMD Professor of Oral Medicine, Director, Programs for Medically Complex Patients, University of Pennsylvania School of Dental Medicine, Philadelphia, PA Barbara E Gooch DMD, MPH Dental Officer, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA John Greene DMD, MPH Dean Emeritus, University of California San Francisco School of Dentistry, San Rafael, CA Deborah Greenspan BDS, DSc, ScD (hc), FDSRCS Ed (hon) Professor of Clinical Oral Medicine, University of California San Francisco School of Dentistry, San Francisco, CA John S. Greenspan BSc, BDS, PhD, FRCPath Professor and Chair, Department of Stomatology, University of California San Francisco School of Dentistry, San Francisco, CA Robert 0. Greer DDS, ScD Professor of Pathology and Medicine, University of Colorado Health Sciences Center, Schools of Medicine and Dentistry, Denver, CO David Grembowski PhD Professor of Health Services and Dental Public Health Sciences, University of Washington, Seattle, WA Ellen R. Gritz PhD Professor and Chair, Department of Behavioral Science, M.D. Anderson Cancer Center, University of Texas, Houston, TX Kenneth A. Gruber PhD Chief, Chronic Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Kevin Hardwick DDS, MPH Captain, USPHS, International Health Officer, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Hazel J. Harper DDS, MPH Private Practice, Washington, DC John Hauth MD Professor, Interim Chairman and Director, Center for Research in Women's Health, University of Alabama at Birmingham, Birmingham, AL Maxine Hayes MD, MPH Assistant Secretary, Community and Family Health, Washington State Department of Health, Olympia, WA Marc W. Heft DMD, PhD Professor and Director of the Claude Pepper Center, University of Florida College of Dentistry, Gainesville, FL Joseph Henry DDS, PhD, ScD Dean Emeritus, Howard University College of Dentistry and Professor, Harvard School of Dental Medicine, Boston, MA Mark C. Herzberg DDS, PhD Professor, University of Minnesota School of Dentistry, Minneapolis, MN Alan R. Hinman MD, MPH Senior Consultant for Public Health Programs, Taskforce for Child Survival and Development, Decatur, GA Cynthia Hodge DMD, MPH Private Practice, Nashville, TN Dorthe Holst DDS, MPH Professor, Department of Community Dentistry, University of Oslo, Oslo, Norway John I? Howe III MD President, University of Texas Health Science Center at San Antonio, San Antonio, TX David Johnsen DDS, MS Dean and Professor of Pediatric Dentistry, University of Iowa College of Dentistry, Iowa City, IA Ralph Katz DMD, PhD Professor, Department of Behavioral Science and Community Health, University of Connecticut School of Dental Medicine, Farmington, CT H. Asuman Kiyak MA, PhD Director, Institute on Aging and Professor, University of Washington School of Dentistry, Seattle, WA xiv ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL k\`znncth S. Komman DDS. PhD Ch,,.f Scientific Officer, Interleukin Genetics, Inc., +n .\ntonio. TX t:linI K;ousvelari DDS, DSc llc31th Scientist Administrator, National Institute of Dcnr.il and Craniofacial Research, National Institutes ,,f Health. DHHS, Bethesda, MD I.,, .inth \: Kumar DDS, MPH \~~,stant Director. Bureau of Dental Health, New York ?t.itc Department of Health, Albany, NY I;.,\ mend Kuthy DDS, MPH Prl,fcssor and Chair, Preventive and Community Ilcntistn: UnivTersity of Iowa College of Dentistry, ~,wn City. IA I r.1 l..imstcr DDS, MMSc Prolcssor and Vice Dean, Columbia University School (11 Dental and Oral Surgery, New York, NY 1'111lil' R. Lee MA, MD I'rolcssor Emeritus of Social Medicine and Senior .\dvtsor. Institute for Health Policy Studies, I `nivcrsity of California San Francisco School of \~cd~c~nc. San Francisco, CA 1c.1~ qucl Z. LeGeros BS, MS, PhD I'rolcssor, Department of Dental Materials Science ,ind Director, Research Center for Minority Oral I lc:ilth, New York University College of Dentistry, Ncn York. NY I).iv~tl Locker BDS, PhD i'rofcssor. Faculty of Dentistry University of Toronto, I~lronto. Canada `111.11 t l-ockwood DDS, MPH I)cntnl Officer/Epidemiologist, Division of Oral Health, ( cntcrs for Disease Control and Prevention, DHHS, .\tl.inta. GA I l.in)td 1.oe DDS Director Emeritus, National Institute of Dental and ~~r.mtofacial Research, National Institutes of Health, [)I IHS, Florida and Norway (1 \I .yana Lopez DDS, MPH I)ema1 Program Manager. City of Austin, Austin, TX wd D. Macek DDS, PhD. MPH .\sststant Professor. Department of Oral Health Care hind Delivery, University of Maryland School of Dcntisrry. Baltimore, MD i)~llOrCS ?.I. Malvitz DrPH c-litef. Surveillance Investigations and Research BrJnch. Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA h'nIllS E Mangan PhD Chief. Infectious Disease and Immunity Branch, rntlonal Institute of Dental and Craniofacial Research. xati"nal Institutes of Health, DHHS, Bethesda. MD Acknowledgments Kathleen Mangskau RDH, MPA Director, North Dakota Oral Health Program, North Dakota Department of Health, Bismarck, ND Georgetta Manning-Cox DDS, MPH Chairman, Community Dentistry and Associate Professor, Howard University College of Dentistry, Washington, DC Don Marianos DDS, MPH Consultant in Public Health, Pinetop, AZ Gary C. Martin DDS, MPH Lieutenant Colonel, U.S. Air Force, T&Service Center for Oral Health Studies, Uniformed Services University of the Health Sciences, Department of Defense, Bethesda, MD . Ricardo J. Martinez MD, MPH Director, Division of Extramural Research, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Richard Mascola DDS Private Practice, Jericho, NY Carolyn Beth Mazzella RN Assistant Surgeon General, USPHS, Office of the PHS Chief Nurse, Health Resources and Services Administration, DHHS, Rockville, MD Kim McFarland DDS, MS Dental Health Director, State of Nebraska, Nebraska Department of Health, Lincoln, NE J. Michael McGinnis MD Senior Vice President and Director, Health Group, The Robert Wood Johnson Foundation, Princeton, NJ Robert Mecklenburg DDS, MPH Coordinator, Tobacco and Oral Health Initiatives for the Tobacco Control Research Branch, National Cancer Institute, DHHS, Bethesda, MD Roseann Mulligan DDS, MS Professor and Chairman, Department of Dental Medicine and Public Health, University of Southern California School of Dentistry, Los Angeles, CA Juan M. Navia PhD Professor Emeritus, University of Alabama at Birmingham, Birmingham, AL Edward O'Neil PhD, MPA Professor, Dental Public Health and Hygiene, Director, Center for Health Professions, University of California, San Francisco, San Francisco, CA Roy C. Page DDS, PhD Professor, Departments of Periodontics and Pathology, Schools of Dentistry and Medicine, University of Washington, Seattle, WA No-Hee Park DMD, PhD Dean, School of Dentistry, University of California Los Angeles, Los Angeles, CA ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xv Acknowledgments Steven Perlman DDS, MScD Associate Professor of Pediatric Dentistry, Boston University Goldman School of Dental Medicine, Boston. MA Poul Erik Petersen DDS, Dr Odont Sci, BA, MSC Professor, University of Copenhagen, School of Dentistry, Copenhagen N, Denmark Kathy Phipps RDH, DrPH Associate Professor, Oregon Health Sciences University, Newport, OR Scott Presson DDS, MPH Captain, USPHS, Chief, Program Services Branch, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Francisco Ramos-Gomez DDS, MS, MPH Associate Professor, Department of Growth and Development, University of California San Francisco, San Francisco, CA E. Diane Rekow DDS, PhD Professor and Chair, Department of Orthodontics, University of Medicine and Dentistry of New Jersey, Newark, NJ Michael Rethman DDS, MS Colonel, U.S. Army, Chief of Periodontics, Tripler Dental Clinic, Honolulu, HI S. Timothy Rose DDS, MS Private Practice, Appleton, WI Bruce Rothwell DMD, MSD Associate Professor and Chairman, University of Washington, Restorative/Hospital Dentistry, Seattle, WA Shirley B. Russell PhD Professor and Chairperson, Department of Microbiology, Associate Dean for Research, Mehany Medical College, Nashville, TN Ann L Sandberg PhD Chief, Neoplastic Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Charles Sanders DDS Dean, Howard University College of Dentistry, Washington, DC Michele J. Saunders DMD, MS, MPH Endowed Professor of Clinical Dentistry, University of Texas Health Science Center, San Antonio, TX Crispian Scully MD, PhD, MDS Dean, Director of Studies and Research, International Centers for Excellence in Dentistry and Eastman Dental Institute for Oral Health Care Sciences, University College of London, London, England Leslie W. Seldin DDS, PC Private Practice, New York, NY Aubrey Sheiham BDS, PhD, DHC Professor, Department of Epidemiology and Public Health, University College London Medical School, London, England Cynthia Sherwood DDS Private Practice, Independence, KS Mark D. Siegal DDS, MPH Chief, Bureau of Oral Health Services, Ohio Department of Health, Columbus, OH Sol Silverman Jr. MA, DDS Professor of Oral Medicine, University of California San Francisco School of Dentistry, San Francisco, CA Susan E Silverton MD, PhD Assistant Professor and Enid Neidle Scholar, University of PennsylvaniaSchool of Dental Medicine. Philadelphia, PA Jeanne Sinkford DDS, MS, PhD Associate Executive Director, American Dental Education Association, Washington, DC Judy A. Small PhD Chief, Craniofacial Anomalies and Injuries Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Christian Stohler DMD, Dr.Med.Dent William R. Mann Professor and Chair, Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI George Stookey PhD Executive Associate Dean, Indiana University School of Dentistry, Indianapolis, IN Michael Till DDS, PhD Dean, University of Minnesota School of Dentistry, Minneapolis, MN Richard Valachovic DMD, MPH Executive Director, American Dental Education Association, Washington, DC Clemencia M. Vargas DDS, MPH, PhD Assistant Professor, University of Maryland School of Dentistry Baltimore, MD Rueben Warren DDS, MPH, DrPH Associate Administrator for Urban Affairs, The Agency for Toxic Substances and Disease Registry, DHHS, Atlanta, GA Reginald Wells PhD Deputy Commissioner, Administration for Children and Families, Administration on Developmental Disabilities, DHHS, Washington, DC Terrie Wetle PhD Deputy Director, National Institute on Aging, National Institutes of Health, DHHS, Bethesda, MD David A. Whiston DDS Private Practice, Falls Church, VA xvi ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL iiLicl~ \\`ilson DDS. MPH Bureau Chief, State of Connecticut Department of Pttblic Health, Avon, CT LL,,lncth ~1. Yamada MD, PhD Br.,nch Chief, Craniofacial Development Biology and Rcseneration. National Institute of Dental and crL,niofacial Research, National Institutes of Health, DHHS. Bethesda. MD EDITORIAL AND PRODUCTION ASSISTANTS Ihi Editorial Staff of the KEVRIC Company, Inc., ~ilvcr Spring, MD PROJECT ASSISTANTS \rinl' Brcncnbach \t.iirrlcc Champagne MA ~tt$~~mie A. Dopson MSW, MPH h.ittirrinc E. Krizek \I,ino I! Maertens I 11~~1~ \IcAllister JD I ,t't,rg:1;1 A. McIntyre ( .ltOcrinc YlcNish RDH, MHS FEDERAL COORDINATING COMMITTEE I (II\ :\lbarelli \g~ng Services Program Specialist, Administration on .\g~ng, DHHS. Washington, DC ( lil.rvl :\ustein-Casnoff MPH Ihrcctor, Public Health Policy, Office of the Assistant yccrcrav for Planning and Evaluation, DHHS, L\`:ishington, DC \\ 1111,1m E Benson \cting Principal Deputy Assistant Secretary for Aging (retired), Administration on Aging, DHHS, \\`,rshington, DC \I~lhmdas Bhat BDS, MDS, DrPH 4c.mor Science Advisor, Office of International ttealth Programs, U.S. Department of Energy, Gcrmsntown, MD [)~~I1113 Blum MS RD ~titrnionist, Department of Agriculture, --\lesandria, VA i-rlc Bothwell DDS, MPH, phD CJPtam USPHS, Assistant Chief, Dental Services Branch (retired), Indian Health Service, DHHS, Rockville, MD (1 Richard Buchanan DMD DePuty Director for Dentistry, Department of Veterans .iffairs, il?`ashington, DC ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments Claude Earl Fox MD, MPH Administrator, Health Resources and Services Administration, DHHS, Rockville, MD Patricia A. Grady PhD, RN, FAAN Director, National Institute of Nursing Research, National Institutes of Health, DHHS, Bethesda, MD Elizabeth Jacobson PhD Deputy Director for Science, Center for Devices and Radiological Health, Food and Drug Administration, DHHS, Rockville, MD Wanda K. Jones Dr. PH. Deputy Assistant Secretary for Health, Office of Women's Health, DHHS, Washington, DC Lireka P Joseph Dr. PH. Captain, USPHS. Director, Office of Health and Industry Programs, Center for Devices and Radiological Health, Food and Drug Administration, DHHS, Rockville, MD Douglas B. Kamerow MD, MPH Assistant Surgeon General USPHS, Director, Center for Practice and Technology Assessment, Agency for Healthcare Research and Quality, DHHS, Rockville, MD Mireille B. Kanda MD, MPH Director of Health and Disability Services, Head Start Bureau, Agency for Children, Youth, and Families, DHHS, Washington, DC Rod F Kirk DDS Captain, USPHS, Chief, Dental Program, Federal Bureau of Prisons, Department of Justice, Washington, DC Kenneth W Kizer MD, MPH Under Secretary for Health (retired), Department of Veterans Affairs, Washington, DC William Kohn DDS Captain, USPHS, Associate Director for Science, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Thomas M. I-eiendecker DDS, MPH Commander, U.S. Navy, Assistant Professor, Tri-Service Center for Oral Health Studies, Uniformed Services University of the Health Sciences, Department of Defense, Bethesda, MD Lawrence McKinley DDS Captain, U.S. Navy, Senior Consultant for Dentistry, Tricare Management ,4ctivity, Department of Defense, Falls Church, VA Edward Sondik PhD Director, National Center for Health Statistics, Centers for Disease Control and Prevention, DHHS, Hyattsville, MD xvii Acknowledgments Sue Swenson Commissioner, Administration on Developmental Disabilities, Administration for Children and Families, DHHS. Washington, DC Jeanette Takamura Ron J. Vogel Acting Deputy Administrator of the Food and Nutrition Programs, Food and Nutrition Service, Department of Agriculture, Alexandria, VA Assistant Secretary for Aging, Administration on Aging, DHHS, Washington, DC . . . XVIII , ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents Executive Summary THE CHALLENGE, 4 THE CHARGE, 4 THE SCIENCE BASE FOR THE REPORT, 5 ORGANIZATION OF THE REPORT, 5 Part One: What Is Oral Health? 5 Part Two: What Is the Status of Oral Health in America? 6' Part Three: What Is the Relationship Between Oral Health and General Health and Well-being? 6 Part Four: How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? 7 Part Five: What Are the Needs and Opportunities to Enhance Oral Health? 9 MAJOR FINDINGS, 10 A FRAMEWORK FOR ACTION, 11 CONCLUSION, 13 REFERENCES, 13 PROJECT TEAM, 13 2ART ONE ( lt;tptcr 1 WHAT IS ORAL HEALTH? The Meaning of Oral Health THE CHALLENGE, 19 THE CHARGE, 19 THE SCIENCE BASE FOR THE REPORT, 19 ORGANIZATION OF THE REPORT, 20 What Is Oral Health? 20 What Is the Status of Oral Health in America? 20 What Is the Relationship Between Oral Health and General Health and Well-being? 20 How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? 21 What Are the Needs and Opportunities to Enhance Oral Health? 21 A Call to Action, 21 The Craniofacial Complex CONTACT AND COMMUNICATION, 23 Taste and Smell, 23 Touch, Temperature, and Pain, 24 Speech, 25 THE ORAL GAVIN, 25 The Oral Mucosa, 25 The Teeth, 26 The Salivary Glands, 26 The Immune System, 27 15 17 23 ORAL HEALTH IN AMERICA: .X REPORT OF THE SURGEON GENERAL xix Contents CRANIOFACIAL ORIGINS, 28 Early Development, 29 Genetic Controls, 30 THE AGING OF CRANIOFACIAL TISSUES, 31 The Teeth, 31 The Jaws, 31 The Oral Mucosa, 32 Sensory and Motor Functioning, 32 The Salivary Glands, 32 FINDINGS, 32 REFERENCES. 33 PART TWO Chapter 3 WHAT IS THE STATUS OF ORAL HEALTH IN AMERICA? Diseases and Disorders , DENTAL AND PERIODONTAL INFECTIONS, 37 Dental Caries, 37 Periodontal Diseases, 39 SELECTED MUCOSAL INFECTIONS AND CONDITIONS, 42 Oral Candidiasis, 42 Herpes Simplex Virus Infections, 43 Oral Human Papillomavirus Infections, 43 Recurrent Aphthous Ulcers, 43 ORAL AND PHARYNGEAL CANCERS AND PRECANCEROUS LESIONS, 44 Heightening the Risk, 44 Prevention and Management, 47 DEVELOPMENTAL DISORDERS, 47 Craniofacial Anomalies Caused by Altered Branchial Arch Morphogenesis, 47 Cranial Bone and Dental Anomalies, 48 Craniofacial Defects Secondary to Other Developmental Disorders, 49 Craniofacial Manifestations of Single-Gene Defects, 49 INJURY, 50 Sports, 50 Falls, 50 Motor Vehicle Collisions, 50 Violence, 51 SELECTED CHRONIC AND DISABLING CONDITIONS, 51 Sjogren`s Syndrome, 51 Acute and Chronic Oral-Facial Pain, 52 Temporomandibular Disorders, 52 A MIRROR. A MODEL, AND A BETTER UNDERSTANDING OF DISEASES AND DISORDERS, 53 FINDINGS, 53 REFERENCES, 53 35 37 xx ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents Chapter -I The Magnitude of the Problem WHO HAS WHAT DISEASES AND CONDITIONS? 63 Dental Caries, Periodontal Diseases, and Tooth Loss, 63 Oral and Pharyngeal Cancers and Precancerous Lesions, 67 Selected Mucosal Infections and Diseases, 70 Developmental Disorders, 71 Injury, 72 Chronic and Disabling Conditions, 73 WHAT IS THE BURDEN OF DISEASE IN SELECTED POPULATIONS? CHALLENGES AND OPPORTUNITIES, 74 Racial and Ethnic Minorities, 74 Women's Health, 77 Individuals with Disabilities, 78 . UTILIZATION OF PROFESSIONAL CARE: WHAT DO WE KNOW ABOUT THE RELATIONSHIP OF ORAL HEALTH AND USE OF DENTAL SERVICES? 79 Dental Care Utilization, 80 Variation by Sex, Race/Ethnicity, Income, and Insurance, 81 61 Variation by Oral Health Status, 82 Reasons for Nonutilization, 83 Unmet Needs, 83 Outcomes of Appropriate Levels of Access and Utilization: An Example, 83 ORAL HEALTH STATUS IN CHANGING TIMES, 87 FINDINGS, 89 REFERENCES, 89 PART THREE t .Il;ipter 5 WHAT IS THE RELATIONSHIP BETWEEN ORAL HEALTH AND GENERAL HEALT.H AND WELL-BEING? Linkages with General Health THE MOUTH AND FACE AS A MIRROR OF HEALTH AND DISEASE, 97 95 97 Physical Signs and Symptoms of Disease and Risk Factors, 97 Oral Manifestations of HIV Infection and of Osteoporosis, 101 Oral-fluid-based Diagnostics: The Example of Saliva, 103 Conclusion, 104 THE MOUTH AS A PORTAL OF ENTRY FOR INFECTION, 104 Oral Infections and Bacteremia, 104 Oral Infections as a Result of Therapy, 105 Infective Endocarditis, 107 Oral Infections and Respiratory Disease, 108 Oral Transmission of Infections, 108 Conclusion, 109 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xxi Contents CRANIOFACIAL ORIGINS, 28 Early Development, 29 Genetic Controls, 30 THE AGING OF CRANIOFACIAL TISSUES, 31 The Teeth, 31 The Jaws, 31 The Oral Mucosa, 32 Sensory and Motor Functioning, 32 The Salivary Glands, 32 FINDINGS, 32 REFERENCES, 33 PART TWO Chapter 3 WHAT IS THE STATUS OF ORAL HEALTH IN AMERICA? Diseases and Disorders DENTAL AND PERIODONTAL INFECTIONS, 37 Dental Caries, 37 35 37 Periodontal Diseases, 39 SELECTED MUCOSAL INFECTIONS AND CONDITIONS, 42 Oral Candidiasis, 42 Herpes Simplex Virus Infections, 43 Oral Human Papillomavirus Infections, 43 Recurrent Aphthous Ulcers, 43 ORAL AND PHARYNGEAL CANCERS AND PRECANCEROUS LESIONS, 44 Heightening the Risk, 44 Prevention and Management, 47 DEVELOPMENTAL DISORDERS, 47 Craniofacial Anomalies Caused by Altered Branchial Arch Morphogenesis, 47 Cranial Bone and Dental Anomalies, 48 Craniofacial Defects Secondary to Other Developmental Disorders, 49 Craniofacial Manifestations of Single-Gene Defects, 49 INJURY, 50 Sports, 50 Falls, 50 Motor Vehicle Collisions, 50 Violence, 5 1 SELECTED CHRONIC AND DISABLING CONDITIONS, 51 Sjogren's Syndrome, 5 1 Acute and Chronic Oral-Facial Pain, 52 Temporomandibular Disorders, 52 A MIRROR, A MODEL, AND A BETTER UNDERSTANDING OF DISEASES AND DISORDERS, 53 FINDINGS, 53 REFERENCES, 53 xx ORAL HE4LTH IN .4MERICA: A REPORT OF THE SURGEON GENERAL Contents The Magnitude of the Problem WHO HAS WHAT DISEASES AND CONDITIONS? 63 Dental Caries, Periodontal Diseases, and Tooth Loss, 63 Oral and Pharyngeal Cancers and Precancerous Lesions, 67 Selected Mucosal Infections and Diseases, 70 Developmental Disorders, 71 Injury, 72 Chronic and Disabling Conditions, 73 WHAT IS THE BURDEN OF DISEASE IN SELECTED POPULATIONS? CHALLENGES AND OPPORTUNITIES, 74 Racial and Ethnic Minorities, 74 Women's Health, 77 Individuals with Disabilities, 78 UTILIZATION OF PROFESSIONAL CARE: WHAT DO WE * KNOW ABOUT THE RELATIONSHIP OF ORAL HEALTH AND USE OF DENTAL SERVICES? 79 Dental Care Utilization, 80 Variation by Sex, Race/Ethnicity, Income, and Insurance, 81 61 Variation by Oral Health Status, 82 Reasons for Nonutilization, 83 Unmet Needs, 83 Outcomes of Appropriate Levels of Access and Utilization: An Example, 83 ORAL HEALTH STATUS IN CHANGING TIMES, 87 FINDINGS, 89 REFERENCES, 89 PART THREE (.Iq)tcr 5 WHAT IS THE RELATIONSHIP BETWEEN ORAL HEALTH AND GENERAL HEALTH AND WELL-BEING? Linkages with General Health THE MOUTH AND FACE AS A MIRROR OF HEALTH AND DISEASE, 97 Physical Signs and Symptoms of Disease and Risk Factors, 97 Oral Manifestations of HIV Infection and of Osteoporosis, 101 Oral-fluid-based Diagnostics: The Example of Saliva, 103 Conclusion, 104 THE MOUTH AS A PORTAL OF ENTRY FOR INFECTION, 104 Oral Infections and Bacteremia, 104 Oral Infections as a Result of Therapy, 105 Infective Endocarditis, 107 Oral Infections and Respiratory Disease, 108 Oral Transmission of Infections, 108 Conclusion, 109 95 97 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xxi Contents ASSOCIATIONS AMONG ORAL INFECTIONS AND DIABETES, HEART DISEASE/STROKE, AND ADVERSE PREGNANCY OUTCOMES, 109 The Periodontal Disease-Diabetes Connection, 109 The Oral Infection-Heart Disease and Stroke Connection. 115 Periodontal Disease and Adverse Pregnancy Outcomes, 120 Conclusion, 122 Chapter 6 IMPLICATIONS OF THE LINKAGES, 122 FINDINGS, 123 REFERENCES, 123 Effects on Well-being and Quality of Life 133 THE CULTURAL CONTEXT, 134 Cultural Models, 134 e Combining Perspectives, 134 ORAL-HEALTH-RELATED QUALITY OF LIFE DIMENSIONS, 135 Functional Dimensions, 135 Psychosocial Dimensions, 137 Indirect Economic Costs, 142 RATINGS OF ORAL HEALTH, 144 Global Ratings, 144 Satisfaction Ratings, 144 ORAL-HEALTH-RELATED QUALITY OF LIFE MEASURES, 144 HEIGHTENED EXPECTATIONS, 146 FINDINGS, 146 REFERENCES, 147 PART FOUR Chapter 7 HOW IS ORAL HEALTH PROMOTED AND MAINTAiNED AND HOW ARE ORAL DISEASES PREVENTED? Community and Other Approaches to Promote Oral Health and Prevent Oral Disease WEIGHING THE EVIDENCE THAT INTERVENTIONS WORK, 155 153 155 PREVENTION AND CONTROL OF DENTAL CARIES, 158 Fluoride, 158 Fluoridation of Drinking Water, 160 School Water Fluoridation, 162 Dietary Fluoride Supplements, 162 Fluoride Mouthrinses, 165 Fluoride Varnishes, 165 Dental Sealants, 166 PREVENTION AND CONTROL OF PERIODONTAL DISEASES, 168 Community Programs to Prevent Gingivitis, 169 Prevention of Periodontitis, 169 Summary, 169 PREVENTION AND CONTROL OF ORAL AND PHARYNGEAL CANCERS, 169 Community-based Interventions, 170 Early Diagnosis of Oral and Pharyngeal Cancers, 171 Summary 172 xxii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents Chilpter 9 PREVENTION AND CONTROL OF CRANIOFACIAL BIRTH DEFECTS, 172 Summary, 173 PREVENTION AND CONTROL OF INTENTIONAL AND UNINTENTIONAL INJURY, 173 Craniofacial Injuries, 173 Summary: Prevention of Craniofacial Injuries, 176 ORAL HEALTH PROMOTION AND DISEASE PREVENTION KNOWLEDGE AND PRACTICES, 176 Dental Caries Prevention, 177 Periodontal Disease Prevention, 178 Oral Cancer Prevention and Early Detection, 178 Summary, 179 BUILDING UPON SUCCESS, 179 FINDINGS, 181 REFERENCES, 181 Personal and Provider Approaches to Oral Health INDIVIDUAL RESPONSIBILITY: PERSONAL APPROACHES TO ORAL HEALTH, 189 Daily Hygiene and Dental Caries Prevention, 189 Daily Hygiene and the Prevention of Periodontal Diseases, 190 Healthy Lifestyles, 190 Care Seeking, 190 PROVIDER-BASED CARE, 191 Risk Assessment, 192 Diagnostic Tests, 193 Oral Health Assessment, 193 Changing Approaches to Selected Diseases and Conditions, 196 Chronic'Craniofacial Pain and Sensorimotor Conditions, 211 Temporomandibular Disorders, 211 Mucosal and Autoimmune Diseases, 212 FACTORS AFFECTING FUTURE HEALTH CARE PRACTICES, 212 Evidence-based Practice, 213 Clinical Practice Guidelines, 213 Science and Technology Contributions, 214 Broadening the Base for the Provision of Oral Health Care, 216 FINDINGS, 216 REFERENCES, 216 Provision of Oral Health Care COMPONENTS OF PROFESSIONAL CARE, 223 The Dental Component, 223 The Medical Component, 225 The Public Health Component, 225 Areas of Overlap, 227 EXPENDITURES FOR ORAL HEALTH CARE, 227 FINANCING AND REIMBURSEMENT, 229 Insurance, 229 The Changing Market, 231 Federal and State Programs, 233 189 223 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL . . . XXIII Contents FACTORS AFFECTING THE CAPACITY TO MEET ORAL HEALTH NEEDS, 234 Numbers of Dental Personnel, 235 Sex and Racial/Ethnic Composition of Dental Personnel, 236 Student Indebtedness and Its Effects, 237 Personnel Needs for Faculty and Clinical Research, 238 Curriculum Needs, 238 Taking Care of Those Most in Need, 239 TWENTY-FIRST CENTURY CHALLENGES: WHAT LIES AHEAD? 239 FINDINGS, 240 REFERENCES, 241 PART FIVE Chapter 10 WHAT ARE THE NEEDS AND OPPORTUNITIES TO ENHANCE ORAL HEALTH? Factors Affecting Oral Health over the Life Span HEALTH IN THE CONTEXT OF SOCIETY, 245 Historical Models, 245 Contemporary Models, 246 CHANGING VULNERABILITIES THROUGHOUT LIFE, 249 Children, 249 Adolescents and Young Adults, 257 Midlife Adults, 258 Chapter 11 Chapter 12 Older Americans, 262 ACHIEVING ORAL HEALTH THROUGHOUT LIFE, 267 FINDINGS, 269 REFERENCES, 269 Facing the Future THE PAST AND PRESENT AS PROLOGUE, 275 The Pioneers, 275 Vital Statistics, 275 Health Improvement, 276 DIVERSITY OF DISEASES AND PATIENTS, 276 TRANSFORMING TREATMENTS, 276 TRANSFORMING HEALTH PROFESSIONAL EDUCATION, 276 TRANSFORMING HEALTH CARE, 277 ORAL HEALTH-NOT YET FOR ALL, 277 HOPE FROM SCIENCE AND TECHNOLOGY, 278 A FRAMEWORK FOR ORAL HEALTH, 280 REFERENCES, 281 A Call to Action MAJOR FINDINGS, 283 A FRAMEWORK FOR ACTION, 284 CONCLUSION, 287 Index 243 245 275 283 289 xxiv ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary publication of this first Surgeon Generals Report on Oral Health marks a milestone in the history of oral health in America. The report elaborates on the meaning of oral health and explains why oral health is essential to general health and well-being. In the course of the past 50 years, great progress has been made in understanding the common oral diseases- dental caries (tooth decay) and periodontal (gum) diseases-resulting in marked improvements in the nations oral health. Most middle-aged and younger Americans expect to retain their natural teeth over their lifetime and do not expect to have any serious oral health problems. The major message of this Surgeon Generals report is that oral health is essential to the general health and well-being of all Americans and can be achieved by all Americans. However, not all Americans are achieving the same degree of oral health. In spite of the safe and effective means of maintaining oral health that have benefited the majority of Americans over the past half century, many among us still experience needless pain and suffering, complications that devastate overall health and well-being, and financial and social costs that diminish the quality of life and burden American society. What amounts to "a silent epidemic" of oral diseases is affecting our most vulnerable citizens- poor children, the elderly, and many members of racial and ethnic minority groups (GAO 2000). (See box entitled "The Burden of Oral Diseases and Disorders.") The word oval refers to the mouth. The mouth includes not only the teeth and the gums (gingiva) and their supporting tissues, but also the hard and soft palate, the mucosal lining of the mouth and throat, the tongue, the lips, the salivary glands, the chewing muscles, and the upper and lower jaws. Equally important are the branches of the nervous, immune, and vascular systems that animate, protect, and nourish the oral tissues, as well as provide con- nections to the brain and the rest of the body. The genetic patterning of development in utero further reveals the intimate relationship of the oral tissues to the developing brain and to the tissues of the face and head that surround the mouth, structures whose location is captured in the word craniofacial. A major theme of this report is that oral health means much more than healthy teeth. It means being free of chronic oral-facial pain conditions, oral and pharyngeal (throat) cancers, oral soft tissue lesions, birth defects such as cleft lip and palate, and scores of other diseases and disorders that affect the oral, dental, and craniofacial tissues, collectively known as the craniofacial complex. These are tissues whose functions we often take for granted, yet they represent the very essence of our humanity. They allow us to speak and smile; sigh and kiss; smell, taste, touch, chew, and swallow; cry out in pain; and convey a world of feelings and emotions through facial expressions. They also provide protection against microbial infections and environmental insults. The craniofacial tissues also provide a useful means to understanding organs and systems in less accessible parts of the body. The salivary glands are a model of other exocrine glands, and an analysis of saliva can provide telltale clues of overall health or disease. The jawbones and their joints function like other musculoskeletal parts. The nervous system apparatus underlying facial pain has its counterpart in nerves elsewhere in the body. A thorough oral examination can detect signs of nutritional defi- ciencies as well as a number of systemic diseases, including microbial infections, immune disorders, injuries, and some cancers. Indeed, the phrase the mouth is a mirror has been used to illustrate the wealth of information that can be derived from examining oral tissues. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 1 Executive Summar) New research is pointing to associations between chronic oral infections and heart and lung diseases, stroke, and low-birth-weight, premature births. Associations between periodontal disease and dia- betes have long been noted. This report assesses these associations and explores mechanisms that might explain the oral-systemic disease connections. The broadened meaning of oral henlth parallels the broadened meaning of Ilealth. In 1948 the World Health Organization expanded the definition of health to mean "a complete state of physical, mental, and social well-being, and not just the absence of infirmity." It follows that oral health must also include well-being. Just as we now understand that nature and nurture are inextricably linked, and mind and body are both expressions of our human biology, so, too, we must recognize that oral health and general health are inseparable. We ignore signs and symptoms of oral disease and dysfunction to our The Burden of Oral Diseases and Disorders Oral diseases are progressive and cumulative and become more com- plex over time.They can affect our ability to eat,the foods we choose, how we look, and the way we communicate.These diseases can affect economic productivity and compromise our ability to work at home, at school, or on the job. Health disparities exist across population groups at all ages. Over one third of the U.S. population (100 million people) has no access to community water fluoridation. Over 108 million chil- dren and adults lack dental insurance, which is over 2.5 times the num- ber who lack medical insurance. The following are highlights of oral. health data for children, adults, and the elderly. (Refer to the full report for details of these data and their sources.) Children o Cleft lip/palate, one of the most common birth defects, is esti- mated to affecl 1 out of 600 live births for whites and 1 out of 1,850 live births for African Americans. o Other birth defects such as hereditary ectodermal dysplasias, where all or most teeth are missing or misshapen,cause lifetime prob- lems that can be devastating to children and adults. o Dental caries (tooth decay) is the single most common chronic childhood disease-5 times more common than asthma and 7 times more common than hay fever. o Over 50 percent of 5- to g-year-old children have at least one cavity or filling, and that proportion increases to 78 percent among 17- year-olds. Nevertheless, these figures represent improvements in the oral health of children compared to a generation ago. o There are striking disparities in dental disease by income. Poor children suffer twice as much dental caries as their more affluent peers, and their disease is more likely to be untreated.These poor-nonpoor detriment. Consequently, a second theme of the report is that oral health is integral to general health. You cannot be healthy without oral health. Oral health and general health should not be interpreted as separate entities. Oral health is a critical component of health and must be included in the provision of health care and the design of community programs. The wider meanings of oral and health in no wa) diminish the relevance and importance of the t\vo leading dental diseases, caries and the periodontal diseases. They remain common and widespread. affecting nearly everyone at some point in the life span. What has changed is what we can do about them. Researchers in the 1930s discovered that people living in communities with naturally fluoridated water supplies had less dental caries than people drinking unfluoridated water. But not until the end differences continue into adolescence. One out of four children in America is born into poverty,and children living below the poverty line (annual income of $17,000 for a family of four) have more severe and untreated decay. o Unintentional injuries,manyofwhich include head,mouth,and neck injuries, are common in children. o Intentional injuries commonly affect the craniofacial tissues. o Tobacco-related oral lesions are prevalent in adolescents who currently use smokeless (spit) tobacco. o Professional care is necessary for maintaining oral health, yet 25 percent of poor children have not seen a dentist before entering kindergarten. o Medical insurance is a strong predictor of access to dental care. Uninsured children are 2.5 times less likely than insured children to receive dental care.Children from families without dental insurance are 3 times more likely to have dental needs than children with either pub- lic or private insurance. For each child without medical insurance, there are at least 2.6 children without dental insurance. o Medicaid has not been able to fill the gap in providing dental care to poor children. Fewer than one in five Medicaid-covered children received a single dental visit in a recent year-long study period. Although new programs such as the State Children's Health Insurance Program WHIP) may increase the number of insured children, many will still be left without effective dental coverage. o The social impact of oral diseases in children is substantial. More than 51 million school hours are lost each year to dental-related illness. Poor children suffer nearly 12 times more restricted-activity days than children from higher-incomefamilies.Pain and suffering due to untreated diseases can lead to problems in eating, speaking, and attending to learning. 2 ORAL HEi4LTH IN .4MERIC;\: A REPORT OF THE SURGEON GENERAL - Executive Summary (,f \\.-orld War 11 were the investigators able to design ,Ind implement the community clinical trials that , which could result in reduced lubrication and contribute to a sensation of mouth dryness. There are also subtle changes in the protective ability of sali- vary secretory IgA antibody (Smith et al. 1987). FINDINGS Natural selection has served Homo sapiens well in evolving a craniofacial complex with remarkable functions and abilities to adapt, enabling the organ- ism to meet the challenges of an ever-changing envi- ronment. An examination of the various tissues reveals elaborate designs that have evolved to serve the basic needs and functions of a complex mammal as well as those that are uniqely human, such as 32 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL speech. The rich distribution of nerves, muscles, and blood vessels in the region as well as extensive endocrine and immune system connections is an indication of the vital role of the craniofacial complex in adaptation and survival over a long life span. In particular, o Genes controlling the basic patterning and segmental organization of human development, and specifically the craniofacial complex, are highly con- served in nature. Mutated genes affecting human development have counterparts in many simpler organisms. . There is considerable reserve capacity or redundancy in the cells and tissues of the craniofacial complex, so that if they are properly cared for, the structures should function well over a lifetime. 0 The salivary glands and saliva subserve tast- ing and digestive functions and also participate in the mucosal immune system, a main line of defense against pathogens, irritants, and toxins. o Salivary components protect and maintain oral tissues through antimicrobial components, buffering agents, and a process by which dental enamel can be remineralized. REFERENCES .Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson JD. Cellular mechanisms of development. In: Molecular biology of the cell. 3rd ed. New York: Garland; 1994. p. 1036-137. Baron S, Poast J, Cloyd MW. Why is HIV rarely trans- mitted by oral secretions? Saliva can disrupt orally shed, infected leukocytes. Arch Intern Med 1999 Feb 8;159(3):303-10, Bhaskar SN. Maxilla and mandible (alveolar process). In: Bhaskar SN. editor. Orban's oral histology and embryology. St. Louis (MO): Mosby Year Book; 1991. p. 239-59. Bhaskar SN, Orban BJ. Orban's oral histology and embryology. 11th ed. St. Louis (MO): Mosby Year Book; 1990. Chapter 1, Development of the face and oral cavity. Baum BJ. Age changes in salivary glands and salivary secretions. In Holm-Pederson P, Lee H, editors. Geriatric dentistry Copenhagen: Munksgaard; 1986. p. 114-22. Baiim BJ and O'Connell BC. The impact of gene thera- py on dentistry J Am Dent Assoc 1995:126:179-89. Caterina MJ, Schumacher MA, Tominaga M, Rosen TA, Levine JD, Julius D. The capsaicin receptor: a heat- activated ion channel in the pain pathway Nature I997;389:816-24. Hajishengallis G, and Michalek SM. Current status of a mucosal vaccine against dental caries. Oral Microbial Immunol 1999;14:1-20. The Craniofacial Complex Johansson CB, Momma S, Clarke DL, Rishng M, Lendahl U, Frisen J. Identification of a neural stem cell in the adult mammalian central nervous system. Cell 1999 Jan 8;96( 1):25-34. Kroes I, Lepp PW, Relman DA. Bacterial diversity with- in the human subgingival crevice. Proc Nat1 Acad Sci USA 1999 Dee 7;96(25):14547-52. Lamkin MS, Oppenheim FG. Structural features of sali- vary function. Crit Rev Oral Biol Med 1993;4(3- 4):251-9. Mandel ID. The role of saliva in maintaining oral home- ostasis. J Am Dent Assoc 1989 Aug;119:298-304. Mandel ID, Ellison SA. The biological significance of the nonimmunoglobulin defense factors. In: Pruit K, Tenovuo J, editors. The lactoperoxidase system. New York: Marcel Dekker; 1985. p. 1-14. McGhee JR, Kiyono H. The mucosal immune system. In: Paul WE, editor. Fundamental immunology. 4th ed. New York: Lippincott-Raven; 1999. p. 909-45. Mestecky J. The common mucosal immune system and current strategies for induction of immune respons- es in external secretions. J Clin Immunol 1987 Jul;7(4):265-76. Mestecky J, Russell MW Mucosal immunoglobulins and their contribution to defense mechanisms: an overview. Biochem Sot Trans 1997 May;25(2):457- 62. Mjor IA. Age changes in the teeth. In: Holm-Pedersen P, Liie H, editors. Geriatric dentistry. Copenhagen: Munksgaard; 1986. p. 94-101. Navazesh M, Mulligan RA, Kipnis V, Denny PA, Denny PC. Comparison of whole saliva flow rates and mucin concentrations in healthy Caucasian young and aged adults. J Dent Res 1992 Jun;71(6):1275-8. Oberg S. Dissector for Netter's atlas of human anatomy: discussions. Vol 2. Summit (NJ): Ciba-Geigy; 1994. Sadler Tw, Langman J. Langman's medical embryology Baltimore: Williams & Wilkins; 1995. Sarosiek J, Scheurich CJ, Marcinkiewicz M, McCaIlum RW. Enhancement of salivary esophagoprotection: rationale for a physiological approach to gastroe- sophageal reflux disease. Gastroenterology 1996;110:675-81. Ship JA. The oral cavity In: Hazzard WR et al., editors. Principles of geriatric medicine and gerontology. New York: McGraw-Hill; 1999. Shugars DC, Wahl SM. The role of the oral environment in HIV-l transmission. J Am Dent Assoc 1998 Ju1;129(7):851-8. Smith DJ, Taubman MA, Ebersole JL. Ontogeny and senescence of salivary immunity J Dent Res 1987 Feb(2);66:451-6. Tabak L. In defense of the oral cavity: structure, biosyn- thesis, and functions of salivary mucins. Annu Rev Physiol 1995;57:547-64. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 33 The Craniofacial Complex Taichman NS. Cruchley AT, Fletcher LM. Hagi-Pavli EP Paleolog EM. Abrams WR, Booth V, Edwards RM, Malamud D. Vascular endothelial growth factor in normal salivary glands and saliva: a possible role in the maintenance of mucosal homeostasis. Lab Invest 1998 Ju1;78(7):869-75. Wilentz J. The senses of man. New York: Thomas Y. Crowell; 1968. Xu T, Levitz SM, Diamond RD, Oppenheim FG. Anticandidal activity of major human salivav his- tatins. Infect Immun 1991 Aug;59(8):2549-54. Young PT. Role of hedonic processes in development of sweet taste. In: Weiffenbach, JM, editor. Taste and development-the genesis of sweet preference. Bethesda (MD): National Institutes of Health, Public Health Service, U.S. Department of Health. Education and Welfare Report no. NIH 77-1068; 1977. p. 399-417. Zelles T, Purushotham KR, Macauley SP Oxford GE, Humphreys-Beher MG. Saliva and growth factors: the fountain of youth resides in us all. J Dent Res 1995 Dec;74( 12):1826-32. Zero DT. Etiology of dental erosion-extrinsic factors. Eur J Oral Sci 1996 Apr;104(2 Pt 2):162-77. 34 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL What Is the Status of Oral Health in America? To begin to answer this question, Chapter 3 guides the reader through a discussion of oral diseases and disorders in such categories as infections, inherited disorders, and neoplasms. Whether or not an individual succumbs to the disease or disorder in question depends on subtle interactions of genetic, environmental, and behavioral variables. Risk factors common to systemic diseases and disorders, such as tobacco use, excessive alcohol use, and inappropriate dietary practices, also contribute to many oral diseases and disorders. As more details on the causes of diseases unfold, specific strategies for disease prevention can be developed. Chapter 4 describes the magnitude of the problem facing the nation due to oral diseases and disorders. These conditions are prevalent and complex, and they affect individuals across the life span. Although major improvements have been seen nationally for most Americans, disparities exist in some population groups as classified by age, sex, income, and race/ethnicity. National and state-based epidemiologic data presented against the backdrop of demographic and socioeconomic variables provide some information on racial and ethnic minorities, but serious shortcomings exist. The paucity of data at national, state, and local levels extends to other populations, including indi- viduals with disabilities, those with alternate sexual orientation, migrant populations, and the homeless, and limits the capacity to fully document the magnitude of the problem and develop needed programs. The chapter provides a basis for understanding disparities in oral health by pre- senting available data on dental visits. More work is needed to understand the dimensions of oral health problems in the United States and the reasons for differences among populations. OR4L Hl%4LTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 35 Diseases and Disorders As the gateway to the body, the mouth is challenged by a constant barrage of invaders-bacteria, viruses, parasites, fungi. Thus infectious diseases, notably dental caries and periodontal diseases, predominate among the ills that can compromise oral health. Injuries take their toll as well, with the face and head particularly vulnerable to sports injuries, motor vehi- cle crashes, violence, and abuse. Less common but very serious are oral and pharyngeal cancers, with a 5-year survival rate of hardly better than 50 percent (Kosary et al. 1995). Birth defects and developmental disorders frequently affect the craniofacial complex. These appear most commonly as isolated cases of cleft lip or palate, but clefting or other craniofacial defects can also be part of complex hereditary dis- eases or syndromes. Additionally, acute and chronic pain can affect the oral-facial region, particulaily in and around the temporomandibular (jaw) joint, and accounts for a disproportionate amount of all types of pain that drive individuals to seek health care. Many systemic diseases such as diabetes, arthri- tis, osteoporosis, and AIDS, as well as therapies for systemic diseases, can directly or indirectly compro- mise oral tissues. The World Health Organization's International Classification of Diseases and Stomatology currently lists more than 120 specific diseases, distributed in 10 or more classes, that have manifestations in the oral cavity (WHO 1992). This chapter concentrates on six major oral dis- ease categories: dental and periodontal infections; mucosal disorders; oral and pharyngeal cancers; developmental disorders; injuries; and a sampling of chronic and disabling conditions, including Sjiigren's syndrome and oral-facial pain. DENTAL AND PERIODONTAL INFECTIONS The most common oral diseases are dental caries and the periodontal diseases. Individuals are vulnerable to dental caries throughout life, with 85 percent of adults aged 18 and older affected. Periodontal dis- eases are most often seen in maturity, with the major- ity of adults experiencing some signs and symptoms by the mid-30s. Certain rare forms of periodontal dis- ease affect young people. The major oral health suc- cess story of the past half century is that both caries and periodontal diseases can be prevented by a com- bination of individual, professional, and community measures. Dental Caries The word.caries derives from the Latin for rotten, and many cultures early on posited a tooth worm as the cause of this rottenness. By the twentieth century, caries came to describe the condition of having holes in the teeth-cavities. This description, although not incorrect, is misleading. In actuality, a cavity is a late manifestation of a bacterial infection. The bacteria colonizing the mouth are known as the oral flora. They form a complex community that adheres to tooth surfaces in a gelatinous mat, or biofilm, commonly called dental plaque. A cariogenic biofilm at a single tooth site may contain one-half- billion bacteria, of which species of mutans streptococci are critical components. These bacteria are able to ferment sugars and other carbohydrates to form lactic and other acids. Repeated cycles of acid generation can result in the microscopic dissolution of minerals in tooth enamel and the formation of an opaque white or brown spot under the enamel surface (Mandel 1979). Frequency of carbohydrate consumption (Gustafsson et al. 1954), physical ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 37 Diseases and Disorders characteristics of food (e.g., stickiness), and timing of food intake (Burt and Ismail 1986) also play a role. The essential role of bacteria in caries initiation was established in landmark experiments in the 1950s. Investigators observed that germ-free ani- mals fed high-sugar diets remained caries-free until the introduction of mutans streptococci (a particular group of bacterial strains having a number of com- mon characteristics, and which adhere tightly to the tooth). Later experiments demonstrated the trans- missibility of the bacteria from mother to litter and from caries-infected to uninfected cage-mates (Fitzgerald and Keyes 1960). Species of Lactobacillus, Actinomyces. and other acid-producing streptococci within the plaque may also contribute to the process (Bowden 1990). If the caries infection in enamel goes unchecked, the acid dissolution can advance to form a cavity that can extend through the dentin (the component of the tooth located under the enamel) to the pulp tissue, which is rich in nerves and blood vessels. The result- ing toothache can be severe and often is accompanied by sensitivity to temperature and sweets. Treatment requires endodontic (root canal) therapy. If untreat- ed, the pulp infection can lead to abscess, destruction of bone, and spread of the infection via the blood- stream. Dental caries can occur at any age after teeth erupt. Particularly damaging forms can begin early, when developing primary teeth are especially vulner- able. This type of dental caries is called early child- hood caries (ECC). Some 6 out of 10 children in the United States have one or more decayed or filled pri- mary teeth by age 5 (U.S. Department of Health and Human Services, National Center for Health Statistics 1997). EGG may occur in children who are given pacifying bottles of juice, milk, or formula to drink during the day or overnight. The sugar con- tents pool around the upper front teeth, mix with cariogenic bacteria, and give rise to rapidly progress- ing destruction (Ripa 1988). Other risk factors for ECC include arrested development of tooth enamel, chronic illness, altered salivary composition and vol- ume (resulting from the use of certain medications or malnourishment), mouth breathing, and blockage of saliva flow in a bottle-fed infant (Bowen 1998, Seow 1998). Although there have been continuing reductions in dental caries in permanent teeth among children and adolescents over the past few decades, caries prevalence in the primary dentition may have stabi- lized or increased slightly in some population groups (Petersson and Bratthall 1996, Rozier 1995). Reductions in caries in permanent teeth also have been proportionately greater on the smooth surfaces rather than on the pit-and-fissure surfaces character- istic of chewing surfaces. The gingival tissues tend to recede over time, exposing the tooth root to cario- genie bacteria that can cause root caries. An impor- tant risk factor for root caries in older people is the use of medications that inhibit salivary flow, leading to dry mouth (xerostomia). Saliva contains components that can directly attack cariogenic bacteria, and it is also rich in calci- um and phosphates that help to remineralize tooth enamel. Demineralization of enamel occurs when pH levels fall as a result of acid production by bacteria. It can be reversed at early stagesif the local environ- ment can counteract acid production, restoring pH to neutral levels. Remineralization can occur through the replacement of lost mineral (calcium and phos- phates) from the stores in saliva. Fluoride in saliva and dental plaque and the buffering capacity of sali- va also contribute to this process. Indeed. it is now believed that fluoride exerts its chief caries-preven- tive effect by facilitating remineralization. Several studies have demonstrated that remineralization results in an increase in tooth hardness and mineral content. rendering the tooth surface more resistant to subsequent acid attack (Larsen 1987, Linton 1996, Retief 1983, Shannon 1978, Vissink et al. 1985, White 1988). Overt caries lesions develop when there is insuf- ficient time for remineralization between periods of acidogenesis, or when the saliva production is com- promised. Over 400 medications list dry mouth as a side effect, notably some antidepressants, antipsy- chotics, antihistamines, decongestants, antihyperten- sives, diuretics, and antiparkinsonian drugs (Sreebny et al. 1992). The effects of xerostomia may be partic- ularly severe in cancer patients receiving radiation to the head or neck because the rays can destroy sali- vary gland tissue rather than simply inhibiting sali- vary secretion. The professional application of dental sealants (plastic films coated onto the chewing surfaces of teeth) is an important caries-preventive measure that complements the use of fluorides, The films prevent decay from developing in the pits and fissures of teeth, channels that are often inaccessible to brushing and where fluoride may be less effective. The rate of caries progression through enamel is relatively slow (Berkey 1988, Ekanayake 1987, Shwartz et al. 1984) and may be slower in patients who have received regular fluoride treatment or who consume fluoridated water (Pitts 1983, Shwartz et al. 1984). Because a large percentage of enamel lesions remain unchanged over periods of 3 to 4 years, and 38 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders because progression rates through dentin are comparably slow (Craig et al. 1981, Emslie 1959, Kolehmainen and Rytomaa 1977), the application of infection control and monitoring procedures to assess caries risk status, lesion activity status, evidence of lesion arrest, and evidence of lesion remrneralization over extended periods of time is recommended. Experts believe that the earlier mutans strepto- cocci are acquired in infancy, the higher the caries risk. Most studies indicate that infants are infected before their first birthday, around the time the first incisors emerge. However, one study found the medi- an age of acquisition to be 26 months, coinciding with the emergence of the primary molars (Bowen 1998, Caufield et al. 1993, Seow 1998). DNA finger- printing has demonstrated that the source of trans- mission is usually the mother (Caufield et al. 1993). It is not clear why some individuals are more sus- ceptible and others more resistant to caries. Genetic differences in the structure and biochemistry of enamel proteins and crystals (Slavkin 1988), as well as variations in the quality and quantity of saliva and in immune defense mechanisms are among the fac- tors under study. Analysis of mutans streptococci genomes may also shed light, indicating which species are particularly virulent and which genes contribute to that virulence. Even the most protective genetic endowment and developmental milieu are unlikely to confer resistance to decay in the absence of positive person- al behaviors. These include sound dietary habits and good oral hygiene, including the use of fluorides, and seeking professional care. There are indications, however, that some destructive oral habits are on the rise, such as the use of smokeless (spit) tobacco products by teenage boys. Although the chief con- cern here lies in the long-term risk for oral cancers, spit tobacco that contains high levels of sugar is also associated with increased levels of decay of both crown and root surfaces (Tomar and Winn 1998). Periodontal Diseases Like dental caries, the periodontal diseases are infec- tions caused by bacteria in the biofilm (dental plaque) that forms on oral surfaces. The basic divi- sion in the periodontal diseases is between gingivitis, which affects the gums, and periodontitis, which may involve all of the soft tissue and bone supporting the teeth. Gingivitis and milder forms of periodontitis are common in adults. The percentage of individuals with moderate to severe periodontitis, in which the destruction of supporting tissue can cause the tooth to loosen and fall out, increases with age. Gingivitis Gingivitis is an inflammation of the gums character- ized by a change in color from normal pink to red, with swelling, bleeding, and often sensitivity and ten- derness. These changes result from an accumulation of biofilm along the gingival margins and the immune system's inflammatory response to the release of destructive bacterial products. The early changes of gingivitis are reversible with thorough toothbrushing and flossing to reduce plaque. Without adequate oral hygiene, however, these early changes can become more severe, with'infiltration of inflammatory cells and establishment of a chronic infection. Biofilm on tooth surfaces opposite the openings of the salivary glands often mineralizes to form calculus or tartar, which is covered by unmin- eralized biofilm-a combination that can exacerbate local inflammatory responses (Mandel 1995). A gin- gival infection may persist for months or years, yet never progress to periodontitis. Gingival inflammation does not appear until the biofilm changes from one composed largely of gram- positive streptococci (which can live with or without oxygen) to one containing gram-negative anaerobes (which cannot live in the presence of oxygen). Numerous attempts have been made to pinpoint which microorganisms in the supragingival (above the gum line) plaque are the culprits in gingivitis. Frequently mentioned organisms include Fusobacterium nucleatum, Veillonella parvula, and species of Campylobacter and Treponema. But as Ranney (1989) notes, "The complexity of the results defies any attempt to define a discrete group clearly and consistently associated with gingivitis." Gingival inflammation may be influenced by steroid hormones, occurring as puberty gingivitis, pregnancy gingivitis, and gingivitis associated with birth control medication or steroid therapy. The pres- ence of steroid hormones in tissues adjacent to biofilm apparently encourages the growth of certain bacteria and triggers an exaggerated response to biofilm accumulation (Caton 1989). Again, thorough oral hygiene can control this response. Certain prescription drugs can also lead to gingi- val overgrowth and inflammation. These include the antiepileptic drug phenytoin (Dilantin); cyclosporin, used for immunosuppressive therapy in transplant patients; and various calcium channel blockers used in heart disease. Treatment often requires surgical removal of the excess tissue followed by appropriate personal and professional oral health care. ORAL HEtZLTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 39 Diseases and Disorders A form of gingivitis common 50 years ago but relatively rare today is acute necrotizing ulcerative gingivitis, also known as Vincent's infection or trench mouth. This aggressive infection is characterized by destruction of the gingiva between the teeth, sponta- neous bleeding, pain, and oral odor. People under extreme stress have an increased susceptibility. Spirochetes and other bacteria have been found in the connective tissue of those affected. An associa- tion between smoking and this type of gingivitis is well recognized and was demonstrated as early as 1946 (Pindborg 1947, 1949). This condition has been seen in some HIV-positive patients (Murray 1994). Treatment requires a combination of profes- sional periodontal treatment and antibacterial thera- py along with professional smoking cessation assis- tance as appropriate. Adult Periodontitis The most common form of adult periodontitis is described as general and moderately progressing; a second form is described as rapidly progressing and severe, and is often resistant to treatment. The mod- erately progressive adult form is characterized by a gradual loss of attachment of the periodontal liga- ment to the gingiva and bone along with loss of the supporting bone. It is most often accompanied by gingivitis (Genco 1990). It is not necessarily preced- ed by gingivitis, but the gingivitis-related biofilm often seeds the subgingival plaque. The destruction of periodontal ligament and bone results in the for- mation of a pocket between the tooth and adjacent tissues, which harbors subgingival plaque. The cal- culus formed in the pocket by inflammatory fluids and minerals in adjacent tissues is especially damag- ing (Mandel and Gaffar 1986). The severity of periodontal disease is determined through a series of measurements, including the extent of gingival inflammation and bleeding, the probing depth of the pocket to the point of resist- ance, the clinical attachment loss of the periodontal ligament measured from a fixed point on the tooth (usually the cemento-enamel junction), and the loss of adjacent alveolar bone as measured by x-ray (Genco 1996). Severity is determined by the rate of disease progression over time and the response of the tissues to treatment. Adult periodontitis often begins in adolescence but is usually not clinically significant until the mid- 30s. Prevalence and severity increase but do not accelerate with age (Beck 1996). One view proposes that destruction occurs at a specific site during a defined period, after which the disease goes into remission (Socransky et al. 1984). The current view is that the disease process may not be continuous but rather progresses in random bursts in which short periods of breakdown of periodontal ligament and bone alternate with periods of quiescence. These episodes occur randomly over time and at random sites in the mouth. Part of the difficulty in determin- ing the pattern of progression reflects variation in the sensitivity of the instruments used to measure the loss of soft tissue and bone. The latest generation of probes finds evidence of both continuous and multi- ple-burst patterns of loss in different patients and at different times (Jeffcoat and Ready 1991). Most researchers agree that periodontitis results from a mixed infection but that a particular group of gram-negative bacteria are key to the process and markedly increase in the subgingival plaque. The bacteria most frequently cited are Porphyromonas gin- givalis, Prevotella intermedia, Bacteroides forsythus, Treponema denticola, and Actinobacillus actino- mycetemcomitans (Genco 1996). Their role in disease initiation and progression is determined in part by their "virulence factors." These include the ability to colonize subgingival plaque, generate products that can directly injure tissues, and elicit an inflammatory or immune response. The potentially noxious bacte- rial products include hydrogen sulfide, polyamines, the fatty acids butyrate and propionate, lipopolysac- charide (also known as endotoxin), and a number of destructive enzymes. The interaction of this arsenal with the host response is at the core of periodontal pathology (Genco 1992, Socransky and Haffajee 1991, 1992). Sequencing of the genomes of several key periodontal pathogens is under way and should provide further insight into these pathogens as well as catalyze new treatment approaches. Delicate Balances. Neutrophils (a type of white blood cell) and antibodies are the major immune defenses against bacterial attack. Neutrophils move to the site of infection, where they engulf bacteria and elaborate antibacterial agents and enzymes to destroy bacteria. Although stimulation of the immune system to attack the offending bacteria is generally protective, immune hyperresponsiveness and hypersensitivity can be counterproductive, leading to the destruction of healthy tissue. Nevertheless, the neutrophiuanti- body axis is critical for full protection against peri- odontal diseases (Genco 1992). Also important is the release of certain potent molecules called cytokines and prostaglandins, especially prostaglandin E2 (PGE,) which can contribute to tissue destruction. Cytokines are proteins secreted by immune cells that help regulate immune responses and also affect bone, epithelial, -lo ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and connective tissues. Most prominent in periodontal diseases are interleukin 1 (IL-l), tumor necrosis factor OL (TNF-a), and interferon y (IFN-?I). These cytokines mediate the processes of bone resorption and connective tissue destruction. Susceptibility and Resistance. PGE, may play a central role in the tissue destruction that occurs in peri- odontal diseases. Levels of PGE, in periodontal tissue are low or undetectable in health, increase in gingivi- tis, and rise significantly in periodontitis. Now there is increasing evidence that the level of PGE, pro- duced in response to bacterial challenge (especially by endotoxin) can be used as a measure of suscepti- bility (Offenbacher et al. 1993). Presumably, the level of PGE, production is sub- ject to genetic influence. Studies of identical and fra- ternal twins, either reared together or apart, provide evidence that genetic factors may indeed influence susceptibility or resistance to the common adult form of periodontitis (Michalowicz 1994). Recently, a commercial test for a genetic marker of susceptibility has been introduced. The marker is associated with increased production of a particular form of inter- leukin lfi (IL-lp) when stimulated by periodonto- pathic bacteria (Kornman et al. 1997). Newman (1996) found that nonsmoking adults who are posi- tive for the marker are 6 to 19 times more likely to develop severe periodontitis. Susceptibility to adult periodontitis has also been explored in relation to a variety of behavioral and demographic variables as well as to the presence of other diseases. One of the strongest behavioral asso- ciations is with tobacco use. The risk of alveolar bone loss for heavy smokers is 7 times greater than for those who have not smoked (Grossi et al. 1995). Cigarette smoking also may impair the normal host response in neutralizing infection (Seymour 199 l), resulting in the destruction of healthy periodontal tissues adjacent to the site of infection (Lamster 1992). Smokers also have decreased levels of salivary and serum immunoglobulins to Prevotella intermedia and Fusobacterium nucleatum (Bennet and Reade 1982, Haber 1994) and depressed numbers of helper T cells as well (Costabel et al. 1986). Finally smok- ing alters the cells that engulf and dispose of bacte- rla-neutrophils and other phagocytes-affecting their ability to clear pathogens (Barbour et al. 1997). Epidemiologic studies have found that such additional factors as increasing age, infrequent dental visits, low education level, low income, co-morbidi- ties, and inclusion in certain racial or ethnic popula- tions are associated with increased prevalence of Diseases and Disorders periodontitis (Page 1995). It is important that epi- demiologic studies also take into consideration the fact that tobacco use, oral hygiene, professional pro- phylaxis, and routine dental care are correlated to socioeconomic status, as are race and ethnicity. Sex is another factor. Males tend to have higher levels of periodontal diseases, presumably because of a histo- ry of greater tobacco use and differences in personal care and frequency of dental visits. However, female hormones may play a protective role (as they do in protecting against osteoporosis) (Genco 1996). Certain systemic diseases heighten susceptibility Epidemiological studies have confirmed that patients with diabetes mellitus, both type 1 and type 2, are more susceptible to periodontal diseases (Genco 1996). Measures such as the gingival index, pocket depth, and loss of attachment are more severe if the diabetic patients are smokers (Bridges et al. 1996). The likelihood of periodontal disease increases markedly when diabetes is poorly controlled. In con- trast, periodontal diseases respond well to therapy and can be managed successfully in patients with well-controlled diabetes. Such therapy can result in improvements in the diabetic condition itself (Mealey 1996) (see Chapter 5). There is some evidence that osteoporosis may be a risk factor for periodontal disease. More clinical attachment loss and edentulousness have been reported in osteoporotic than in nonosteoporotic women (Jeffcoat and Chestnut 1993). Two studies in 1996 showed that estrogen replacement therapy in postmenopausal women not only gives protection against osteoporosis, but also results in fewer teeth lost to periodontal disease (Grodstein et al. 1996, Jacobs et al. 1996). The less common rapidly progressive form of adult periodontitis typically affects people in their early 20s and 30s. It is characterized by severe gingi- val inflammation and rapid loss of connective tissue and bone. Many patients have an inherent defect in neutrophil response to infection. Several systemic diseases have been associated with this form of peri- odontal disease, including type 1 diabetes, Down syndrome, Papillon-Lefevre syndrome, Chediak- Higashi syndrome, and HIV infection (Caton 1989). Specific bacteria associated with rapidly progressive disease include Porphyrornonas gingivalis, PrevoteIla inter-media, Eikenella corrodens, and Wolinella recta (Scheutz et al. 1997). Most recently, mutations in the cathepsin C gene have been associated with the Papillon-Lefevre syndrome (Hart et al. 1999) and how the defect can result in periodontal disease (Toomers et al. 1999). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 41 Diseases and Disorders Refractory Periodontitis. Refractory periodontitis is not a specific form of disease, but refers to cases in which patients continue to exhibit progressive dis- ease at multiple sites despite aggressive mechanical therapy to remove biofilm and calculus, along with the use of antibiotics. Refractory sites exhibit elevat- ed levels of a number of different bacteria, with the dominant species different in different subjects. It is not known whether variations in pathogenicity of the bacteria, defects in the subject's defense systems, or combinations of these factors are responsible for the refractory nature of the disease (Haffajee et al. 1988). The adoption of new diagnostic technology to detect predominant bacterial species, followed by selective antibiotic treatment, may help resolve infection and disease in these patients. Early-onset Periodontitis The forms of periodontitis occurring in adolescents and young adults generally involve defects in neu- trophil function (Van Dyke et al. 1980). Localized juvenile periodontitis (LJP) mainly affects the first molar and incisor teeth of teenagers and young adults, with rapid destruction of bone but almost no telltale signs of inflammation and very little supragingival plaque or calculus. Actinobacillus actin- ornycetemcomitans has been isolated at 90 to 100 per- cent of diseased sites in these patients, but is absent or appears in very low frequency in healthy or mini- mally diseased sites (Socransky and Haffajee 1992). It is possible that the bacteria are transmitted among family members through oral contacts such as kiss- ing or sharing utensils, because the same bacterial strain appears in affected family members. However, evidence of a neutrophil defect argues for a genetic component. Another organism frequently associated with LJP is Capnocytophaga ochracea. Neither of these bacteria dominate in the generalized adult form of the disease, where Porphyromonas gingivalis is con- sidered of greatest significance (Schenkein and Van Dyke 1994). Prepubertal periodontitis is rare and can be either general or localized. The generalized form begins with the eruption of the primary teeth and proceeds to involve the permanent teeth. There is severe inflammation, rapid bone loss, tooth mobility, and tooth loss. The localized form of the disease is less aggressive, affecting only some primary teeth. The infection involves many of the organisms associ- ated with periodontitis, but the mix may differ some- what, with Actinobacillus actinomycetemcomitans, Prevotella interned@ Eikenella corrodens, and several species of Capnocytophaga implicated (Caton 1989). Defects in neutrophil function noted in both forms of the disease (Schenkein and Van Dyke 1994) may explain why patients are highly susceptible to other infections as well (Suzuki 1988). SELECTED MUCOSAL INFECTIONS AND CONDITIONS Like the skin, the mucosal lining of the mouth serves to protect the body from injury This lining is itself subject to a variety of infections and conditions, ranging from benign canker sores to often fatal cancers. Oral Candidiasis Chronic hyperplastic candidiasis is a red or white lesion that may be flat or slightly elevated and may adhere to soft or hard tissue surfaces, including den- tal appliances. It is caused by species of Candida, especially Candida albicans, the most common fungal pathogen isolated from the oral cavity. Normally, the fungi are present in relatively low numbers in up to 65 percent of healthy children and adults and cause no harm (McCullough et al. 1996). Problems arise when there is a change in oral homeostatis-the nor- mal balance of protective mechanisms and resident oral flora that maintain the health of the oral cavity- so that defense mechanisms are compromised (Scully et al. 1994). Under these circumstances the fungal organisms can overgrow to cause disease. A primary disruption in homeostasis occurs with the use of antibiotics and corticosteroids, which can markedly change the composition of the oral flora. Deficiencies in the immune and endocrine systems are also important. Indeed, the diagnosis of candidiasis in an otherwise seemingly healthy young adult may be the first sign of HIV infection. Other causes of candidia- sis include cancer chemotherapy or radiotherapy to the head and neck, xerostomia resulting from radia- tion to the head and neck, medications, chronic mucosal irritation, certain blood diseases, and other systemic conditions. Also, tobacco use has been iden- tified as a cofactor. Candidiasis often causes symptoms of burning and soreness as well as sensitivity to acidic and spicy foods. Patients may complain of a foul taste in the mouth. However, it can also be asymptomatic. Genomic analysis of the Candida albicans genome is helping investigators identify numerous genes that code for virulence factors, including enzymes that can facilitate adhesion to and penetration of mucous membranes. At the same time, researchers are explor- ing novel gene technologies to increase production of 42 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL `I family of native salivary proteins, the histatins, that halve known anticandidal and other antimicrobial effects. The most common form of oral candidiasis is denture stomatitis. It occurs when tissues are trau- matized by continued wearing of ill-fitting or inade- quately cleaned dental appliances and is described as chronic erythematous candidiasis. Another form, candidal angular cheilosis, occurs in the folds at the angles of the mouth and is closely associated with denture sore mouth (Tyldesley and Field 1995). Other common forms of Candida infection are pseudomembranous candidiasis (thrush), which may affect any of the mucosal surfaces, and acute erythe- matous candidiasis, a red and markedly painful vari- ant commonly seen in AIDS patients. In most cases, Candida infection can be con- trolled with antifungal medications used locally or systemically Control is difficult, however, in patients with immune dysfunction, as in AIDS, or other chronic debilitating diseases, Often the organisms become resistant to standard therapy, and aggressive approaches are necessary (Tyldesley and Field 1995). The spread of oral candidiasis to the esophagus or lungs can be life-threatening and is one of the crite- ria used to define frank AIDS (Samaranayake and Holmstrup 1989). Herpes Simplex Virus Infections In any given year, about one-half-million Americans will experience their first encounter with the herpes simplex virus type 1 (HSV-l), the cause of cold sores. That first encounter usually occurs in the oral region and may be so mild as to go unnoticed. But in some people, particularly young children and young adults, infection may take the form of primary her- petit stomatitis, with symptoms of malaise, muscle aches, sore throat, and enlarged and tender lymph nodes, prior to the appearance of the familiar cold sore blisters. These blisters usually show up on the lips, but any of the mucosal surfaces can be affected. Bright-red ulcerated areas and marked gingivitis may also be seen (Tyldesley and Field 1995). Herpes viruses also cause genital infections, which are transmitted sexually Both HSV- 1 and HSV- 2 have been found in oral and genital infections, with HSV-1 predominating in oral areas and HSV-2 in gen- ital areas (Wheeler 1988). Herpes viruses have also been implicated as cofactors in the development of oral cancers. Crowded living conditions can result in greater contact with infected individuals, which aids in transmission of HSV (Whitley 1992). Diseases and Disorders Normally the immune system mounts a success- ful attack on the viruses, with symptoms abating by the time neutralizing antibodies appear in the blood- stream, in about 10 days. However, herpes viruses are notorious for their ability to avoid immune detection by taking refuge in the nervous system, where they can remain latent for years. In oral herpes the virus commonly migrates to the nearby trigeminal gan- glion, the cluster of nerve cells whose fibers branch out to the face and mouth. In about 20 to 40 percent of people who are virus-positive, the virus may reac- tivate, with infectious virus particles moving to the oral cavity to cause recurrent disease (Scott et al. 1997). The usual site of a recurrent lesion is on or near the lips. Recurrences are rarely severe, and lesions heal in 7 to 10 days without scarring (Higgins et al. 1993). The recurrences may be provoked by a wide range of stimuli, including sunlight, mechanical trau- ma, and mild fevers such as occur with a cold. Emotional factors may play a role as well. Oral Human Papillomavirus Infections There are more than 100 recognized strains of oral human papillomavirus (HPV), a member of the papovavirus family, implicated in a variety of oral lesions (Regezi and Sciubba 1993). Most common are papillomas (warts) found on or around the lips and in the mouth. HPV is found in 80 percent of these oral squamous papillomas (de Villiers 1989). The virus has also been identified in 30 to 40 percent of oral squamous cell carcinomas (Chang et al. 1990) and has been implicated in cervical cancer as well. Whether a cancer or nonmalignant wart develops may depend on which virus is present or on which viral genes are activated. Oral warts are most often found in children, probably as a result of chewing warts on the hands. In adults, sexual transmission from the anogenital region can occur (Franchesi et al. 1996). In general, viral warts spontaneously regress after 1 or 2 years. The immune system normally keeps HPV infections under control, as evidenced by the increased prevalence of HPV-associated lesions in HIV-infected patients and others with immuno- deficiency Recurrent Aphthous Ulcers Recurrent aphthous ulcers (RAU), also referred to as recurrent aphthous stomatitis, is the technical term for canker sores, the most common and generally ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 43 mild oral mucosal disease. Between 5 and 25 percent of the general population is affected, with higher numbers in selected groups, such as health profes- sional students (Axe11 et al. 1976, Embil et al. 1975, Ferguson et al. 1984, Kleinman et al. 1991, Ship 1972, Ship et al. 1967). The disease takes three clinical forms: RAU minor, RAU major, and herpetiform UU. The minor form accounts for 70 to 87 percent of cases. The sores are small, discrete, shallow ulcers surrounded by a red halo appearing at the front of the mouth or the tongue. The ulcers, which usually last up to 2 weeks, are painful and may make eating or speaking diffi- cult. About half of RAU patients experience recur- rences every 1 to 3 months; as many as 30 percent report continuous recurrences (Bagan et al. 1991). RAU major accounts for 7 to 20 percent of cases and usually appears as 1 to 10 larger coalescent ulcers at a time, which can persist for weeks or months (Bagan et al. 1991). Herpetiform R4U has been reported as occurring in 7 to 10 percent of RAU cases. The ulcers appear in crops of 10 to 100 at a time, concentrating in the back of the mouth and lasting for 7 to 14 days (Bagan et al. 1991, Rennie et al. 1985). R4U can begin in childhood, but the peak peri- od for onset is the second decade (Lehner 1968). About 50 percent of close relatives of patients with R4U also have the condition (Ship 1965), and a high correlation of R4U has been noted in identical but not fraternal twins. Associations have been found between R4U and specific genetic markers (Scully and Porter 1989). R4U has also been associated with hypersensi- tivities to some foods, food dyes, and food preserva- tives (Woo and Sonis 1996). Nutritional deficien- cies-especially in iron, folic acid, various B vita- mins, or combinations thereof-have also been reported, and improvements noted with suitable dietary supplements (Nolan et al. 1991). The two factors that have been found to have the strongest association with R4U are immunologic abnormality, possibly involving autoimmunity, and trauma (Lehner 1968, Ship 1996. Woo and Sonis 1996). Volunteers with and without a history of RAU were studied for their reaction to the trauma of a nee- dle prick to the inner cheek tissue. No ulcers devel- oped in non-R4U subjects, but nearly half of those prone to canker sores had a recurrence (Wray et al. 1981). R4U also can occur in a number of systemic dis- eases, including HIV infection, ulcerative colitis, Crohn's disease, and Behcet's disease (Ship 1996). In general, people who are immunocompromised are more susceptible to RAU, as are people with a variety of blood diseases. EWU itself does not give rise to other illnesses but is uncomfortable. Symptomatic treatment includes topical analgesics, antibacterial rinses, topi- cal corticosteroids, and a new prescription medica- tion that reduces pain and healing time (Khandwala et al. 1997, Ship 1996). ORAL AND PHARYNGEAL CANCERS AND PRECANCEROUS LESIONS In 2000, oral or pharyngeal cancer will be diagnosed in an estimated 30,200 Americans and will cause more than 7,800 deaths (Greenlee et al. 2000). Over 90 percent of these cancers are squamous cell carci- nomas-cancers of the epithelial cells. The most common oral sites are on the tongue, the lips, and the floor of the mouth. Oral cancer is the sixth most common cancer in U.S. males and takes a dispropor- tionate toll on minorities; it now ranks as the fourth most common cancer among African American men (Kosary et al. 1995). The prominent role of tobacco use, especially in combination with alcohol, in caus- ing these cancers is a major incentive to develop effective health promotion and disease prevention efforts. Heightening the Risk Oral cancer develops as a clone from a single geneti- tally altered cell (Solt 1981). It generally has a long latency period and invariably develops from a pre- cancerous lesion on the oral mucosa, such as a white leukoplakia, or more commonly, a reddish erythro- plakia (Mashberg 1978, Shklar 1986). Both kinds of lesions are usually induced by tobacco use alone or in combination with heavy use of alcohol. The develop- ment of squamous cell carcinoma from initial ery- throplakia lesions has been well demonstrated exper- imentally. Silverman (1998) reported rates of malig- nant transformation for leukoplakias of between 0.13 and 17.5 percent. However, there is considerable debate as to the actual malignant potential of the leukoplakia lesion associated with the use of smoke- less (spit) tobacco. Meaningful data for determining a specific malignant transformation rate or relative risk of oral cancer due to smokeless tobacco use are difficult to obtain because of the confounding effects of other habits such as concurrent smoking and alco- hol consumption and because of the variations in smokeless (spit) products and how they are used. 44 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL .\nother oral precancerous lesion that has r,cclved attention is submucous fibrosis. It is com- ,nonly seen in India and Southeast Asia and is relat- (`1 to betel nut use (Canniff et al. 1986). Early epidemiologic studies identified behaviors Guch as smoking and environmental factors such as ,sposure to solar radiation and x-rays as causes of ,rttraoral and lip cancers (Pindborg 1977). Researchers then sought experimentally to explain the mechanisms of initiation. In the 1980s and I99Os. investigators exploited the techniques of riiolecular biology and genetics to probe what was going on deep inside the cell. These studies revealed `m abundance of systemic and local factors, including \,iral and fungal infections, that affect cell behavior. Some factors stimulate cell division and others ttthibit it-even to the point of initiating a program of cell "suicide," called apoptosis. How a given cell behaves at any given time in its life cycle is the net result of the signals it receives from neighboring cells and molecules, from circulating factors in the blood or immune system, and from its own internal controls. The following sections provide a brief description of these factors and how they may participate in enhancing the risk for the development of oral cancers. Tobacco and Alcohol Tobacco and alcohol are the major risk factors for oral cancers, and their effects have been studied for many years (Rothman and Keller 1972, Decker and Goldstein 1982). Tobacco contains substances that are frankly carcinogenic or act as initiators or pro- moters of carcinogenesis. Among these are N- nitrosonornicotine. 4-nitroquinoline-N-oxide, and benzpyrene. The most damaging carcinogens are found in the tars of tobacco smoke, but many forms of smokeless (spit) tobacco, including snuff, have been implicated in the development of mouth cancer (Advisory Committee to the Surgeon General 1986, International Agency for Research on Cancer 1985, Winn 1984). Other habits that have been related to oral cancer include chewing betel nut in the presence of tobacco, as is done primarily in Southeast Asia (Hirayama 1966, Mehta et al. 1981), and, more recently, using marijuana (Donald 1986). The role of alcohol in oral carcinogenesis has been demonstrated experimentally (Wight and Ogden 1998) and appears to be related to its damag- ing effect on the liver, Major metabolites of alcohol, such as acetaldehyde-a known carcinogen in ani- mals-may also be important. Alcohol is also thought to act as a solvent that facilitates the pene- Discscs and Disorders tration of tobacco carcinogens into oral tissues. That observation may partly explain why the combined use of tobacco and alcohol produces a greater risk for oral cancer than use of either substance alone. Indeed, tobacco and alcohol, working in tandem, are thought to account for 75 to 90 percent of all oral and pharyngeal cancers in the United States (Blot et al. 1988). Viruses The role of viruses in causing cancer in animals was established early in the century when Rous showed that a virus, later named the Rous sarcoma virus (RSV), caused tumors in chickens. The issue of whether viruses could cause cancer in humans remained unexplored until the mid-1970s when Varmus and Bishop showed that RSV had a special gene, which they called src (for sarcoma), that could transform the cell it infected into a malignant cell (Bishop et al. 1978). It was an oncogene, or cancer- causing gene. The researchers subsequently, and sur- prisingly, discovered that src was not native to the virus, but had been picked up by some ancestor virus from a chicken cell's own genome, where src had pre- sumably played a role in the chicken cell's normal growth and development. Somehow RSV was able to subvert src when it infected a chicken cell to cause the cell to divide uncontrollably. Varmus and Bishop called the normal cellular src gene a proto-oncogene, meaning that it had the potential to be converted to an oncogene. Subsequent research led to the discov- ery of other viruses that could cause tumors in ani- mals and revealed the presence of proto-oncogenes in birds and mammals. These genes could also be con- verted to oncogenes, behaving exactly like those car- ried by cancer viruses. In 1982 an oncogene isolated from a human bladder cancer turned out to be virtu- ally identical to rus, the oncogene found in a rat sar- coma virus (Parada et al. 1982). Viruses that have been implicated in oral cancer include herpes simplex type 1 and human papillo- mavirus. Epstein-Barr virus, also a herpes virus, is now accepted as an oncogenic virus responsible for Burkitt's lymphoma, occurring primarily in Africa, and nasopharyngeal carcinoma, occurring primarily in China. HPV is a major etiologic agent in cervical cancer (Howley 1991), and has been found in associ- ation with oral cancer as well (Sugerman and Shillitoe 1997). HPV DNA sequences have been found in oral precancerous lesions as well as in squa- mous cell carcinomas (Adler-Storthz et al. 1986, Syrjanen et al. 1988), and experimental evidence has shown that HPV-16 can be an important cofactor in ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 45 46 - Diseases and Disardcrs oral carcinogenesis (Park et al. 1991, 1995). Herpes simplex type 1 antibodies were demonstrated in patients with oral cancer, and herpes was found to induce dysplasia (abnormal cellular changes) in the lips of hamsters when combined with the application of tobacco tar condensate (Park et al. 1986). More recently, human herpes virus 8, a newly identified member of the herpes virus family, has been found in Kaposi's sarcoma, an otherwise rare cancer occurring in patients with AIDS. These tumors often appear initially within the oral cavity (Epstein and Scully 1992). Other uncommon oral malignant tumors, such as Hodgkin's lymphoma and non-Hodgkin's lymphoma, can also occur in the mouths of AIDS patients. tions in the ~53 gene detected in many types of can- cer (Greenblatt et al. 1994, Hollstein et al. 1991), including oral and pharyngeal cancer (Langdon and Partridge 1992, Somers et al. 1992). The ~53 gene has been called the "guardian of the genome" (Lane 1992) because of its ability to recognize damage to a cells DNA and stop the process of growth and divi- sion until the damage is repaired. If repair is not pos- sible, ~53 can trigger apoptosis. Mutations in the ~53 gene in oral cancer have been linked to smoking and alcohol use (Brennan et al. 1995). Loss of Immunosurveillance and Control In addition to viruses, infection with strains of the fungus Candida albicans has been linked to the development of oral cancers via the fungal produc- tion of nitrosamines, which are known carcinogens. The immune system can, at first noted by Paul Ehrlich in 1909, seek and destroy initial clones of transformed cancer cells (Ehrlich 1957). Ehrlich called this process immunosuweillance, and it has been confirmed in experimental animals (Burnet 1970, Shklar et al. 1990) and in humans with induced immunosuppression (Penn 1975). Genetic Derangements Of the more than 50 known oncogenes, many have been reported to be present in oral cancer, and mul- tiple oncogenes have been reported in oral and pha- ryngeal cancer (Spandidos et al. 1985). Some of these are &l-l, c-erb-B2, c-myc, ins-2, and members of the rus family (Berenson et al. 1989, Bos 1989, Riviere et al. 1990, Somers et al. 1990, 1992). The genetic derangements that can give rise to oral cancer, including many mutations associated with the transformation of proto-oncogenes, have received notable attention (Sidransky 1995, Wong et al. 1996). In some instances a change in a single nucleotide base-a point mutation-in a gene encoding a proto-oncogene is enough to transform it into an oncogene. Cancerous changes may also involve alterations, deletions, and break points in chromosomes that affect the position of genes. One mechanism of immunosurveillance involves stimulating cytotoxic macrophages and lymphocytes to migrate to the tumor site and release tumor necro- sis factors (Y and l3 (Shklar and Schwartz 1988). Another mechanism operative in oral cancer appears to be stimulation of Langerhans cells, a special group of immune cells, in the oral mucosa (Schwartz et al. 1985). Other immune cells implicated in tumor rejection are natural killer cells and lymphokine-acti- vated killer cells (Reif 1997). There is an increased incidence of cancer in patients with AIDS or other immunodeficient condi- tions or with induced immunosuppression prior to organ transplantation. In addition, there is evidence that smoking depresses the immune system (Chretien 1978), and this may be one of the ways in which smoking acts as a major risk factor in oral cancer. Mutations that disarm the cells DNA repair mechanisms, as well as mutations in tumor suppres- sor genes, which inhibit abnormal cell growth, play a major role in cancer development. If an individual inherits or acquires a mutation in one or more tumor- suppressor genes, for example, the loss of this pro- tective mechanism reduces the number of other dele- terious changes needed for cancer to develop. Growth Factors Tumor suppressor genes suspected to be mutated in oral and pharyngeal cancers include those for Rb, ~16 (MTSI, CDKNZ, or IN4a), and ~53. Todd et al. (1995) recently reported a novel oral tumor suppres- sor gene, named "deleted in oral cancer-l (doe-11." Of the group of tumor suppressor genes, that coding for ~53 is considered of major importance, with muta- Immune cells are potent generators of growth factors and other molecules that can stimulate other cells to migrate and proliferate. This capacity is important in normal cell growth and turnover, in wound healing, and in coping with infection. Unfortunately, the release of growth factors can contribute to oral can- cer by stimulating keratinocyte (oral epithelial cell) proliferation (Aaronson 1991, Issing et al. 1993, Wong 1993). Increased levels of transforming growth factor (Y (TGF-a) and epidermal growth factor have been found in oral and pharyngeal cancers and there- fore could serve as markers for malignancy (Grandis and Tweardy 1993). Nicotine at high doses stimulates ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL rhe release of growth hormones, among other endocrine effects (Pomerleau and Pomerleau 1984, se),ler et al. 1984, 1986). prevention and Management Studies of experimental carcinogenesis are elucidat- ing the role of micronutrients in tumor development & progression. Alpha tocopherol (vitamin E) also has been studied as an antioxidant in nutritional npproaches to the prevention or control of oral can- cer. Antioxidants can trap free radicals, the highly reactive molecules that build up in cells and can damage DNA. The control of oral cancer and precan- cerous lesions has been demonstrated experimental- ly using a variety of antioxidant micronutrients, such as retinoids, carotenoids, and glutathione, as well as alpha tocopherol. For example, it was found that alpha tocopherol inhibited tumor development and tumor angiogenesis (blood vessel formation) in ham- sters, as well as the expression of TGF-c~, a potent angiogenesis stimulator (Shklar and Schwartz 1996). *Animal research and tissue culture studies using ani- mal- and human-derived cancer cell lines have shown combinations of micronutrients to be more effective than single micronutrients and to work syn- ergistically. The nutrients not only were able to inhib- it experimental carcinogenesis, but also could com- pletely prevent tumor development and cause estab- lished squamous cell carcinomas to regress (Shklar and Schwartz 1993). The mechanisms of cancer con- trol by micronutrients are gradually becoming clari- fied and involve common pathways of activity at the molecular level (Shklar and Schwartz 1994). Clinical studies in humans have shown an inhibitory effect on oral leukoplakia (Benner et al. 1993, Blot et al. 1993, Garewal 1993, Garewal et al. 1990, Hong et al. 1986), suggesting a potential role for nutrients in the overall prevention and management of early oral cancer and precancerous leukoplakia. However, a recommenda- tion to employ such approaches clinically at this time is premature. DEVELOPMENTAL DISORDERS The importance of the face as the bearer of identity, character, intelligence, and beauty is universal. Craniofacial birth defects, which can include such manifestations as cleft lip or palate, eyes too closely or widely spaced, deformed ears, eyes mismatched in color, and facial asymmetries, can be devastating to the parents and child affected. Surgery, dental care, psychological counseling, and rehabilitation may ORAL HErlLTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 47 Diseases and Disorders help to ameliorate the problems but often at great cost and over many years. Although each developmental craniofacial dis- ease or syndrome is relatively rare, the number of children affected worldwide is in the millions. In addition, craniofacial defects form a substantial com- ponent of many other developmental birth defects, largely because they occur very early in gestation, when many of the same genes that orchestrate the development of the brain, head, face, and mouth are also directing the development of the limbs and many vital internal organs, such as the heart, lungs, and liver. By about the third week after fertllization, the three germ layers of the embryo-the ectoderm, endoderm, and mesoderm-have formed, as well as the first of four sets of paired swellings-the branchial arches-that appear at the sides of the head end of the embryo. (See Chapter 2 for more details on this process.) Some craniofacial defects result from failure of the arches to complete their morphogenet- ic development. Other craniofacial defects are the result of the abnormal differentiation of cells derived from the ectoderm and endoderm or from ectomes- enchyme cells, which originate in a part of the ecto- derm (the neural crest), in interaction with future connective tissue (the mesenchyme). Craniofacial Anomalies Caused by Altered Branchial Arch Morphogenesis Cleft Lip/Palate and Cleft Palate The most common of all craniofacial anomalies-and among the most common of all birth defects-are clefts of the lip with or without cleft palate and cleft palate alone; these occur at a rate of 1 to 2 out of 1,000 births, resulting in over 8,000 affected new- borns every year. Cleft lip/palate and cleft palate are distinct conditions with different patterns of inheri- tance and embryological origins (Lidral et al. 1997, Murray et al. 1997). The male to female ratio of cleft lip/palate is 2:l; the ratio for cleft palate alone is just the reverse, 1:2. These anomalies result from the failure of the first branchial arches to complete fusion processes (Murray 1995, Robert et al. 1996). Clefting can occur independently or as part of a larger syndrome that may include mental retardation and defects of the heart and other organs. Not all cases of clefting are inherited; a number of teratogens (environmental agents that can cause birth defects) have been impli- cated, as well as defects in essential nutrients such as Diseases ;tnd Disorders folic acid. Smoking by the mother during pregnancy also increases the risk. It is becoming increasingly evident that most diseases and disorders, not just craniofacial anomalies, result from interactions involving multiple genes and environmental factors. Infants with clefts have difficulty with vital oral functions such as feeding, breathing, speaking, and swallowing. They are also susceptible to repeated res- piratory infections. As these children grow. they must cope with the social consequences of a facial defor- mity, delayed and altered speech, frequent illness, and repeated surgeries that may persist through late adolescence. Current molecular epidemiology investigations have examined both syndromic and nonsyndromic (isolated) cleft lip/palate and cleft palate. Linkage studies have identified a number of candidate genes (Lewanda and labs 1994), including MSXl , RAR, an X-linked locus, and the genes for TGF-B3 and TGF- a. The pattern of inheritance in cleft lip/palate and cleft palate suggests that between 2 and 20 genes may be involved, with one gene representing a major component in the development of the cleft. One of the common syndromic forms of cleft lip/palate, the Van der Woude syndrome, is caused by an autosomal dominant form of inheritance at a locus on chromo- some 1 (Sander et al. 1995). Future molecular genet- ic studies will be needed to provide the information necessary for prenatal diagnosis, calculation of risk, and potential gene therapy. The Treacher Collins Syndrome- Mandibulofacial Dysostosis Children with the Treacher Collins syndrome have downward-sloping eyelids; depressed cheekbones; a large fishlike mouth; deformed ears with conductive deafness; a small, receding chin and lower jaw; a highly arched or cleft palate; and severe dental mal- occlusion (Dixon 1996). These defects result from defective cranial neural crest cell differentiation, migration, and proliferation (see Chapter 2). Consequently, the first branchial arch structures are deficient, and all derivative craniofacial components are affected. The underdeveloped facial structures can con- tribute to airway blockage and repeated upper respi- ratory infections, either of which can be fatal. The faulty development of the ears leads to a conductive deafness. The severe facial deformities exacerbate the psychological difficulties these youngsters face. Investigators have identified the gene involved in an autosomal dominant form of the syndrome (Wise et al. 1997). The function of the gene is not yet known, but its identity will provide opportunities for prenatal diagnosis, gene therapy, and further under- standing of craniofacial development. The Pierre Robin Syndrome Deficient development of the first-branchial-arch- derived mandibular portion results in the lower jaw's being set far back in relation to the forehead. As a result, the tongue is set back and may obstruct the posterior airway, compromising respiration (Elliott et al. 1995, Tomaski et al. 1995) and, in severe cases, leading to inadequate aeration and failure to thrive. The infant is also at risk for the development of car pulmonale, an enlargement of the right ventricle of the heart that occurs secondarily to a chronic lung condition. Cleft palate may be another consequence. The DiGeorgeNelocardiofacial Syndrome The primary defect in the DiGeorge syndrome results from altered development of the fourth branchial arch and the third and fourth pharyngeal pouches (Goldmuntz and Emanuel 1997). Deficiencies affect- ing the thymus, parathyroid glands, and the great vessels that derive from these structures result. The facial features are subtle and include a squared-off nasal tip, small mouth, and widely spaced eyes. Similar facial features, along with heart defects, are seen in the velocardiofacial syndrome. Both syn- dromes are associated with deletions on the long arm of chromosome 22 (22qll) (Gong et al. 1997, Gottlieb et al. 1997). Further characterization of this chromosomal deletion region will provide informa- tion on the specific gene(s) affected and its function in craniofacial development. The thymus defects severely compromise cellular immunity, depriving the body of thymus-derived T cells and paving the way for severe infectious disease. Inadequate or missing parathyroid glands cause severe hypocalcemia (low blood calcium levels) and seizures. The great vessel abnormalities alter cardiac output and lead to compromised circulation to heart tissues. Cranial Bone and Dental Anomalies Defects in the timing of developmental events can cause premature fusion of cranial bones. Impairments of tooth development can result from interruptions of the developmental sequence at sev- eral different stages. 48 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL CraniosyIIoStOSeS Some craniofacial anomalies are associated with so- called master genes that orchestrate a program by Ivhich the embryo assumes its basic shape. Craniosynostosis, which occurs in approximately 1 out of 3,000 births, is one such anomaly. It results in the premature fusion of the cranial sutures, a danger- ous condition that puts pressure on the developing brain. A number of diseases and syndromes, includ- ing Crouzon's, Apert's, Boston-type craniosynostosis, pfeiffer's, and Saethre-Chotzen, share this anomaly, but differ in other features, which can include struc- tural defects such as webbing of the hands and feet as well as mental retardation. Boston-type craniosynos- tosis has been linked to MSX2, one of the master genes. Several of the other syndromes involve point mutations at one or another locus in genes that code for fibroblast growth factor receptors (FGFR 1,2, and 3) (Howard et al. 1997, Meyers et al. 1996). Collectively, these genes are associated with cell reg- ulation, either through mediating growth factor effects or by serving as transcription factors (Cohen 1997). Hereditary Hypodontia or Anodontia Conditions of underdeveloped teeth (hypodontia) or their complete absence (anodontia) have been corre- lated with specific genes, such as MSXl and LEFl. The complete absence of teeth alters the bony devel- opment of the mandible and maxilla. Amelogenesis Imperfecta and Dentinogenesis Imperfecta Amelogenesis imperfecta and dentinogenesis imper- fecta are linked to defects in structural genes that code for proteins essential to the development of tooth enamel (amelogenesis imperfecta) or dentin (dentinogenesis imperfecta). The teeth are weak and extremely sensitive to temperature and pressure. The ordinary forces of chewing are painful and can lead to further wear and pain. The enamel matrix genes include tuftelin, ameloblastin, and amelogenin; researchers have begun to link mutations in these genes with amelo- genesis imperfecta. Similarly, genes labeled DSP and DPP have been characterized for dentin matrix and are associated with the inheritance of dentinogenesis imperfecta. Diseases and Disorders Craniofacial Defects Secondary to Other Developmental Disorders A number of genetic diseases occur in which cranio- facial defects are secondav to a more generalized structural or biochemical defect. Osteogenesis Imperfecta Inherited mutations of collagen genes lead to a num- ber of "brittle bone" diseases characterized by defects in mineralized tissues that form from a collagen-rich matrix. Osteogenesis imperfecta presents a spectrum of deficiencies that includes fragile bones, clear or blue sclera, deafness, loose ligaments, and painful dentinogenesis imperfecta-like chaages in the teeth. Epidermolysis Bullosa-Recessive Dystrophic TYPe The gene defect in epidermolysis bullosa-recessive dystrophic type-manifests as blisters or bullae that appear shortly after birth on skin areas following minor trauma. Mutations in keratin genes that con- tribute to the epithelial cell cytoskeleton have been correlated with this condition. The oral manifestations include both mucosal bullae and altered teeth. Altered teeth with hypoplas- tic enamel develop and exhibit an increased suscepti- bility to caries. Oral bullae develop from even the slightest mucosal trauma. The condition is painful and dangerous because of the constant risk that the bullae will become infected. Craniofacial Manifestations of Single-Gene Defects In many craniofacial defects, mutations within a sin- gle gene manifest as complex syndromes with varied organ and limb defects as well as facial anomalies. Ectodermal Dysplasias The ectodermal dysplasias (EDs) are a family of hereditary diseases first observed by Charles Darwin over a century ago. They involve defects in two or more tissues derived from the ectoderm-skin, hair, teeth, nails, and sweat glands. The ectodermal struc- tures fail to differentiate properly owing to altered epithelial-mesenchymal signaling. A gene, EDA, at an X-linked locus has been linked to the syndrome, and ongoing research is aimed at determining the func- tion of the gene and the molecular mechanism of the syndromes (Kere et al. 1996, Zonana et al. 1994). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 49 Diseases and Disorders More recently, investigators have discovered genes linked to autosomal (i.e., non-sex-linked) forms of ED, displaying both dominant and recessive inheri- tance (Monreal et al. 1999). Oral manifestations of the ectodermal dysplasias are associated with the teeth. Alterations in tooth delrelopment can include hypodontia, anodontia, and conically shaped teeth. The Waardenburg Syndrome The Waardenburg syndrome has been subdivided into several types. All involve a variety of abnormali- ties in the position and appearance of the nose and eyes, with pigment changes that may cause one eye to differ in color from the other. Other signs include deafness, a mildly protruding jaw. cleft lip and palate, and skeletal deformities (Reynolds et al. 1995). The syndrome is inherited in an autosomal dominant manner with complete penetrance and variable expression. Specific genes associated with this syn- drome are members of the homeobox family that reg- ulate the transcription of other genes: Waardenburg type 1 with PAX3; Waardenburg type 2 with IMITF, 3q14.1; and Waardenburg type 3 with PAX3, 2q35 (Asher et al. 1996). Cleidocranial Dysplasia The inheritance of a regulatory gene defect in clei- docranial dysplasia leads to features that include delayed tooth eruption, supernumerary teeth, altered or missing collarbones, short stature. and possible failure of cranial suture closure. The exact mecha- nism of the associated gene, CBFAI, located on chro- mosome 6, has not been determined but appears to be essential for bone development. INJURY The common perception is that injuries are random occurrences that are unpredictable and hence unpre- ventable. In actuality, experts in the field make the point that there are no basic scientific distinctions between injury and disease (Haddon and Baker 1981). Injuries have been categorized as "intention- al" and "unintentional." People identified as being at risk for certain injuries. as well as the causes of those injuries, can be targeted for appropriate prevention strategies. Such an approach is broadly applicable to sports, falls, and motor vehicle injuries (unintention- al) as well as to injuries caused by abusive and vio- lent behaviors (intentional). Injuries are a major public health problem. out- ranking cancer and heart disease as a leading cause of death in some age groups of the population (Kraus and Robertson 1992). Cranial injuries in particular are a leading cause of mortality Oral-facial injuries can bring disfigurement and dysfunction, greatly diminishing the quality of life and contributing to social and economic burdens (Reisine et al. 1989). The leading causes of oral and craniofacial injuries are sports. violence, falls, and motor vehicle collisions (Kraus and Robertson 1992). Oral cavity injuries may also be caused by foreign objects in food (Hyman et al. 1993). sports Craniofacial sports injuries occur not only in contact sports, but also in individual activities such as bicy- cling, skating, and gymnastics, especially on trampo- lines. Each sport predisposes its participants to a spe- cific array of extrinsic risk factors (Pinkham and Kohn 1991). These include physical contact, projec- tiles such as balls and pucks, and the quality of the playing field and equipment. In contact sports the absence of protective equipment such as headguards and mouthguards is a major risk factor. In a recent survey of school-aged children in organized sports, football was the only sport in which the majority of participants used mouthguards and headgear (Nowjack-Raymer and Gift 1996). There are intrinsic risk factors as well, relating to characteristics of the individual participant. These include age, sex, injury history, body size, aerobic fit- ness and muscle strength, central motor control, and general mental ability (Taimela et al. 1990). Falls Falls are a major cause of trauma to teeth, primarily to incisors. Unlike bone fractures, fractures of the crowns of the teeth do not heal or repair, and affect- ed teeth often have an uncertain prognosis. Problems may develop later due to damage to the pulp. Motor Vehicle Collisions The effects of motor vehicle collisions may range from minor and reversible effects to long-term med- ical. surgical, and rehabilitative consequences. Post- traumatic headaches and chronic oral-facial pain can occur. Neuromuscular and glandular damage may cause short- or long-term problems with chewing, swallowing, and tearing or result in facial tics or paralysis. 50 ORAL HEALTH IN :lILlERICS: ;I REPORT OF THE SURGEON GENERAL Violence The family is the single most frequent locus of vio- lence in Western society Domestic violence includes child abuse, spousal and elder abuse, and abuse of the disabled. Child abuse is of particular concern to the oral health community because 65 percent of cases involve head and oral-facial trauma (Mathewson 1993, Needleman 1986) and dentists are required to report suspected cases of child abuse. fn the young child, head injury is the most common cause of death. Psychological trauma from abuse can result in sleep disturbances, eating disorders, devel- opmental growth failure in young children, and nerv- ous habits such as lip and fingernail biting and thumb sucking. Effects may also include chronic underachievement in school and poor peer relation- ships (Mathewson 1993). In abusive families, physi- cal neglect is commonplace, with inadequate provi- sion of basic needs, including medical and oral health care (Mathewson 1993). SELECTED CHRONIC AND DISABLING CONDITIONS Oral, dental, or craniofacial signs and symptoms play a critical role in autoimmune disorders such as SjGgren's syndrome and in a number of chronic and disabling pain conditions. Sjiigren's Syndrome Sjogren's syndrome is one of several autoimmune dis- orders in which the body's own cells and tissues are mistakenly targeted for destruction by the immune system. Like other autoimmune conditions, Sjogren's syndrome is more prevalent among women. The ratio of females to males affected is 9:1, with symptoms usually developing in middle age. There are an esti- mated 1 to 2 million individuals in the United States with Sjogren's syndrome (Talal 1992). The disease occurs in two forms. Primary Sjogren's involves the salivary and lacrimal (tear) glands. In secondary Sjogren's the glandular involve- ment is accompanied by the development of a con- nective tissue or collagen disease, most often rheumatoid arthritis, lupus erythematosis, scleroder- ma, or biliary cirrhosis. The glandular involvement causes a marked reduction in fluid secretion, resulting in xerostomia and xerophthalmia (dry eyes). The constant oral dry- ness causes difficulty in speaking, chewing, and swal- lowing; the dry eyes often itch and feel gritty. There Diseases and Disorders is no cure for Sjogren's, and patients often carry eye- drops and water bottles or saliva substitutes in an attempt to provide symptomatic relief. Clinically, the reduction in salivary flow changes the bacterial flora, which, in addition to the reduction in salivary pro- tective components, increases the risk of caries and candidiasis (Daniels and Fox 1992). Recent studies have indicated that there is a reduction in masticato- r-y function (Dusek et al. 1996) and an increased prevalence of periodontal disease (Najera et al. 1997). In advanced stages the salivary glands may swell because of obstruction and infection or lym- phatic infiltration, In both forms of the disease, other systems may eventually become* affected. Nasal, laryngeal. and vaginal dryness may occur, as well as abnormalities in internal organs (Oxholm and Asmussen 1996). Diagnosis is difficult in the early stages, and women often report that it took many years and con- sultations with many specialists before they received the correct diagnosis. Diagnosis involves demonstra- tion of specific antibodies in the blood characteristic of an autoimmune disorder, a labial (minor) salivary gland biopsy, and a series of eye tests to measure flow rate and tissue characteristics. Confirmatory tests include an evaluation of salivary flow and chemistry. Patients with Sjogren's syndrome are at some risk of developing diseases such as non-Hodgkin's lym- phoma; clinical data indicate that such lymphomas develop in 5 percent of patients with Sjogren's syn- drome (Moutsopoulos et al. 1978). Histological examination shows that immune cells infiltrate the glands and cluster around the secretory elements, resulting in a breakdown of the normal structure of the gland. The mechanisms by which this occurs involve immune-cell-mediated inflammation and stimulation of the salivary gland cells themselves to produce tissue-destructive mole- cules such as cytokines. Another hypothesis is that a viral infection of the glands may trigger the immune response that leads to autoimmunity, whereas genet- ic or regulatory alterations might lead to abnormali- ties in apoptosis (Fox and Speight 1996). In addition to saliva substitutes and artificial tears, some medications, such as pilocarpine and cevimeline, are prescribed to increase salivary flow from the residual healthy gland tissue, again provid- ing symptomatic relief only The problems that develop in the other organ systems are also treated symptomatically At advanced stages, steroids are employed intermittently to alleviate problems. ORAL HEALTH IN AMERICA: .4 REPORT OF THE SURGEON GENERAL 51 Diseases and Disorders Acute and Chronic Oral-Facial Pain Since the nineteenth century when two dentists, Horace Wells and Frederick Morton. demonstrated the analgesic powers of nitrous oxide and ether, oral health investigators have been recognized leaders in the field of pain management worldwide. Their analyses of the cells, pathways, and molecules involved in the transmission and modulation of pain have given rise to a growing variety of medications, often combined with other approaches, that can con- trol acute and chronic pain. Pain researchers today stress that chronic pain can become a disease in itself, causing long-term detrimental changes in the nerv- ous system. These changes may affect resistance to other diseases as well as effectively destroy quality of life. Most people have experienced acute pain involv- ing teeth and the oral tissues at one time or another. Atypical Facial Pain Atypical facial pain is characterized by a continuous dull ache on one or both sides, most frequently in the region of the maxilla (the upper jaw). The pain tends to be episodic and is aggravated by fatigue, worry, or emotional upset. It is often accompanied by pain elsewhere in the body and depression. Once a dental cause can be ruled out, pain resolution depends on the successful use of antidepressants, psychotherapy, or both (Tyldesley and Field 1995). Tic Douloureux The oral-facial region is also subject to pain that can be paroxysmal or continuous along a distinct nerve distribution. The most frequently encountered of these oral facial neuralgias is tic douloureux, or trigeminal neuralgia, a disease of unknown etiology affecting one, two, or all three branches of the trigeminal nerve. The pain is highly intense and of a stabbing nature, and lasts for a few seconds. This transient attack may be repeated every few minutes or several hours. There may be no precipitating fac- tor, or it may occur in response to a gentle touch or a breeze wafting across the face-a condition experts call allodynia, the feeling of pain in response to a nor- mally nonpainful stimulus. On other occasions, there may be a specific trigger zone. Although spontaneous remission for weeks or months may occur, it is rarely permanent. Given the unknown, unpredictable nature of tic douloureux, it is not surprising that fear of pain comes to dominate these patients' lives, as they avoid doing anything that might trigger an attack. Trigeminal neuralgia generally occurs in later life, but also occurs in younger individuals affected by multiple sclerosis, where it is assumed to be asso- ciated with lesions (multiple sclerosis "plaques") in the brain stem. Medical treatment depends largely on the use of a drug that has become a virtual specific, the antiepileptic drug carbamazepine. For those patients with no consequential adverse effects, it can control the disease. An alternative for chronic suffer- ers is the surgical removal of a small vein or artery that may be exerting pressure on the nerve root or the selective destruction of the nerve fibers them- selves using chemical or electrical methods. In many cases, these procedures can produce complete relief from pain (Tyldesley and Field, 1995). Temporomandibular Disorders Various etiological factors, including trauma, can give rise to pain and dysfunction in the temporo- mandibular joint and surrounding muscles, condi- tions collectively called temporomandibular disor- ders (TMDs). The pain may be localized or radiate to the teeth, head, ears, neck, and shoulders. Abnormal grating, clicking, or crackling sounds, known as crepitus, in the joint often accompany localized pain. Pain is also found in response to clinical palpation of the affected structures. TMDs are common, occur- ring in as many as 10 million Americans. Although surveys indicate that both sexes are affected, the majority of individuals seeking treatment are women of childbearing age, a phenomenon. suggesting that hormonal influences should be investigated. Several factors can contribute to the onset or exacerbation of TMD symptoms. These factors include certain developmental anomalies; injury to the jaw from accidents or abuse; oral habits that greatly stress the joint and musculature, such as tooth grinding (bruxism); jaw manifestations of sys- temic diseases such as fibromyalgia and arthritic dis- eases; and some irreversible treatments for initial signs and symptoms. The multiplicity of factors that may cause or con- tribute to TMDs has unfortunately led to a multiplic- ity of treatments. Most of these treatments have not been tested in randomized controlled clinical trials. During the 1970s and 1980s many individuals underwent surgery, which proved unsuccessful in many cases. Leading investigators have proposed standard- ized research diagnostic criteria to clarify the kinds of pathology that can give rise to TMDs and to classify the most common forms of TMDs. Such criteria could be used in designing clinical trials and could ultimately lead to better diagnostics. treatments, and prevention. The criteria use two dimensions or axes: 52 ORAL HEliLTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Diseases and Disorders axis I delineates various forms of joint or muscle pathology; axis II explores pain-related disability and psvchologic 1 t t a s a us. The approach requires detailed clinical examinations and patient histories (Dworkin ,md LeResche 1992). A MIRROR, A MODEL, AND A BETTER UNDERSTANDING OF DISEASES AND DISORDERS Studying the diseases and disorders that affect cran- iofacial tissues can provide scientists with models of systemic pathology Because some craniofacial tis- sues, such as bones, mucosa, muscles, joints, and nerve endings, have counterparts in other parts of the body and these tissues are often more accessible to research analysis than deeper-lying tissues, researchers studying craniofacial tissues can gain valuable insights into how cancer develops, the role of inflammation in infection and pain, the effects of diet and smoking, the consequences of depressed immunity, and the changes that can arise from a mutated gene. Other craniofacial tissues-teeth, gingiva, tongue, salivary glands, and the organs of taste and smell-are unique to the craniofacial complex. Study of the diseases affecting these tissues has revealed a wealth of information about their special nature as well as the molecules and mechanisms that normally operate for the protection, maintenance, and repair of all the oral, dental, and craniofacial tissues. When factors perturb these nurturing elements, the oral health scale can tip toward disease. When those fac- tors stem from systemic diseases or disorders, the mouth can sometimes mirror the body's ill health. Similarly underscoring the connection between oral and general health are studies suggesting that poor dental health, mainly due to chronic dental infec- tions, may heighten the risk for both cardiovascular disease and stroke independently of factors such as social class and established cardiovascular risk fac- tors (Grau et al. 1997). The interplay between cran- iofacial and systemic health and disease has become a lively focus of interest and research, as discussed in Chapter 5. Current research on developmental disorders and diseases affecting the craniofacial complex is facilitating and complementing the intense effort of the Human Genome Project to map and sequence all 100,000 genes. This goal should be accomplished early in the twenty-first century and should begin to yield information on the genetic program that gov- erns morphogenesis, organ development, and disease etiology and pathogenesis, with the potential for ORAL HE.4LTH IN AMERICr\ interventions that can correct errors in the program. The continued sequencing of the genomes of micro- bial pathogens involved in oral diseases also should lead to new diagnostic and preventive approaches. FINDINGS o Microbial infections, including those caused by bacteria, viruses, and fungi, are the primary cause of the most prevalent oral diseases. 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Zonana J, Jones M, Clarke A, Gault J, Muller B, Thomas Tyldesley WR, Field AE. Oral medicine, 4th ed. Oxford: NS. Detection of de novo mutations and analysis of Oxford University Press; 1995. their origin in families with X linked hypohidrotic ectodermal dysplasia. J Med Genet 1994 Apr;31(4): 287-92. Diseases and Disorders ORAL HEALTH IN AMERICA: .4 REPORT OF THE SURGEON GENERAL 59 The range of oral, dental, and craniofacial diseases and conditions that take a toll on the U.S. population is extensive. This chapter provides highlights of dis- eases and conditions affecting the U.S. population using available national and state data to describe the burden of disease in the United States. To capture the dimensions and extent of these diseases and condi- tions, the data are presented where possible by demo- graphic measures such as racefethnicity, sex, age, education, and economic status. Statistics and trends are presented for each of the six categories of oral dis- eases and disorders whose etiology and pathogenesis are described in Chapter 3: dental and periodontal infections, oral and pharyngeal cancers, mucosal infections and conditions, developmental disorders, intentional and unintentional injuries, and chronic and disabling conditions. Included are conditions as common as dental caries and periodontal diseases as well as relatively rare clefting syndromes. Also men- tioned are conditions that are more common in cer- tain demographic subpopulations-for example, Sjiigren's syndrome and temporomandibular disor- ders, which are more common in women, and injuries, which are more common in men. (See Box 4.1 for a glossary of terms used in this chapter.) There is no single measure of oral health or the burden of oral diseases and conditions, just as there is no single measure of overall health or overall dis- ease. As a result, this chapter assembles clinical and epidemiologic measures for specific conditions affecting the craniofacial structures. Note too that the chapter presents an incomplete picture. State-specif- ic data on oral diseases are extremely limited. There is a paucity of national data on rare conditions as well as on the health of selected populations and their subgroups. Some characteristics and unique needs of these populations are highlighted, and a number of questions raised. More extensive analyses of the differences among racial/ethnic, sex, and income groups are warranted. The relationship of oral health to the use of dental services is described. However, the effects of health care visits and of spe- cific services rendered need further study. Most of the data in the figures and tables pre- sented in this chapter are derived from large, nation- ally representative surveys of the U.S. civilian, nonin- stitutionalized population. These include complex sample surveys, such as the National Health and Nutrition Examination Survey (NHANES), which use a sample of individuals selected with known probability to estimate the prevalence of particular characteristics and conditions in the nation as a whole. The multipurpose NHANES provides data on the frequency of the most common oral diseases and conditions. The most recent survey, NHANES III, was conducted by the National Center for Health Statistics (NCHS) of the Centers for Disease Control between 1988 and 1994. Trained interviewers gath- ered demographic, health, and related data from eli- gible households. Selected persons in these house- holds were invited to a mobile examination center, where they underwent multiple health assessments, including an oral examination by a trained dentist (NCHS 1996). Related surveys such as the National Health Interview Survey (NHIS) also use complex survey sampling and household interviews to obtain health information about the U.S. population (Kovar 1989). The NHIS conducted in 1989 included data on oral-facial pain conditions; several of these sur- veys have captured data on dental visits. The most extensive dental utilization survey that provides demographic and socioeconomic data and data on reasons for not visiting a dentist was conducted in 1989. Surveys conducted by the National Institute of Dental and Craniofacial Research of a probability sample of U.S. schoolchildren in 1979-80 and 1986- 87 (Snowden and Miller-Chisholm 1992) used ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 61 The Magnitude of the Problem BOX 4.1 Glossary Complex sample survey. A survey of individuals selected with known probability to estimate the prevalence and/or extent of particular characteristics and conditions. dfs. The count (number) of decayed (untreated) or filled primary tooth surfaces per person. dft. The count (number) of decayed (untreated) or filled primary teeth per person. DMFS.The count (number) of decayed (untreated), misiing (due to caries), or filled permanent tooth surfaces per person. DMFT.The count (number) of decayed,missing (due to caries),' 0; filled permanent teeth per person. Epidemiology.The study of the distribution and determinants of disease frequency in human populations. Incidence. The number of cases of a disease, or condition, that occurs during a specified period of time. Incidence rate. The number of cases of a disease, or condition, that occurs during a specified period of time, per specified unit of population. Loss of periodontal attachment.' The distance from the cementoenamel junction to the bottom of the gingival sulcus. Mortality rate. The number of deaths during a stated period of time divided by the total number of persons in the population. Prevalence. The number of existing cases of a disease, or condi- tion, at a designated point in time. Prevalence rate. The number of existing cases of a disease, or condition, at a designated point in time, per the number of per- sons in the population. Relative survival rate. Survival rates for persons with a partic- ular disease or condition corrected for the expected occurrence of death in persons in the age group. Survival rate. The number of persons surviving over a specified time period divided by the number of persons alive at the start of the time period. `In theThird National Health and Nutrition Examination Survey,the M (miss- ing) component of the DMFl (S) index reflects teeth (or tooth surfaces) miss- ing because of dental caries or periodontal disease. Teeth missing because of trauma, orthodontic treatment or other non-disease-related reasons were not scored. *Periodontal disease status is assessed by measuring the distance from the gingivai margin (FGM) to depth of the gingival sulcus, or pocket depth, and the distance from thegingival margibto the cementoenamel junction (FGM- CEl).A third measure,loss of attachment,is determined by calculating the dif- ference between pocket depth and the FGM-CU distance. Loss of attachment is important because it serves as a measure of how much support from the tissues surrounding the tooth has been lost. similar oral examination procedures as in NHANES. Because school attendance is high in the United States, these surveys are considered representative of noninstitutionalized children throughout the United States and are used in this chapter. Record-based surveys are another approach to obtaining health data for the nation as a whole or for selected broad areas. Mortality statistics are obtained by determining the number of deaths in the United States and dividing that figure by the total U.S. pop- ulation as determined from U.S. Census data (Kovar 1989). Cancer statistics are derived from population- based cancer registries in selected large geographic areas of the United States usirig reports of cancer occurrences from hospitals, doctors, and laborato- ries. This data system, maintained by the National Cancer Institute, is called the Surveillance, Epidemiology, and End Results program (Ries et al. 1999). Birth certificate registries in geographic areas and surveys of health care facilities provide valuable information from record-based systems about other aspects of oral and craniofacial health such as birth defects (Schulman et al. 1993). The Centers for Disease Control and Prevention's Behavioral Risk and State Surveillance System provides essential state data on edentulousness (Tomar 1997). In selected cases, survey findings other than from national prob- ability surveys are used. State-specific data are pro- vided for those conditions for which there are data from most states--that is, cancer mortality statistics and self-reports of edentulism. Economic status is derived from annual income data. Unless otherwise stated, "poor" is defined in this chapter as an annual income below the U.S. poverty level. For both national and other surveys, the race and ethnicity terms used in this report are consistent with the terms used in the supporting documentation as referenced in the text and cited in the reference list. Available national data for most conditions are limited primarily to Hispanic, non- Hispanic black, and non-Hispanic white populations, due to the sampling design of the national surveys. The NHANES III oversampled Mexican Americans, so the data from that survey are available for this sub- population of Hispanics. 62 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem WHO HAS WHAT DISEASES AND CONDITIONS? Dental Caries, Periodontal Diseases, and Tooth Loss Dental Caries Dental caries is one of the most common childhood diseases. In this section, decayed refers to teeth with caries that have not been treated. The term filled refers to treated caries. Dental caries refers to both decayed and filled teeth. Among 5- to 17-year-olds, dental caries is more than 5 times as common as a reported history of asthma and 7 times as common as hay fever (Figure 4.1). Prevalence increases with age. The majority (51.6 percent) of children aged 5 to 9 years had at least one carious lesion or filling in the coronal portion of either a primary or a permanent tooth. This proportion increased to 77.9 percent for 17-year-olds and 84.7 percent for adults 18 or older. Additionally, 49.7 percent of people 75 years or older had root caries affecting at least one tooth (NCHS 1996, NHANES III). Despite progress in reducing dental caries, indi- viduals in families living below the poverty level experience more dental decay than those who are economically better off. Furthermore, the caries seen in these individuals is more likely to be untreated than caries in those living above the poverty level (Figure 4.2); more than one third (36.8 percent) of poor children aged 2 to 9 have one or more untreat- ed decayed primary teeth, compared to 17.3 percent of nonpoor children. In addition to poverty level, the proportion of teeth affected by dental caries also varies by age and race/ethnicity. Poor Mexican American children aged FIGURE 4.1 Dental caries is one of the most common diseases among S-to 17-year-olds Caries I]\ 58.6 0 10 20 30 40 so 60 70 Percentage of children and adolescents aged 5 to17 Note: Data include decayed or filled primary and/or decayed,Rlled, or mlsring permanent teeth. Asthma, chronic bronchitis, and hay fever based on report of household respondent about thesampled S- to 17-year-olds. Source: NCHS 1996. 2 to 9 have the highest number of primary teeth affected by dental caries (a mean of 2.4 decayed or filled teeth) compared to poor non-Hispanic blacks (mean 1.5) and non-Hispanic whites (mean 1.9). Among the nonpoor, Mexican American 2- to g-year- olds have the highest number of affected teeth (mean 1.8)) followed by non-Hispanic blacks (1.3) and non- Hispanic whites (1 .O). There are also differences by race/ethnicity and poverty level in the proportion of untreated decayed teeth for all age groups. Poor Mexican American chil- dren aged 2 to 9 have the highest proportion of untreated decayed teeth (70.5 percent), followed by poor non-Hispanic black children C67.4 percent) (Figure 4.3). Nonpoor children have lower propor- FIGURE 4.2 A higher percentage of poor people than nonpoor have at least one untreated decayed tooth so * Poor teeth only) and permanent teeth) teeth only) Age iource: NCHS 1996. FIGURE 4.3 Poor children aged 2 to 9 in each racial/ethnic group have a higher percentage of untreated decayed primary teeth than nonpoor children 80 c & 70 01x4 cs 6o 55 50 55 w 40 XC rts 00) 3o i; 20 w- x 10 2 0 Non-Hispanic black Mexican American Non-Hispanic white * Poor children W Nonpoor children Source: NCHS 1996. ORAL HEALTH IN AMERICA: A REPORT OF THE WRGEON GENERAL 63 The Magnitude of the Problem tions of untreated decayed teeth, although the group with the lowest proportion (non-Hispanic whites) still has an average of 37.3 percent of decayed teeth untreated. Poor adolescents aged 12 to 17 in each raciaueth- nit group have a higher percentage of untreated decayed permanent teeth than the corresponding nonpoor adolescent group (Figure 4.4). Poor Mexican American (47.2 percent) and poor non- Hispanic black adolescents (43.6 percent) have more than twice the proportion of untreated decayed teeth than poor non-Hispanic white adolescents (20.7 per- cent). For nonpoor adolescents the proportion of untreated decayed permanent teeth is highest in non- Hispanic black adolescents (41.7 percent)-a pro- portion only slightly lower than for this group's poor counterparts (43.6 percent). The mean number of permanent teeth affected by dental caries (decayed or filled) for this age group is similar among Mexican Americans (2.7), non-Hispanic whites (2.5), and non-Hispanic blacks (2.3). As income level increases, the percentage of adolescents with decayed teeth decreases and the proportion of decayed teeth that have been filled increases (Vargas et al. 1998). Adult populations (aged 18 and older) show a similar pattern, with the proportion of untreated decayed teeth higher among the poor than the non- poor (Figure 4.5). Regardless of poverty level status, adult non-Hispanic blacks and Mexican Americans have higher proportions of untreated decayed teeth than their non-Hispanic white counterparts. FIGURE 4.4 Poor children aged 12 to 17 in each racial/ethnic group have a higher percentage of untreated decayed permanent teeth than nonpoor children Non-Hispanic black Mexican American `Non-Hispanic white W Poor children H Nonpoor children Source: NCHS 1996. Improvements have been noted over the past 25 to 30 years with regard to dental caries. Among most age groups, the average number of teeth per person affected by dental caries has decreased, and the aver- age number of teeth per person that show no signs of infection, as well as the proportion of the population that is caries-free, has increased. Since 1971-74, major increases have been noted in the percentage of children and adolescents aged 5 to 17 who have never experienced dental caries in their permanent teeth. Younger adults have experi- enced a decline in dental caries during this time period, as measured by the average number of teeth without decay or fillings (Figure 4.6). These trends are not found among those 55 to 74 years of age. I 1 FIGURE 4.5 Poor adults aged 18 and older have a higher percentage of untreated decayed teeth than nonpoor adults 50 45 5 5 40 =E r c 35 sg F z 30 f= 25 15 `s t - g#E 20 s `, 15 5s E It! 10 5 0 * Poor adults Source: NCHS 1996. O Nonpoor adults FIGURE 4.6 Since 1971-74, the average number of permanent teeth without decay or fillings has increased among 18- to 54-year-olds 7 1971-74 1988-94 Survey year Sources: NCHS 1975,1996. 64 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem The number of untreated decayed teeth per per- son across all age groups has also declined. periodontal Diseases The presence of periodontal disease is measured clin- ically in several ways, one of which is by calculating the loss of periodontal attachment. Figure 4.7 shows that most adults 25 years and older have at least 2 mm or more loss of attachment. The disease is more serious as the amount of attachment loss and number of tooth sites affected increase. More severe disease can be defined as having 4 mm or more loss of attach- ment in at least one site. The percentage of adults with 6 mm or more loss of attachment at one or more sites increases at older age groups, with 19.0 percent of 55- to 64-year-olds and 23.4 percent of 65 to 74- year-olds having this amount of loss or more. Figure 4.8 displays these data in a different format and shows that a small but increasing percentage of the popula- tion at each older age group has severe disease. At all ages, men are more likely than women to have at least one tooth site with a 6 mm or more loss of attachment (Figure 4.9). In addition to age and sex, the prevalence of periodontal loss of attachment also varies by racial/ethnic group (Figure 4.10). A higher percentage of non-Hispanic black persons at each age group have at least one tooth site with 6 mm or more of periodontal attachment loss as compared to other groups. Within each racial/ethnic group, the highest percentage affected is found among individu- als 70 years and older. At every age, a higher propor- tion of those at the lowest socioeconomic status FIGURE 4.7 The proportion of adults with at least one site with loss of periodontal attachment of 2 mm or more, 4 mm or more, and 6 mm or more increases with age 94.5 95.7 89.8 v 86.4 i 3 2 80 ,1 - Loss of attachment 3 14.9 t $4.6 .% 2 mm or more `s 60 60.5 - 1 50.2 :54.9 m 4 mm or more L m * 6 mm or more s . z 40 - 37.3 38.0 2! 81 " ? 22.1 20- ; .12.0 $3.0 0 - 0.2 I 1 , I , 18-24 25-34 35-44 45-54 55-64 65-74 75+ Age group Sources: Adapted from NCHS 1996,Burt and Eklund 1999 FIGURE 4.8 Although older adults have more periodontal attachment loss than younger adults, severe loss is seen among a small percentage of individuals at every age Age + la-44 - 45-M - 65+ 3 5 7 9 11 Loss of periodontal attachment (mm) Sources: Adapted from NCHS 1996, Burt and Eklund 1999. FIGURE 4.9 Males are more likely than females to have at least one tooth site with 6 mm or more of periodontal loss of attachment 40 f 35 g 30 B 25 E 20 g 1s #j 10 5 0 Age vw O Female * Male SourcesAdapted from NCHS 1996,Burtand Eklund 1999. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 65 The Magnitude of the Problem (SES) level have at least one site with attachment loss of 6 mm or more, compared to those at higher SES levels (Figure 4.11) (Burt and Eklund 1999).' Gingivitis as measured by gingival bleeding, a sign of inflammation, is more evident among Mexican Americans (63.6 percent) than among non- Hispanic blacks (55.7 percent) and non-Hispanic whites (48.6 percent) (Albandar et al. 1999). Early-onset periodontitis, a severe, rapidly pro- gressive disease occurring in individuals under age FIGURE -t.lO Non-Hispanic blacks are more likely than other groups to have at least one tooth site with 6 mm or more of periodontal loss of attachment 50 47.1 45 a8 40 H 35 E 30 5 25 5 20 5 15 = 10 5 0 30-49 SO-69 70+ Age group Race/ethnicity W Non-Hispanic black Mexican American PI Non-Hispanic white Source: NCHS 1996. 35, has been reported to be 4 times more common in males than in females (Lee and Brown 1991); among 13- to 17-year-olds, it has been found to be highest among African Americans (10.0 percent), as com- pared with Hispanics (5.0 percent) and whites (1.3 percent) (Albandar et al. 1997). Tooth Loss and Edentulism Although teeth are lost for a number of reasons, including trauma, orthodontic treatment, and removal of third molars (wisdom teeth), most teeth are lost because of periodontal disease or dental caries (Phipps and Stevens 1995, Neissen and Weyant 1989). By age 17, mom than 7.3 percent of U.S. children have lost at least one permanent tooth because of caries; by age 50, Americans have lost an average of 12.1 teeth, including the third molars. Men and women are nearly equally likely to be edentulous. Overall, a higher percentage of individu- als living below the poverty level are edentulous than are those living above (Figure 4.12). Individuals with incomes equal to or above twice the poverty level have a rate of edentulism of 6.9 percent. This rate is less than half the rate for those with incomes below twice the poverty level (14.3 percent). Although the overall rate of edentulism for adults 18 and older is approximately 10 percent (9.7 per- cent), the rate increases with age, so that about a third (33.1 percent) of those 65 and older are edentulous. Comparisons across raceIethnicity for the population 18 years and older indicate that the edentulous rate FIGURE 4.11 The percentage of adults with at least one tooth site with 6 mm or more of periodontal attachment loss is greater among persons of low socioeconomic status at all ages 40 37.8 36.2 Y 35 e 30 x 25.8 25.5 t 25 ii 20 E 15 E 81 10 5 0 18-24 25-34 35-44 45-54 55-64 65-74 75+ Age group Socioeconomicstatus tow B Middle * High Sources: Adapted from NCHS 1996,Burt and Eklund 1999. `In this section, income levels are defined as low (less than 185 percent of the U.S. poverty level or below), middle (185.1 percent to 350 percent of the poverty level), and /rig/l (350.1 percent of the poverty level or higher). 66 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL for non-Hispanic whites is 10.9 percent; for non- Hispanic blacks, it is 8.0 percent; and for Mexican ,\mericans, 2.4 percent. Non-Hispanic whites, both poor and nonpoor, have the highest rates of eden- tufism compared to non-Hispanic blacks and \tesican Americans. Of the three population groups, \lexican Americans are the least likely to lose all of their teeth, and the proportion of Mexican Americans \vho are edentulous varies only slightly by economic status. A lower proportion of U.S. adults have lost all their natural teeth now than was the case two decades ago (Figure 4.13). The decline is most pro- nounced at older ages. Edentulism is one of a few conditions for which state-specific data exist. These data reveal a wide variation in the percentages of the population aged 65 and older who have no teeth, from a low of 13.9 percent in Hawaii to a high of 47.9 percent in West Virginia; this is more than a threefold difference (Table 4.1) (Tomar 1997). Reasons for these differ- ences are unknown at this time. Oral and Pharyngeal Cancers and Precancerous Lesions Oral and Pharyngeal Cancers Every year, about 1.2 million people develop cancer in the United States (based on 2000 estimates). Sites FIGURE 4.12 Complete tooth loss varies by race/ethnic@ and poverty status: a higher percentage of poor and nonpoor non-Hispanic white adults (18 and older) have no teeth compared with non-Hispanic blacks and Mexican Americans Non-Hispanic black Mexican American Non-Hispanic white * Poor adults II Nonpoor adults Source: NCHS 1996. The Magnitude of the Problem in the oral cavity and pharynx (throat) account for about 30,200 cases, or 2.4 percent of all cancers, and about 7,800 Americans die from these cancers each year (ACS 1999). The life of each person with these cancers is shortened by an average of 16.5 years. The median age at diagnosis of oral and pharyngeal can- cer is 64, and the rate of occurrence increases with age. More than 95 percent of oral cancers occur in individuals aged 35 and older (Ries et al. 1999). The overall 5-year survival rate for people with oral and pharyngeal cancers is 52 percent, which is worse than that for-among others-cancers of the prostate, corpus and uterus, breast, bladder, larynx, cervix, colon, and rectum in both blacks and whites (Ries et al. 1999). People with oral cancers detected at an early stage have a 5-year survival rate of 81.3 percent; however, only 35 percent of individuals with oral and pharyngeal cancers are diagnosed at an early stage. The 5-year survival rate drops to 21.6 percent FIGURE 4.13 The percentage of people without any teeth has declined among adults over the past 20 years 28.6 12& is.2 Age +65-74 +55-64 +35-54 * 18-34 2.0 .c 0.4 / 1971-74 1988-94 Survey years Sources: NCHS1975,1996. TABLE 4.1 Five states with highest and lowest percentages of edentulous persons aged 65 and older States with Highest Percentage Percentage State Edentulous West Virginia 47.9 Kentucky 44.0 Louisiana 43.0 Arkansas 39.2 Maine 37.8 Source: Tomar 1997. States with Lowest Percentage Percentage State Edentolous Hawaii 13.9 California 16.2 Oregon 16.5 Arizona 18.5 Wisconsin 19.4 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 67 among people diagnosed with advanced-stage can- cers (Ries et al. 1999). Compared to patients with other types of cancer, oral and pharyngeal cancer patients who survive have the highest rate of devel- opment of new cancers in the mouth or in other parts of the body (Winn and Blot 1985). Incidence rates for oral and pharyngeal cancers are higher for black individuals than for whites: 12.5 cases versus 10.0, respectively, per 100,000 people each year. In the United States, Asians and Pacific Islanders (7.9 per lOO,OOO), American Indians and Alaska Natives (6.4 per lOO,OOO), and Hispanics (5.8 per 100,000) have lower incidence rates than whites and blacks (Wingo et al. 1999). Figure 4.14 provides incidence rates for selected racial/ethnic groups by sex. Males have higher inci- dence rates than females; specifically, they are 2.6 times more likely to develop oral and pharyngeal cancers than women (Ries et al. 1999). The incidence rates of oral and pharyngeal cancers for black males FIGCRE -4.1-t Males have higher incidence rates of oral and pharyngeal cancers than females Z Female H Male are 39.6 percent higher than for white males (20.8 versus 14.9, respectively, per 100,000 males per year). Rates for black and white females are the same (6.0 per 100,000 females per year) (Ries et al. 1999). Oral and pha- ryngeal cancers are the seventh most common cancer among white males and the fourth most frequently diagnosed cancer among black males (Figure 4.15) (Wing0 et al. 1999). Black White Asian and Pacific Islander American Indian and Alaska Native Hispanica 0 5 10 15 20 25 Rate per 100,000 Nate: Age adjusted to the 1970 U.S.standard. 1 Data are unavailable for Hispanic females. Sources: Adapted from Wingo et al. 1999;SEER Program, 1990-96, Ries et al. 1999. As for many other cancer sites, the overall 5-year survival rate for oral and pharyngeal can- cers is lower for blacks than for whites: 34 versus 56 percent FIGURE -t.15 Cancers of the oral cavity and pharynx are the seventh most common cancers in white males and the fourth most common in black males Prostate gland Lung & bronchus Colon/rectum Urinary bladder tymphomas Melanoma of skin Oral cavity & pharynx Leukemia Kidney/renal Pancreas 0 50 100 150 200 250 Prostate gland Lung&bronchus Colon/recrum Oral cavity&pharynx Stomach Urinary bladder Lymphomas Pancreas Kidney/renal Esophagus 0 50 100 150 200 250 White males Note: Age adjusted to the 1970 U.S.standard. Sources: Adapted from Wingo et al. 1999; SEER Program, 1990-96, Ries et al. 1999. Incidence rate per lW,OOO Black males a; ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL (Ries et al. 1999) (Figure 4.16). However, only 19 percent of blacks with oral and pharyngeal cancers are diagnosed when the cancer is at the local, and more easily treatable, stage, compared to 38 percent for whites (Figure 4.17). At every stage of diagnosis, the survival rate for blacks is lower than for whites (Figure 4.18). The occurrence of cancers in specific sites with- in the oral cavity and pharynx varies by sex and race/ethnicity A relatively rare subtype of pharyngeal cancer, nasopharyngeal cancer, occurs more often in ,American males and females of Chinese descent than among other raciauethnic groups (Miller et al. 1996). Blacks are twice as likely as whites to develop cancers of the pharynx: 6.0 and 2.9 per 100,000 per year, respectively (Ries et al. 1999). Individuals with can- FIGURE 4.16 Five-year relative survival rates for selected cancers for whites and blacks 0 16 2d io 4 5b ti 70 io io 100 Five-year relative survival rates H White patients W Black patients Note: NOS = not otherwise specified. Source: Korary 1996. cers of the pharynx generally have a worse survival rate than those with cancers in oral cavity sites: 5- year pharyngeal cancer survival rates range from 53.3 to 29.5 percent, depending on the subsite, whereas oral cavity cancer survival rates range from 94.3 to 48.3 percent. The incidence of lip cancer, a highly treatable cancer, is more common in whites than among blacks (1.2 per 100,000 persons per year compared to 0.1). Overall, the incidence rate for oral cavity and pharyngeal cancers is decreasing, with an estimated annual percentage decrease of 0.5 percent per year between 1973 and 1996. There are wide variations in the incidence of site-specific cancers. The largest . FIGURE 4.17 Blacks are less likely to be diagnosed with a localized oral or phatyngeal cancer than whites 60 I White patients Stage at diagnosis Source: Adapted from SEER Program, 1989-95, Ries et al. 1999. FIGURE 4.18 At every stage of diagnosis, the S-year relative survival rates for blacks with oral and pharyngeal cancers are lower than for whites 90 80 * White patients Stage at diagnosis Source: Adapted from SEER Program, 1989-95, Ries et al. 1999. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 69 The Magnitude of the Problem annual declines in incidence were noted for lip can- cer (-3.4 percent per year between 1973 and 1996) (Ries et al. 1999). In contrast, the incidence of tongue cancer, the most common form of oral and phar)-ngeal cancer, may be increasing among young men (Day et al. 1994). Although overall mortality rates for oral and pha- ryngeal cancers declined by 1.6 percent per year between 1973 and 1996, the 5-year survival rate for individuals with oral and pharyngeal cancers has shown no improvement for the past 25 years (Ries et al. 1999). Mortality statistics by state allow for analysis of deaths due to oral cavity and pharyngeal cancers. Table 4.2 highlights the wide variation in mortality found in the country The highest rate is in the District of Columbia-6.7 per 100,000 population; this is nearly 5 times the lowest rate, 1.4 in Utah. Again, reasons for this variation need to be studied (Ries et al. 1999). Tobacco-related Lesions Tobacco use has been estimated to account for over 90 percent of cancers of the oral cavity and pharynx (Peto et al. 1995) and thus represents the greatest single preventable risk factor for oral cancer. Both smoking and spit (smokeless) tobacco (moist snuff and chewing tobacco) are associated with a number of other oral conditions, including oral mucosal lesions, that may progress to oral cancer (Silverman 1998). One type of tobacco-related lesion.is seen in peo- ple who use spit tobacco. A national survey of U.S. schoolchildren in 1985-86 showed that 6.1 percent of males and 0.1 percent of females used spit tobacco. The survey also showed that 34.9 percent of current snuff users aged 12 to 17 and 19.6 percent of current adolescent chewing tobacco users had a spit tobacco lesion (Figure 4.19) (Tomar et al. 1997). The preva- TABLE 4.2 Five states with highest and lowest oral and pharyngeal cancer mortality rates States with Highest Rates States with Lowest Rates Mortality Rate per Mortality Kate per State 100,000 Population State 100,000 Population District of Columbia 6.7 Minnesota 2.0 Delaware 4.0 Wyoming 2.0 South Carolina 3.9 Colorado 2.0 Louisiana 3.5 North Dakota 1.8 Florida 3.4 Utah 1.4 Note: Ages adjusted to the 1970 standard population. Source: Ries et al. 1999. lence of tobacco-related lesions increased with increasing duration and frequency of spit tobacco use. In some American Indian tribes, both adolescent males and females commonly use spit tobacco and have an especially high frequency of spit tobacco lesions. On a Sioux reservation, 37.0 percent of stu- dents in grades 7 through 12 used spit tobacco. Spit tobacco lesions occurred in over one third of those tobacco-using adolescents (CDC 1988). In another study of Navajo adolescents, three fourths of male adolescents (75.4 percent) and one half of female adolescents (49.0 percent) used spit tobacco. Of Navajo adolescents who used spit tobacco, 25.5 per- cent had spit tobacco lesions-29.6 percent of males and 17.0 percent of females (Wolfe and Carlos 1987). Selected Mucosal Infections and Diseases Oral Herpes Simplex Virus Infections The prevalence of recurrent herpes lesions is estimat- ed to be between 15 and 40 percent (Scully 1989). The proportion of the U.S. population with herpes simplex virus type 1 (HSV-1) antibodies is 68.2 per- cent (as evidenced by positive antibody titer). The proportion reporting a history of herpes lesions in the past 12 months is 17.7 percent. The presence of anti- bodies and occurrence of herpes lesions vary by age (Figure 4.20). The frequency of recurrence also varies greatly, ranging from once to several times per year. Infection with the oral herpes simplex virus has been related to socioeconomic factors, with 75 to 90 percent of individuals from lower socioeconomic FIGURE 4.19 Tobacco-related oral lesions are more common in 12-to 17- year-olds who currently use spit tobacco 35 -I c 30- .,0 f 25- .= B s 20- & g 15- aI g lo- 5 2 5- O-- L m Current user Snuff user Chewing tobacco user Source: Adapted from Tomar et al. 1997. 70 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL populations developing antibodies by the end of the first decade of life (Whitley 1993a,b). In comparison, 30 to 40 percent of individuals from middle and upper socioeconomic groups evidence antibodies by the middle of the second decade of life. The prevalence of one or more herpes labialis lesions within the past 12 months is 8.4 percent for non-Hispanic blacks. 16.2 percent for Mexican Americans, and 19.7 percent for non-Hispanic whites (NHANES III). Recurrent Aphthous Ulcers Various epidemiologic studies of recurrent aphthous ulcers have indicated that the prevalence in the gen- eral population can vary from 5 to 25 percent (Axe11 et al. 1976, Embil et al. 1975, Ferguson et al. 1984, Ship 1972, Ship et al. 1967). In NHANES III, 17.2 percent of persons reported having a recurrent aphthous ulcer within the past 12 months, and occurrences were most common among young adults (18 to 24 years old) (Figure 4.21). In selected population groups, the prevalence of recurrent aphthous ulcers can be as high as 50 to 60 percent (Miller and Ship 1977, Ship et al. 1961, 1977). Other Mucosal Lesions Other mucosal conditions contribute to the burden of oral diseases. The following are among the most FIGURE 4.20 Herpes simplex type 1 virus infection is widespread, and oral herpes lesions (cold sores/fever blisters) are common 100 90 80 a 5 70 Q, f 60 5 50 z 8 40 % 30 88.9 Age * 8-11 * 12-17 O l&24 O 25-44 :$45-64 >65 0 Orul candidiasis (commonly called thrush) is a particular prob- lem for individuals with impaired immune function. A prevalence of 9.4 percent has been reported in renal transplant patients (King et al. 1994); Samaranayake (1992) reports prevalences between 43 and 93 percent among HIV-infect- ed patients. It is estimated that 3.6 percent of full denture wearers have candidiasis. 20 10 0 Positive antibody to HSV-la 2 Data not available for the 8- to 1 l-year-old age group. Source: NCHS 1996. Had oral herpes lesion in past 12 months FIGURE 4.21 A substantial percentage of the population, particularly among young adults, has experienced recurrent aphthous lesions (canker sores) in the past 12 months 26.9 o Denture stomatins, a condi- tion in which the mucosa under- neath a denture becomes inflamed and sometimes painful, affects 25.6 percent of people aged 18 and older who have two full dentures. Additionally, 32.2 percent of those with one full denture are affected, 26.7 percent of those with one or more partial den- tures, and 0.87 percent of those who do not have full or partial dentures. 0 Oral human papillomavirus infections, oral and genital papillomas (or condyloma acuminata, also called venereal warts), are especially common among HIV-positive patients. Human papilloma- viruses may be associated with some oral leukopla- kias with a high risk for malignant transformation (Palefsky et al. 1995). Age group Source: Adapted from NCHS 1996 The Magnitude of the Problem common: Developmental Disorders Numerous developmental disorders affect the oral, dental, and craniofacial complex. These include con- genitally missing teeth [all or specific tooth types); congenital problems involving tooth enamel, pulp, or dentin; and craniofacial birth defects or syndromes. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 71 The Magnitude of the Problem Cleft lip and palate are the most common congenital anomalies and may occur as isolated defects or as part of other syndromes. Other craniofacial defects and syndromes that have been the focus of recent genet- ics research include ectodermal dsyplasia, Treacher Collins syndrome, Apert's syndrome, and Waarden- burg syndrome. Craniofacial defects and syndromes have many serious consequences including unusual facial features; severe functional problems; and the need for extensive surgical, medical, and rehabilita- tive interventions and prosthetic devices. Cleft Lip/Palate Oral clefts are one of the most common classes of congenital malformations in the United States, with prevalence rates in the general population of 1.2 per 1,000 births for cleft lip with or without cleft palate and 0.56 per 1,000 births for cleft palate alone (Schulman et al. 1993). These conditions affect facial appearance throughout life. The rate of oral clefts for whites is more than 3 times that for blacks (1.7 versus 0.5 per 1,000 live births) (Figure 4.22). Oral clefts are more common among North American Indians (3.7 per 1,000 births) (Lowry et al. 1989). Cleft palate occurs more fre- quently in females, whereas cleft lip or cleft lip/palate - FIGURE 4.22 Cleft lip and cleft palate are among the most common congenitai malformations, and prevalence varies by race Hydrocephalus Trisomy 21 Microcephalus Obstruction kidney/ureter Cleft lip & palate Pyloric stenosis 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 Prevalence perl,OOOlivebirths Source: Schulman et al. 1993. * Whites * Blacks is more common in males (Burman 1985, Fraser and Calnan 1961, Habib 1978, Owens et al. 1985). Malocclusions Malocclusions can occur due to congenital or acquired misalignments (crowding) of the teeth or jaws. In a national study of individuals between 8 and 50 years old, 25 percent were found to have no crowding of the incisors (front teeth), whereas 11 percent were found to have severe crowding (Bnmelle et al. 1996). About 9 percent had a posteri- or crossbite, where there is poor contact of the back upper and lower chewing surfaces. This crossbite was most common in non-Hispanic \nlhites. Severe over- jet-where the upper front teeth project far for- ward-was found in approximately 8 percent of this population, with a similar percentage demonstrating a severe overbite-where the front top and bottom teeth greatly overlap when the mouth is closed. Less than 5 percent of non-Hispanic whites had an open bite, an inability to bring the upper and lower front teeth together. Injury Injuries to the head, face, and teeth are very com- mon. They can range in severity from the very mild to those that cause death. Although injuries have a major impact on oral health, data on the number and severity of head and face injuries in the United States are very limited.2 Most of our knowledge about the number of injuries that occurs comes from more severe injuries that involve a visit to the emergency room. In 1993 and 1994, there were 20 million visits per year to emergency departments for craniofacial injuries. Less serious injuries can be treated on an outpatient basis. More than 5.9 million injuries in 1991 were treated by dentists in private offices (Gift and Bhat 1993). Overall, 25 percent of all persons aged 6 to 50 have had an injury that resulted in dam- age to one or more anterior teeth (Kaste et al. 1996a). An estimated 2.9 million emergency room visits for all age groups related to tooth or mouth injuries between 1997 and 1998. Twenty-five percent of these injuries were seen in children under the age of 4 (NCHS 1997b). The leading causes of head and face injuries that result in emergency room visits include falls, assaults, IThis section reporrs national data that should provide some estimation of the scope of craniofacial injuries in the population. However, the findings may not be directly comparable because they are from different sources at different times, and because those at risk for each type of injury are not quantified in most cases. 72 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL sports injuries, and motor vehicle collisions (De Wet 1981, Pinkham and Kohn 1991, Sane 1988). In the yational Health Care Survey of emergency rooms, ,lssaults and falls each accounted for 31 percent of visits related to head and face injury. Other studies have reported that up to 19 percent of head and face Injuries are sports-related (McDonald 1994), and 5 percent of head and 19 percent of face injuries result from riding bicycles and tricycles (U.S. Consumer Product Safety Commission 1987). There are differences in rates of emergency room visits for head and face injuries among demographic groups. Males had higher rates than females, except among older adults. The rates of injury were higher for younger and older adults than for those in the middle years. Chronic and Disabling Conditions Oral-Facial Pain Oral-facial pain can greatly reduce quality of life. These types of pain may be due to tooth-related infections, mucosal sores, and irritations, and may include burning sensations, pain in the jaw joint area, and aching pain across the face or cheek. Over 39 million people, or 22 percent of adults 18 years of age and older in the civilian U.S. population, experi- enced at least one of five types of oral-facial pain dur- ing a recent 6-month period (Lipton et al. 1993). Based on the results of a national study of the preva- lence and distribution of oral-facial pain, it is esti- mated that during a 6-month period, 1 American adult in 8 (12.2 percent) suffers from toothache, 1 in 12 (8.4 percent) from painful oral sores, 1 in 19 (5.3 percent) from jaw joint pain, and 1 in 71 (1.4 per- cent) from face or cheek pain (Lipton et al. 1993). The prevalence of toothache and pain due to oral sores decreases with age, whereas the prevalence of burning mouth pain increases with age. Women are twice as likely as men to report two specific types of oral-facial pain: jaw joint pain and face/cheek pain (Figure 4.23). Non-Hispanic blacks and Hispanics were slightly more likely to report toothache than non-Hispanic whites (Lipton et al. 1993). Adults liv- ing in poverty were more likely to report toothaches than adults living above the poverty level (Vargas et al. 2000). Temporomandibular Disorders Symptoms of temporomandibular disorders (TMDs) vary but may include severe pain in the jaw muscu- lature, severe pain or difficulty when opening the The Magnitude of the Problem mouth and chewing, headaches, and ear pain. Based upon assessments of pain in or around the jaw joint, these disorders are estimated to affect 10 million Americans (Lipton et al. 1993). Data from the few available population-based epidemiologic studies indicate that the prevalence of self-reported pain symptoms and clinical signs of TMD pain is between 5 and 15 percent, with peak prevalence in young and middle-aged adults (20 to 40 years of age) (Von Korff 1995). i\lthough physical signs associated with TMDs have been shown to occur with nearly equal fre- quency among men and women, clinical studies have found that women in the third and fourth decades of life were much more likely than men pf the same age to have sought care for reported facial pain in the tem- poromandibular region (Carlsson and LeResche 1995). Sjiigren's Syndrome Sjogren's syndrome, an autoimmune disorder that causes xerostomia (dry mouth), difficulty in swal- lowing, and xerophthalmia (dry eyes), is estimated to affect 1 to 2 million people in the United States (Talal 1992). The diagnosis is most often made in women in middle age. One estimate of the average annual incidence rate for Sjogren's syndrome, based on the Olmsted County, Minnesota, medical database, is about 3 to 5 cases per 100,000 population; this may be low, however (Pillemer et al. 1995). As with most other autoimmune conditions (e.g., rheumatoid arthritis, systemic lupus erythematosis), Sjogren's syndrome affects more women than men. The femalelto-male ratio depends on the study, but may be as high as 9:l (Fox 1996). FIGURE 4.23 Toothache is the most common source of oral-facial pain 14 P g 12 ," 8 10 ; 8 L ; 6 P 4 f 2 0 I Toothache Oral sores Jaw joint Face/cheek Burning Pain category * Female m Male Note: Data are for persons aged 18 and older looking back over the past 6 months. Sources: Adapted from NCHS 1989, Lipton et al.1993. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 73 The &lagnitude of the Problem WHAT IS THE BURDEN OF DISEASE IN SELECTED POPULATIONS? CHALLENGES AND OPPORTUNITIES The national data provide a broad-brush picture of America's oral health. For selected populations, how- ever, oral health and disease status has a different profile. By 2050 about 50 percent of the U.S. popula- tion is expected to be Asian, non-Hispanic black, Hispanic, and American Indian (Council of Economic Advisers 1998). Currently available data for these groups present a picture of disease that is generally poorer than that for non-Hispanic whites. These subgroups present a unique cluster of health, socioeconomic, and cultural issues. At the same time, data for the subgroups within each of these categories are lacking. In addition to raciauethnic groups, other groups such as individuals with disabilities, the homeless, incarcerated individuals, and migrant workers have unique needs and challenges. Cutting across all subgroups are gender-specific health issues. For improvements to be made in America's overall health, a better understanding of the full dimension of the problems faced by these populations and development of specific solutions are part of the chapter examines each greater depth. needed. This subgroup in Racial and Ethnic Minorities Although there have been gains in oral health status for the population as a whole, they have not been evenly distributed across subpopulations. Non- Hispanic blacks, Hispanics, and American Indians and Alaska Natives generally have the poorest oral health of any of the racial and ethnic groups in the U.S. population. Other health statistics, such as life expectancy and infant mortality, indicate that the general health of these groups is varied and also poor compared to other population groups (Council of Economic Advisers 1998). To address the elimination of these disparities in health-and also in housing, education, and other indicators of social and eco- nomic well-being-the administration has launched "The President's Initiative on Race: One America in the 2lst Century" Recommendations for improving the oral and general health status of racial and ethnic minorities are also a prominent feature of Healthy People 2010, the goal-setting health agenda devel- oped for the decade by the USDHHS (2000). African Americans Numerous studies over the decades have compared the health status of blacks and whites in American 74 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL society, but relatively little systematic attention has been focused on the oral health of blacks. Although the overall oral health status of Americans has been improving, many oral diseases and conditions among blacks remain a serious problem--despite the fact that for almost three decades these disparities have been highlighted and recommendations made for addressing health issues including research, educa- tion, human resources, and delivery systems (National Dental Association 1972). These recom- mendations still represent opportunities for improve- ment in the oral health status of African Americans. Baseline data for the Healthy People 2010 objec- tives establish that, for children aged 2 to 4 years, 24.0 percent of non-Hispanic `blacks have experi- enced dental caries in their primary teeth, compared to 15.0 percent for their non-Hispanic white coun- terparts. For children aged 6 to 8, there were no dif- ferences among the' races; but for 15year-olds, a higher percentage of non-Hispanic blacks were affected than of whites. In addition the percentage of people of all ages who had untreated caries was sub- stantially higher for blacks than for whites-about twice as many Higher levels of gingivitis and peri- odontal loss of attachment were also seen in non- Hispanic blacks as compared to non-Hispanic whites. A greater percentage of non-Hispanic blacks 18 years and older have missing teeth when compared to non-Hispanic whites. Relative to non-Hispanic whites, however, non-Hispanic blacks aged 18 and older are less likely to have lost all their teeth (eden- tulism) regardless of whether they are poor. African American males have the highest inci- dence rate of oral cavity and pharyngeal cancers in the United States compared with women and other racial/ethnic groups (Wingo et al. 1999). The distr-i- bution of oral cancer cases reveals that blacks also have a higher proportion of pharyngeal cancer than oral cavity cancer compared to whites. Also, the 5- year relative survival rate (1989-95) for oral cancer was much lower among blacks than whites: 34 ver- sus 56 percent (American Cancer Society (ACS) 1999). This latter finding may be related to the fact that a high percentage of these cancers are diagnosed in later stages of disease in blacks as compared to whites (ACS 1999). On the other hand, for several conditions, African Americans have a lower disease burden than do whites. The incidence rate for cleft lip and cleft palate in African Americans is 0.54 per 1,000, about a third the rate for whites (1.70 per 1,000). Also the prevalence of having one or more herpes labialis lesion within the past 12 months is 50 percent less than that for Mexican Americans and non-Hispanic whites. Hispanics Disparities in oral and general health status between Hispanic and non-Hispanic populations in the United States have been long recognized. Yet the health profile of Hispanics is incomplete due to insuf- ficient sampling of subgroups in national surveys, inconsistent or inadequate assessment of ethnicity, or ambiguities in reporting of ethnic identity (Hahn 1992). Recent efforts to improve data collection, identify subgroups, and provide more baseline data for Hispanics have addressed the situation somewhat, but much work remains to ensure accurate data for health planning and research (Delgado and Estrada 1993). Among preschool Hispanic children early child- hood caries is a particular concern. Two reports have documented early childhood caries among 12.9 per- cent of Hispanic children examined in San Antonio and 37 percent of predominantly Hispanic children in San Francisco (Garcia-Godoy et al. 1994, Ramos- Gomez 1999). Most recently, national survey data suggest that a higher proportion of Mexican American children ages 12 to 23 months may experi- ence dental caries than other racdethnicity groups (Kaste et al. 1996b). Preliminary data from NHANES III indicate that young Mexican American children aged 2 to 4 are more likely to have experienced dental caries in their primary teeth, have on average more decayed and filled tooth surfaces, and have more untreated disease than either non-Hispanic white or non-Hispanic black children (Kaste et al. 199613). Mexican American children aged 2 to 5 years-especially those from lower-income households-were more likely than their African American and non-Hispanic white counterparts to have one or more decayed primary teeth (Vargas et al. 1998). Dental caries continues to affect large numbers of school-age children and youth, as only 30 percent of Mexican Americans, 32 percent of non-Hispanic whites, and 41 percent of non-Hispanic blacks 12 to 17 years of age were free of caries in their permanent teeth (USDHHS 1996). However, most of the dental caries in the permanent teeth of non-Hispanic white children aged 12 to 17 had been treated or filled (87 percent), compared to 63 percent for Mexican Americans and 60 percent for non-Hispanic blacks. The only large-scale survey that permits compar- ison among Hispanic subgroups is the Hispanic Health and Nutrition Examination Survey (HHANES 1982-84). After controlling for age, sex, income, and - The Magnitude of the Problem education, HHANES results show that Cuban American and Puerto Rican adults had about twice as many missing teeth as Mexican Americans. Puerto Ricans and Cuban Americans also had on average more filled teeth than Mexican Americans. Puerto Rican children and adults under 45 years old had more gingivitis than Cuban Americans and Mexican Americans; the highest prevalence of periodontal dis- ease was reported among Puerto Ricans compared to the two other Hispanic groups (Ismail and Szpunar 1990). A national survey found that employed Hispanic adults were twice as likely to have untreated dental caries as non-Hispanic whites. In this study, gingivi- tis and periodontal problems (attachment loss and pockets) were also among the more common prob- lems among the Hispanic adults studied (Watson and Brown 1995). Analysis of a more recent survey (NHANES III) that sampled Mexican Americans is particularly revealing. After adjusting for age, sex, educational attainment, and annual family income, Mexican American adults are similar to their white non- Hispanic counterparts on most oral health indicators. However, among Mexican Americans, individuals in families with less than $20,000 annual income were 1.6 times less likely to have an intact dentition, 3.1 times more likely to have any untreated decay on the crowns of their teeth, and 4.2 times more likely to have severely decayed teeth (very large cavities or only the roots of teeth remaining) than non-Hispanic whites (Garcia and Drury 1999). Also, Mexican Americans were less likely to be edentulous regard- less of poverty status than either non-Hispanic whites or non-Hispanic blacks (Drury et al. 1999). These findings confirm the importance of con- trolling for sociodemographic factors in reporting on oral health status as well as the need to assess other factors related to health status. As a group, Hispanics have lower median incomes, higher poverty rates, more unemployment, and less education than non- Hispanic whites (Ramirez 1999). However, sociode- mographic factors are just one aspect of the questions raised when attempting to understand differences in oral health. The effect of financial barriers and nonfi- nancial factors such as language, culture, dietary pat- terns, and behaviors on access, care seeking, and health outcomes must also be examined. Variations in conditions such as diabetes also may contribute to differences in oral health. It is estimated that Hispanics will surpass African Americans as the country's largest minority group by 2020 (U.S. Bureau of the Census 2000). Aggregate statistics obscure substantial variations within ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 7s The Magnitude of the Problem Hispanic subgroups. More than 20 different coun- tries of varied cultural, socioeconomic, and political backgrounds are currently included in this category of the U.S. population. Narrowing the gap in oral health between Hispanic and non-Hispanic groups will require improved data on health status, barriers to access, and disease factors underlying differences in oral health in these populations. Asians, Native Hawaiians, and Other Pacific Islanders National data for the oral health of Asian, Native Hawaiian, and other Pacific Islander (ANHPI) groups that can be generalized to the U.S. population are not available. Instead the profile of disease and health in this category is only available through studies of spe- cific states and locales. Among all ethnic groups in California in 1993 and 1994, Asian and Pacific Islander American (APIA) children in Head Start had the highest prevalence of early childhood caries-20 percent compared to 14 percent for all Head Start children (Pollick et al. 1997). These data are compa- rable to other survey findings of 16 to 20 percent and 29 percent early childhood caries among APIA chil- dren in Hawaii and California, respectively (Greer unpublished, Louie et al. 1990). A California study of 6- to 8-year-olds found dis- parities in the oral health status of APIA children in the state when compared to all children nationally. Among the California APIA children, 7.I percent had untreated dental caries, with a significant portion of this group requiring urgent dental treatment. By comparison, NHANES III data indicate that in 1988 94, 29 percent of children in the United States aged 6 to 8 years had untreated dental decay There is variation in oral health status among subgroups of ANHPI children. In a recent survey in Hawaii, the prevalence of early childhood caries among APIA children was 16 percent, ranging from a low of 8 percent among Japanese children to a high of 25 percent among Filipino children. The preva- lence of untreated dental caries in 6- to 8-year-old APIA children was 39 percent, which ranged from a low of 16 percent among Japanese children to 40 per- cent among Native Hawaiians, 48 percent among Southeast Asians, and 62 percent among non-Native Hawaiian Pacific Islanders (Greer 1999). Oral cancer incidence and mortality rates for APIAs are lower than those for white non-Hispanics and African Americans. However, nasopharyngeal cancer incidence and mortality rates among Chinese and Vietnamese populations are many times higher than other groups (Miller et al. 1996), and therefore pose a unique health problem for these subgroups. Until recent years, vital statistics and other health-related data were virtually nonexistent for the APIA population. Data for this group generally appeared in the "other" category of national surveys, and thus were not helpful in determining specific population-based oral or general health needs. Little national focus has been given to defining and meas- uring the oral health problems and related health care needs of the APIA population. These needs are now highlighted in the 2010 Healthy People Oral Health Objectives. A few statewide oral health data exist for some APIA child populations, but no ethnic subgroupings can be assessed. Again, this category of the U.S. population is extremely heterogeneous. It is estimated that 76 percent is from one of five ethnic origins and that 74 percent in 1990 were foreign born. More than 63 percent live in four states: California, New York, Hawaii, and Texas. Con- sequently, determining the reasons for variations in oral health will require additional data. American Indian/Alaska Native Populations Data on the oral health of American Indians and Alaska Natives (AVAN) are available through studies conducted by the Indian Health Service (IHS) (Niendorfs 1994). The AVAN people constitute about 1 percent of the U.S. population, or an esti- mated 2.5 million people in 2000. Little is known or can be easily determined about the general or oral health status of the 1 million AVAN people not served by the IHS system. For this reason, with the exception of overall death rates obtained from census data, the statistics described in this section will be limited to the 1.5 million AVAN served by the IHS. By and large, this group represents AVAN people liv- ing on or near reservations. Preliminary analyses of the IHS-wide Oral Health Status Survey of over 13,000 dental patients in 1999 revealed that some conditions have worsened and some improved since an earlier survey conducted in 1991 (IHS 1994, 2000). Across the IHS service pop- ulation there was a statistically significant increase in caries among adults over 55 as measured by the decayed, missing, and filled teeth index. The decayed and filled tooth rate increased from 7.5 to 8.8 teeth, with no change in the average number of missing teeth for this age group. Among AVAN children across the IHS, there was a significant decline in caries in the permanent den- tition and a significant increase in caries in the pri- mary dentition. Among children aged 2 to 5 years, the increase in decayed and filled primary teeth sur- faces went from 8.6 to 11.4. In general, AVAN popu- lations have much greater rates of dental caries and 76 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL periodontal disease in all age groups than the gener- al U.S. population. AVAN children aged 2 to 4 years have 5 times the rate of dental decay compared to all children, and 6- to 8-year-old AVAN children have about twice the rate of dental caries experience. Rates for untreated decay in these age groups are 2 to 3 times higher than in the same age groups in the gen- eral U.S. population. Periodontal disease in AVAN adults is 2.5 times greater than in the general U.S. population. High prevalence rates of diabetes among AVAN populations are a significant contributing fac- tor to this periodontal disease (IHS 2000). Substantial unmet dental needs and quality of life issues have also been identified in IHS surveys, which included studies of representative AWAN com- munities with regard to the effect of oral conditions on well-being and quality of life (Chen et al. 1997). (See Chapter 6 for a general discussion.) One third of schoolchildren report missing school because of den- tal pain. Twenty-five percent of schoolchildren avoid laughing or smiling, and 20 percent avoid meeting other people because of the way their teeth look. As a consequence of dental pain, almost a quarter of the adults are unable to chew hard foods, almost 20 per- cent report difficulty sleeping, and 15 percent limit their work and leisure activities. Three quarters of the elderly experience dental symptoms, and half perceive their dental health as poor or very poor and are unable to chew hard food. Almost half the adults avoid laughing, smiling, and conversation with oth- ers because of the way their teeth look. . Again, the available data allow for obtaining a picture only of the AVAN population residing on reservations where services, including dental servic- es, have been provided by the IHS or contracted to tribes or urban AI/AN organizations. In 1989, American Indians, residing in the current reservation states had a median household income of $19,897. Almost one third (31.6 percent) of AVANs lived below the poverty level. For some groups, diabetes and high rates of tobacco and alcohol use are preva- lent and contribute to poor oral health. Women's Health Analysis of data from NHANES III indicates that women have benefited from the trend in general improvements in oral health that has been enjoyed by the U.S. population overall. Many, but not all, sta- tistical indicators show women to have improved their oral health status as compared to men (NHANES III, Redford 1993). Adult females are less likely than males at each age group to have severe periodontal disease as measured by periodontal loss ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem of attachment of 6 mm or more for any tooth. Both black and white females (6.0 and 6.0 per 100,000) have a substantially lower incidence rate of oral and pharyngeal cancers compared to black and white males, respectively (20.8 and 14.9 per 100,000). A higher prevalence of females than males have oral- facial pain, including pain from oral sores, jaw joints, face/cheek, and burning mouth syndrome. However, there are large areas for which information for either sex, even at the descriptive level, is only partial or nonexistent. Data gaps regarding craniofacial in- juries, soft tissue pathologies, and salivary gland dys- functions are notable examples. Most oral diseases and conditions are complex and represent the product of interactions between genetic, socioeconomic, behavioral, environmental, and general health influences (Chapters 3 and 5). Multiple factors may act synergistically to place sub- groups of women at higher levels of risk for oral dis- eases. For example, the comparative longevity of women, compromised physical status over time, and the combined effects of multiple chronic conditions often with multiple medications, can result in increased risk of oral disease (Redford 1993). Many women live in poverty, are not insured, and are the sole head of their household. For these women, obtaining needed oral health care may be difficult. In addition, gender-role expectations of women may also affect their interaction with dental care providers and could affect treatment recommendations as well (Redford 1993). During the past decade, women's health has emerged as a significant issue in the nation's health agenda. The scientific community is beginning to respond to this concern by studying and reporting the effects of sex and gender differences on health and disease management. Although most of the effort has focused upon women, comparisons with men's health have begun to elucidate sex- and gender- specific differences. Research has demonstrated sex and gender dif- ferences in the response to kappa opioid analgesics for the control of postoperative pain (Gear et al. 1996). These findings have heightened conjecture about differences in the female and male nervous sys- tems in response to pain stimuli. There are studies in mice that suggest that there are sex-specific respons- es to pain and analgesics (Mogil et al. 1996, 1997). Taken together, these findings could help explain why women report certain painful conditions more than men; for example, temporomandibular joint disorders, trigeminal neuralgia, migraine headaches, and burning mouth syndrome (USDHHS 1999). 77 The Magnitude of the Problem Recent research has also demonstrated sex and gender differences in taste perception. Women are more likely than men to be "supertasters" of a bitter compound known as 6-n-propylthyiouracil (PROP) (Bartoshuk et al. 1994). PROP supertasters experi- ence more intense tastes (particularly for bitter and sweet>, a greater sensation of oral burning in response to alcohol, and more intense sensations from fats in food (Bartoshuk et al. 1994, 1996, Tepper and Nurse 1997). PROP supertasters also have more fungiform papillae on their tongues than medium PROP tasters or those who cannot taste PROP at all. ioral and environmental differences-to name a few-decreases the utility of those data that are avail- able. For example, women are reported to be more inclined to self-care, to visit the dentist more often, and to be more likely to report symptoms such as pain. However, the effects of these behaviors on their oral health status cannot be determined fully Figure 4.24 suggests content areas in the study of women's oral health. Individuals with Disabilities The Agenda for Research on Women`s Health for No national studies have been conducted to deter- the 2lst Century noted that the ability to interpret mine the prevalence of oral and craniofacial diseases oral health in the context of sex and gender was lim- among the various populatiops with disabilities. ited by large gaps in knowledge. For example, perti- Several local and regional reports, however, provide nent oral health data, even at the descriptive level, are some relevant data in this regard. For example, some partial or nonexistent for many conditions and dis- smaller-scale studies show that the population with eases for either sex. In addition, limited knowledge of mental retardation or other developmental disabili- etiologic factors, natural history of diseases, behav- ties has significantly higher rates of poor oral hygiene FIGURE 4.24 Content areas in the study of women's health Oral Influences on Systemic Health Evidence for links between oral infection and diabetes Women and the Health Care System Treatment decision making lization of professional services Systemic influences on Oral Health Longevity Multiple chronic conditions Medication usage - Cognitive impairments Physical confinement Compromised functional status Postmenopausal bone loss HIV Diabetes Diseases More Common in Women Than Men TMD, oral-facial pain, Sjogren's / syndrome,saiivary gland dysfunction, burning mouth, alterations in taste, pregnancy-associated oral changes Societal Influences on Women's Caregiving Poverty Gender role expectations Underinsurance Concern for aesthetics Access to care Craniofacial trauma Oral Diseases Affecting the Most Women Caries Periodontal diseases \ Gender Influences on Health Risk Dental care utilization Self-care Eating disorders Unprotected sexual activity Source: Adapted from Chesney and Ozer 1995 and reprinted in USOHHS 1999. 78 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and needs for periodontal disease treatment than the general population, due, in part, to limitations in individual understanding of and physical ability to perform personal prevention practices or to obtain needed services. There is a wide range of caries rates among people with disabilities, but overall their rates are higher than those of people without disabilities. Much of the variation stems from where people reside (e.g., in large institutions where services are available versus in the community where services must be secured from community practitioners). Almost two thirds of community-based residential facilities report that inadequate access to dental care is a significant issue (Beck and Hunter 1985, White et al. 1995, Waldman et al. 1998, Dwyer, Northern Wisconsin Center for the Developmentally Disabled unpublished data, 1996). Parents consistently report dental care as one of the top needed services for their children with disabilities regardless of age (Haveman et al. 1997). Local studies of independent living cen- ters reported that 24 to 30 percent of adults with cerebral palsy, 14 percent with spinal cord injuries, 30 percent with head injuries, and 17 percent who were deaf had dental problems (Arnett 1994). Results from 1999 oral assessments of U.S. Special Olympics athletes (all ages), based on an extremely conserva- tive assessment protocol (without the use of x-rays, mirrors, or explorers), and carried out by the Special Olympics Special Smiles Program in 20 states, indi- cate that 12.9 percent of the athletes reported some form of oral pain, 39 percent demonstrated signs of gingival infection. and nearly 25 percent had untreat- ed decay (Special Olympics, Inc., unpublished data). Note that this is a population that tends to be from higher-income families. The oral health problems of individuals with dis- abilities are complex. These problems may be due to underlying congenital anomalies as well as to inabil- ity to receive the personal and professional health care needed to maintain oral health. There are more than 54 million individuals defined as disabled under the Americans with Disabilities Act, including almost a million children under age 6 and 4.5 million chil- dren between 6 and 16 years of age. A greater per- centage of males than females and of African Americans than Hispanics and whites have disabili- ties (Federal Interagency Forum 1997, Waldman et al. 1999). Children with disabilities have chronic physical, developmental, behavioral, and emotional limitations, including mental retardation, autism, attention deficit hyperactivity disorders, and cerebral palsy. Also, children from families with incomes below the poverty level are about one third more like- ly than children in nonpoor families to have an exist- The Magnitude of the Problem ing special health care need. Similarly, children from less educated households exhibit a higher likelihood of a special health care need. Children in single-par- ent families are about 40 percent more likely than children from two-parent households to have special health care needs (Newacheck et al. 1998). Deinstitutionalization has resulted in highlighting the problem these individuals have regarding access to dental care as they move from childhood to adult- hood. Availability of dental providers trained to serve special needs populations and limited third-party support for the delivery of complex services (see Chapter 9) further complicate the issues entailed in addressing the needs of this population. Given the wide variability among groups with disabilities, this review of oral health status and needs is quite limited. More in-depth assessment and analysis of the determinants of oral health status, access to care, and the role of oral health in the over- all quality of life and life expectancy of individuals with disabilities are needed (see Chapter 10). UTILIZATION OF PROFESSIONAL CARE: WHAT DO WE KNOW ABOUT THE RELATIONSHIP OF ORAL HEALTH AND USE OF DENTAL SERVICES? With few exceptions, maintenance of oral health through a lifetime requires timely receipt of advice for self-care, preventive therapies, early detection and treatment of problems, and restoration of function. Chapter 7 describes community-based and profes- sional interventions that have played a significant role in the improvement of oral health achieved over the past 50 years; their full promise has not, howev- er, been realized. Chapter 8 describes current and emerging strategies for personal and provider approaches to maintain and restore oral health, with tooth-conserving approaches being employed more and more frequently. As noted earlier, almost every- one experiences oral diseases and conditions over the course of a lifetime, and, unlike the common cold, most diseases do not resolve over time. Consequently, receipt of dental services complements self-care as a critical factor in achieving and main- taining good oral health. Although certain counseling and screening serv- ices provided by physicians are recommended (U.S. Preventive Services Task Force 1996), data to indi- cate how many persons receive such services or oral- health-related recommendations from their physi- cian are very limited. There are also no data on physi- cian-based services for oral and craniofacial condi- tions. The data that are available describe utilization ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 79 The Magnitude of the Problem of dental visits. Unfortunately, most of these data are cross-sectional, describing the experience of the pop- ulation in any given year, but providing little detail about how patterns of care over time contribute to oral health. Nevertheless, utilization of care is used as a surrogate measure of an individual's or a popula- tion`s capacity to maintain or improve health status. An understanding of utilization of dental visits and differences in such visits among age, racial/ethnic, sex, and income groups is important in identifying opportunities for improvement in oral health that would follow from timely receipt of professional care. Characteristics of groups with different levels of dental care utilization suggest barriers to care as well as factors that predispose or enable access to dental care. Explanations for variation in utilization are alluded to in the following section, and are discussed in further detail in Chapter 10. More studies are needed to understand the dimensions of disease and the role of professional care and use of services. Also, for oral health in particular, the contributions of all health professions and the interdisciplinary nature of care need to be emphasized. Dental Care Utilization Visiting a health care provider at least once per year and the number of visits made within the past year are used as indicators of an individual's ability to access professional services. Dental care utilization statistics are traditionally based on an individual's reporting "at least one dental visit in the past year," although there are variations with shorter recall intervals and different forms of the question. Depending on the question and survey method, annual dental care use estimates vary The 1996 Medical Expenditures Panel Survey (MEPS) esti- mates that 43 percent of the U.S. population 2 years and older had at least one dental visit that year (MEPS 2000). Responding to a variation of a ques- tion that had been asked in many previous surveys, some 65.1 percent of the U.S. population 2 years and older reported in 1997 that they had visited a dentist in the preceding year (NCHS 1997b), up from 55.0 percent in 1983 (Bloom et al. 1992). The average number of visits per person remains at about two per year. Further research is needed to understand rea- sons for variations in estimates from different survey approaches, but differences among persons with dif- ferent characteristics are quite similar regardless of survey method. Data from the 1997 National Health Interview Survey, reprinted in Healthy People 2010, indicate that the highest percentage reporting at least one rABLE 4.3 Percentage of persons 25 years of age and older with a dental kit within the preceding year, by selected patient character- istics, selected years 1983d 19896 1990 1991 1993 lotalbrC be 25 to 34 years 35 to 44 years 45 to 64 years 65 years and older 65 to 74 years 75 years and older Sex' Male Female Poverty statusLd Below poverty At or above poverty Race and Hispanic origin' White, non-Hispanic Black, non-Hispanic HispanV Education' Less than 12 years 12 years 13 years or more Education, race, and Hispanic origin' Fewer than 12 years White, non-Hispanic Black, non-Hispanic Hispanif 12 years White, non-Hispanic Black, non-Hispanic Hispanif 13 years or more White, non-Hispanic Black,non-Hispanic Hispanif 53.9 58.9 62.3 58.2 60.8 59.0 60.9 65.1 59.1 60.3 60.3 65.9 69.1 64.8 66.9 54.1 59.9 62.8 59.2 62.0 39.3 45.8 49.6 41.2 51.7 43.8 50.0 53.5 51.1 56.3 31.8 39.0 43.4 41.3 44.9 51.7 542 58.8 55.5 58.2 55.9 61.4 65.6 60.8 63.4 30.4 33.3 38.2 33.0 35.9 55.8 62.1 65.4 61.9 64.3 56.6 61.8 64.9 61.5 64.0 39.1 43.3 49.1 44.3 47.3 42.1 48.9 53.8 43.1 46.2 35.1 36.9 41.2 35.2 38.0 54.8 58.2 61.3 56.7 58.7 70.9 73.9 75.7 72.2 73.8 36.1 39.1 31.7 32.0 33.8 36.5 56.6 59.8 40.5 44.8 48.7 56.5 72.6 75.8 54.4 57.2 58.4 66.2 41.8 37.9 42.7 62.8 51.1 59.9 77.3 64.4 67.9 38.1 41.2 33.0 33.1 28.9 33.0 58.8 60.4 43.1 48.2 49.5 54.6 74.2 75.8 61.7 61.3 61.2 61.8 a Data for 1983 and 1989 are not strictly comparable with data for later years. Data for 1983 and 1989 are based on responses to the question "About how long has it been since you last went to a dentist?"Starting in 1990,data are based on the question "During the past 12 months, how many visits did you make to a dentist?" blncludes all other races not shown separately and unknown poverty status and educa- tion level. `Age adjusted. dPoverty status is based on family income and family size using Bureau of the Census poverty thresholds. ePersons of Hispanic origin may be of any race. Notes: Data are based on household interviews of a sample of the civilian noninstitu- tionalized population.Denominators exclude persons with unknown dental data. Estimates for 1983 and 1989 are based on data for all members of the sample house- hold. Beginning in 1990, estimates are based on one adult member per sample house- hold. Estimates for 1993 are based on responses during the last half of the year only. Source: Data from NCHS 1989. 80 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem dental visit was third-grade children (82 percent). Variation by Sex, RacelEthnicity, Income, Those aged 25 years and older with less than a high and Insurance school education had the lowest rates (41 percent) for annual dental visits as compared to those with at Dental care utilization varies with sex and race/eth- least some college education (74 percent) (USDHHS nicity for individuals 25 and older (NCHS 1997a). 2000>. Females had slightly higher rates of utilization (67 percent) than males (63 percent). Hispanic individuals had the low- TABLE 4.4 est utilization (53 percent), and Age-adjusted percentage distribution of persons 2 years and older by interval since non-Hispanic whites had the high- last dental visit, by selected characteristics, 1989 est rates (68 percent). Table 4.3 Interval Since Last Dental Visit provides an overview of utilization from 1983 through 1993. A higher 1 Year to 2Years to percentage of females reported a All LessThan LessThan LessThan SYears dental visit than males in each sur- Intervals 1 Year 2 Years 5 Years or More Never vey year. Fewer non-Hispanic All ages 100.0 57.3 9.5 12.3 11.0 4.6 blacks and Hispanics reported a Sex dental visit than non-Hispanic Male 100.0 54.1 9.6 13.4 12.1 4.9 whites in each survey year. Income Female loo.0 59.9 9.4 11.2 10.1 4.4 and education are also key vari- Race ables in utilization. In 1993, White 100.0 59.5 9.1 11.6 10.5 4.4 almost twice as many individuals Black 100.0 43.2 12.3 16.9 15.1 5.8 25 and older living at or above the Other 100.0 51.6 9.7 14.0 10.8 6.7 poverty line had a dental visit than Hispanic origin did those living below the poverty Non-Hispanic 100.0 58.5 9.4 12.0 10.8 4.1 line in 1993 (64.3 versus 35.9 per- Hispanic 100.0 46.0 10.5 14.6 13.0 9.7 cent). Similarly, almost twice as Mexican American 100.0 40.5 8.9 15.3 15.8 13.1 many individuals with 13 years or Other Hispanic 100.0 53.2 12.3 13.7 9.9 5.1 more of education had a visit than Place of residence did those with fewer than 12 years MSA' 100.0 58.4 9.4. 11.9 10.1 4.5 of education (73.8 versus 38.0 per- Central city 100.0 54.9 10.1 12.9 10.9 5.1 cent) in that same year. Not central city 100.0 60.6 9.0 11.3 9.6 .4.2 Data from the 1989 National Not MSA' 100.0 53.6 9.7 13.6 14.1 5.1 Health Interview Survey showed Geographic region that the overall age-adjusted num- Northeast 100.0 60.7 10.4 10.7 9.0 3.5 ber of visits for blacks was 1.2 vis- Midwest 100.0 61.5 6.3 11.3 10.7 3.5 South 100.0 52.2 10.3 13.9 13.6 5.9 its compared to 2.2 visits for et West 100.0 57.8 8.6 12.3 9.1 4.9 whites (Bloom al. 1992). Table 4.4 shows the percent- Education level Less than 9 years 100.0 30.6 9.9 18.4 30.6 5.9 age distributions of the interval since their most recent dental visit 9 to 11 years 100.0 39.0 10.7 20.3 23.5 1.3 12 years 100.0 54.6 10.6 15.0 14.4 0.5 for people aged 2 and older in 13 years or more 100.0 70.2 8.5 10.3 6.9 0.2 selected demographic and socioe- conomic categories. Individuals Family income who have never visited a dentist Less than $10,000 100.0 42.2 10.9 16.3 20.1 7.0 100.0 43.9 11.8 17.4 16.1 6.6 ranged from high of 13.1 a percent $10,000 to $19,999 $20,000 to 534,999 100.0 58.2 10.5 3.2 10.4 4.6 of Mexican Americans to 5.8 per- $35,000 or more 100.0 72.5 7.8 8.5 5.5 2.9 cent of blacks and 4.4 of percent Dental insurance coverage whites. Eleven percent of the pop- ulation had not had a dental visit With private dental insurance 100.0 70.4 8.7 9.2 6.6 3.3 Without private dental insurance 100.0 50.8 10.7 15.4 14.2 6.0 in 5 or more. Individuals years with fewer than 9 years of educa- ' MSA = metropolitan statistical area. tion represented the highest pro- Source:Bloom et al. 1992. portion, 30.6 percent, of those reporting no dental visit in 5 years ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 81 The Magnitude of the Problem or more, compared with 6.9 percent of those with 13 years or more of education. A larger proportion of individuals without private dental insurance had not had a dental visit in 5 years or more compared with those with private dental insurance (14.2 versus 6.6 percent). Hispanic individuals have the lowest rate of dental insurance coverage-29.0 percent, compared with 32.4 percent for non-Hispanic blacks and 41.8 percent for non-Hispanic whites (U.S. Bureau of the Census 1997). Professional care is necessary for several critical dental disease prevention measures, such as the application of dental sealants. Unfortunately, dental sealants are 3 times less likely to be found on the teeth of Mexican American and African American children than among white children aged 5 to 17 (Selwitz et al. 1996). Asian and Pacific Islander American children in California also demonstrated a low rate of sealant use (Pollick et al. 1997). Variation by Oral Health Status Utilization of dental care is associated with self- reported health status, as shown in Table 4.5. Of those who reported "excellent" or "very good" health, 61.4 percent had had a dental visit within the past year, compared with about 45.1 percent of those reporting "fair" or "poor" health. Functional limita- TABLE 4.5 Age-adjusted percentage distribution of persons 2 years and older by interval since last dental visit, by selected health characteristics, 1989 Interval Since Last Dental Visit Assessed health status Excellent or good very Good Fair or poor Limitation of activity Unable to carry on usual activity Limited in amount or kind of major activity Limited, but not in major activity Not limited in activity Dentition status Dentate Edentulous Source: Bloom et al. 1992. All Less Than 1 Year to Intervals 1 Year 2 Years 100.0 61.4 9.3 100.0 ST.9 10.1 100.0 45.1 10.0 100.0 46.6 9.8 100.0 52.3 9.8 100.0 59.1 8.3 100.0 58.5 9.5 100.0 65.5 9.6 100.0 14.3 6.4 A study comparing individuals who had had a dental visit in the past 12 months with those who had not reported that dentate adults who had a recent visit were less likely to have untreated coronal and root caries, pulpal pathology, and retained tooth roots. They also were more likely to rate the general condition of their teeth and gums as excel- lent or very good (Drury and Redford 2000). 2 Years to Less Than 5 Years 5 Years or More Never 11.2 9.0 4.3 13.9 12.6 5.8 16.6 17.4 5.9 15.6 16.6 5.1 14.0 14.4 4.1 12.8 11.7 4.2 12.0 10.1 4.6 12.8 10.1 0.5 19.8 55.2 0.4 Examination of NHANES III data by low socioeconomic status (SES) provides an additional per- spective. In a recent analysis, SES was measured by a composite index based on educational attain- ment and the ratio of annual fami- ly income to the poverty threshold. Among all adults, people with lower SES scores were nearly 9 times more likely to be edentulous than those with higher SES scores. Among the dentate, those with lower SES scores were 6 times more likely to have coronal decay and nearly 4 times less likely to have visited a dentist in the past 12 months (Drury et al. 1999). tions are also related to dental service utilization. Of those who reported no physical limitations in activi- ties, 58.5 percent reported a dental visit within the past year, compared to 46.6 percent of those who were unable to carry out their usual activities (Table 4.5) (Bloom et al. 1992). Whether a person had natural teeth was strongly associated with dental care utilization (Table 4.5). Dentate persons were more than 4 times more likely to report a dental visit within the past year than eden- tulous people: 65.5 versus 14.3 percent. Over half (55.2 percent) of those who were edentulous reported that they had not had a dental visit in 5 years or more. Recent analyses of data from NHANES III show that adults 18 and older who reported a dental visit in the past 12 months were nearly 9 times more like- ly to be dentate and 4.4 times more likely to have a complete dentition than adults who did not report visiting a dentist within the preceding 12 months. Dentate adults who reported a dental visit in the past 12 months were 3.1 times less likely to have untreat- ed coronal decay and 1.5 times less likely to have gingivitis than dentate adults who did not report a recent dental visit (T. Drury, NIDCR, personal com- munication, 1999). a2 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL -- Reasons for Nonutilization Reasons for nonutilization of dental services are com- plex. Principal reasons cited by respondents of all ages (Bloom et al. 1992) are given in Table 4.6. Slightly less than half of those reporting no dental visit in the past year (46.8 percent) said that they per- ceived having no dental problem. This perception was the predominant response of individuals in all demographic categories, except for those 65 and older, who gave having no teeth as the predominant reason. Younger individuals were more likely than older to cite "no dental problem." Blacks were more likely to report "no problems" (58.5 percent) as a rea- son for no dental visit, compared to 44.3 percent of whites (Bloom et al. 1992). Having no teeth (14.3 percent) was the next most frequently reported reason for no dental visit. About half of the people 65 and older in the 1989 survey gave this as their reason for no dental visit- 39.2 percent of blacks compared to 51.2 percent of whites. The third most frequently cited reason was the cost of care, mentioned by 13.7 percent of respon- dents. Whites (14.3 percent) were more likely than blacks (11.4 percent) to cite cost. Other surveys have reported substantially higher percentages of individ- uals indicating cost as a barrier, particularly those in underserved or low-income areas (Bloom et al. 1992). The age group most sensitive to the cost of care was 18- to 34-year-olds, 19.1 percent of whom gave cost as the reason for no dental visit, Finally, a small proportion of respondents (4.3 percent) report- ed fear as a personal barrier to receipt of care. Unmet Needs Unmet health needs can be assessed in many ways. Because oral diseases are common and do not resolve over time in the absence of intervention, the lack of dental visits is used as an indicator of unmet health needs. In addition, the National Access to Care Survey documented the extent of dental care that individuals wanted but could not obtain ("wants") in the total population and among various population subgroups (Mueller et al. 1998). About 8.5 percent of the U.S. population wanted, but did not obtain, den- tal care in 1994 (Table 4.7). In contrast, only 5.6 per- cent reported unmet medical or surgical care wants. Adult women aged 19 to 64 reported the greatest level of dental care wants; elderly people 65 and older had the lowest level. Blacks, people in fair or poor health or with one or more chronic conditions, and people living in the South reported higher levels of dental care wants than comparable groups. About The Magnitude of the Problem 16.4 percent of those in households whose family income was less than 150 percent of the poverty level reported dental care wants. More than 22 percent of the uninsured reported dental care wants. Insured children with special health care needs were 4 times more likely to report unmet need for dental care (23.9 percent versus 6.1 percent) if they were unin- sured than if they were insured, according to a recent analysis of data from the National Health Interview Survey (Newacheck et al. 2000). Outcomes of Appropriate Levels of Access and Utilization: An Example The effects on health of a system of care with assured access and positive expectations of care-seeking and utilization behavior have been demonstrated by the U.S. Department of Defense. There are currently over 1.4 million men and women on active duty in the U.S. military. The population is predominantly male (86 percent). The racial distribution is 68 percent white, 20 percent black, 7 percent Hispanic, 3 per- cent Asian, and 2 percent other groups. Slightly over 30 percent of active duty personnel are between the ages of 20 and 24, and 91 percent are younger than 40. In 1997, 59 percent were married. Seventy-six percent had a high school degree, and 19 percent were college graduates. Free dental care, one of the benefits provided to active duty military personnel, eliminates one of the significant barriers that has been identified as limiting access to care for many in the civilian population. In addition, military personnel are required to receive a dental examination annually, even if the individual perceives that he or she has "no problem." Dental care is available to most military personnel at their duty station, eliminating the need to travel long distances. A comparison of the oral health and utilization of dental care of the military and civilian populations illustrates the impact of elimination of these barriers to care on oral health, even for persons from demographic groups that are traditionally underserved. In 1994 the Tri-Service Comprehensive Oral Health Survey examined and administered question- naires to 13,050 active duty military personnel using a complex, weighted survey design to examine the oral health status, dental treatment needs, dental uti- lization, and perceived need for care in this popula- tion (York et al. 1995). The study found that nearly all (99.2 percent) active duty military personnel had seen a dentist within the past 2 years. Eighty percent of active duty personnel received a dental examina- tion within the past year, 60 percent had a dental ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 83 The Magnitude of the Problem TABLE 4.6 Percentage of persons with no dental visit in past year by reason reported, by selected characteristics, 1989 All with No Visits in PastYear Fear cost Access No Dental Problem Problem NoTeeth Not Other Important Reason All ages 2to 17 years 18to34years 35to 64years 65 yearsandolder Sex Male All ages 2to 17 years 18to 34years 35to64years 65 yearsandolder Female Allages 2to17years 18to 34years 35to64years 65 yearsand older Race White All ages 2to 17years 18to34years 35to 64years 65yearsandolder Black All ages 2to 17 years 18to 34years 35to64 years 65 yearsand older Other All ages 2to17 years 18to 34years 35to 64years 65yearsandolder Hispanic origin Non-Hispanic All ages 2tol7years 18to34years 3Sto64 years 65yearsandolder Hispanic,total All ages 2to 17 years 18to34years 35to64years 65yearsandolder 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 loo.0 loo.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 100.0 loo.0 100.0 100.0 100.0 4.3 13.7 1.1 46.8 14.3 2.3 8.7 1.3 15.0 1.5 56.8 0.2 1.9 11.9 5.9 19.1 2.4 52.4 0.7 3.2 9.5 5.8 12.8 1.5 43.3 17.8 2.2 a.4 2.2 4.1 1.1 31.2 49.7 1.1 3.9 4.0 13.0 1.5 49.1 12.1 2.6 9.3 1.2 14.9 1.3 56.2 o 0.2 2.0 12.1 5.5 17.5 2.0 54.8 0.6 * 3.4 9.7 5.4 11.2 1.5 45.4 16.1 2.8 9.5 1.7 4.0 1.0 33.6 48.6 1.3 3.5 4.6 14.3 1.8 44.4 16.6 1.9 a.1 1.5 15.2 1.6 57.4 o 0.2 1.8 11.6 6.5 21.0 2.9 49.5 0.8 3.0 9.3 6.2 14.4 1.5 41.1 19.5 1.6 7.3 2.5 4.2 1.2 22.5 50.6 0.9 4.1 4.4 14.3 1.8 44.3 15.7 2.4 9.4 1.3 16.4 1.7 54.0 0.2 2.0 13.3 6.2 20.7 2.6 49.6 0.7 3.4 10.6 5.8 13.0 1.6 41.3 19.0 2.4 9.1 2.1 3.7 1.1 30.5 51.2 1.1 3.9 4.0 11.4 1.0 58.5 8.8 1.5 5.1 1.3 10.7 "0.7 68.3 "0.2 1.2 6.6 4.9 13.3 1.5 63.8 "0.7 2.5 4.6 6.0 11.7 0.9 52.8 13.0 1.1 4.9 3.0 7.0 "1.0 36.6 39.2 "0.9 3.4 3.7 10.8 1.6 52.1 6.1 2.2 9.2 "1.7 11.4 "0.3 49.8 *o.o '2.4 12.6 4.6 11.7 "2.5 59.4 "0.3 "2.2 8.8 4.6 10.8 "1.9 51.0 a.2 *2.6 7.7 "2.8 o 4.2 o 0.7 31.4 44.9 o 0.7 "5.9 4.3 13.0 1.7 45.7 15.6 2.2 9.1 1.3 14.4 1.3 56.2 0.2 1.9 12.8 6.0 18.9 2.5 51.6 0.7 3.2 10.1 5.8 12.0 1.5 42.5 18.8 2.2 a.7 2.1 4.0 1.1 30.9 50.4 1.1 3.9 4.0 19.1 1.8 56.1 3.5 2.6 5.9 1.6 18.4 2.4 59.5 '(0.1 2.2 7.3 5.2 20.1 1.5 57.9 "0.2 3.3 5.6 5.3 20.7 1.6 52.2 6.5 2.3 5.2 "4.6 a.2 "1.4 40.7 31.9 *1.6 *3.4 84 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem All with No Visits Access No Dental Not Other in Past Year Fear cost Problem Problem No Teeth Important Reason Hispanic, Mexican American All ages 100.0 3.6 20.7 1.7 56.2 2.4 2.3 5.3 2 to 17 years 100.0 o 1.4 19.4 2.6 60.7 "0.1 2.2 5.5 18 to 34 years 100.0 4.7 21.0 "0.9 57.5 "0.1 2.8 4.8 35 to 64 years 100.0 5.2 24.3 o 1.4 50.1 4.5 o 1.7 6.4 65 and older years 100.0 "4.3 *11.1 "1.4 38.7 30.5 "1.8 *1.8 Hispanic, other All ages 100.0 4.7 16.3 2.0 55.9 5.3 3.1 7.0 2 to 17 years 100.0 o 1.8 16.3 "1.9 56.9 "0.2 "2.0 11.3 18 to 34 years 100.0 6.2 18.5 *2.4 58.7 `0.4 4.4 7.0 35 to 64 years 100.0 5.5 16.3 o 1.8 54.9 8.9 `3.1 3.8 65 and older years 100.0 o ??? o 5.7 `1.4 42.8 33.2 "1.4 "4.9 Place of residence MSA, total" All ages 100.0 4.4 13.4 1.8 46.6 12.8 2.4 9.0 2 to 17 years 100.0 1.3 14.1 1.4 55.7 0.3 2.0 12.1 18 to 34years 100.0 5.7 18.5 2.6 51.6 0.5 3.3 9.6 35 to 64 years 100.0 6.1 12.6 1.6 43.1 16.0 2.4 8.7 65 and older years 100.0 2.3 4.2 1.1 31.4 47.6 1.2 4.0 MSA, central ciryd All ages 100.0 4.4 14.0 1.7 48.0 11.9 2.6 7.8 2 to 17 years 100.0 1.6 14.6 1.4 56.5 "0.2 2.0 10.0 18 to 34 years 100.0 5.3 17.9 2.5 54.2 0.4 3.6 8.4 35 to 64 years 100.0 6.4 14.1 1.3 43.9 14.8 2.5 7.3 65 and older years 100.0 2.5 4.7 1.3 31.5 46.3 1.7 4.2 MSA, not central cityd All ages 100.0 4.3 13.0 1.8 45.5 13.5 2.3 9.9 2 to 17 years 100.0 1.2 13.7 1.4 55.1 "0.4 2.0 13.7 18 to 34 years 100.0 6.0 19.0 2.6 49.5 0.6 3.1 10.6 35 to 64 years 100.0 5.8 11.6, 1.7 42.6 16.8 2.4 9.6 65 and older years 100.0 2.1 3.9 1.0 31.3 48.5 0.8 4.0 Not MSA' All ages 100.0 4.1 14.4 1.4 47.7 18.8 1.7 8.0 2 to 17 years 100.0 1.3 18.0 1.6 60.0 *0.1 1.5 11.2 18to34years 100.0 6.9 21.1 1.7 55.4 1.2 2.7 9.1 35 to 64 years 100.0 4.9 13.1 1.2 43.8 23.1 1.6 7.7 65 and older years 100.0 2.0 3.9 1.0 30.7 55.2 0.9 3.5 Family incomeb Less than $10,000 All ages 100.0 3.8 19.7 1.7 42.8 22.5 1.4 6.4 2 to 17 years 100.0 o 1.1 19.4 2.6 60.0 "0.3 1.9 9.6 18 to 34 years 100.0 5.7 28.8 2.4 51.7 *0.9 1.9 7.2 35 to 64 years 100.0 6.3 25.2 "1.1 35.5 25.1 1.4 5.4 65 and older years loo.0 2.0 6.6 "0.9 27.4 57.4 *0.7 3.9 $10,000 to $19,999 All ages 100.0 4.0 18.8 1.5 47.0 17.4 1.7 6.5 2 to 17 years 100.0 1.4 21.9 1.4 58.8 -0.1 1.3 7.9 18 to 34 years 100.0 6.1 27.8 1.8 53.2 -0.5 2.4 7.9 35 to 64 years 100.0 4.7 19.2 1.5 43.6 21.7 1.6 5.7 65 and older years 100.0 3.0 3.4 1.2 31.4 51.9 1.3 4.3 $20,000 to $34,999 All ages 100.0 4.8 13.7 1.7 51.3 11.5 2.3 11.1 2 to 17 years 100.0 1.6 14.4 0.9 59.7 o 0.1 1 .7 13.8 18to34years 100.0 6.4 18.1 2.8 54.7 0.8 3.3 12.3 35 to 64 years 100.0 6.4 12.5 1.4 46.2 18.5 2.0 10.2 65 and older years 100.0 1.8 2.4 *1.3 38.5 47.7 "1.5 4.7 (continues) ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 85 The Magnitude of the Problem TABLE 4.6 continued All with No Visits in Past Year 535,000 or more All ages 100.0 2to17years 100.0 18 to 34 years 10u.o 35 to 64 years 100.0 65 and older years 100.0 lental insurance coverage With dental insurance All ages loo.0 2 to 17 years 100.0 la to 34 years 100.0 35 to 64 years loo.0 65 and older years 100.0 Without dental insurance All ages 100.0 2 to 17 years 100.0 18 to 34 years 100.0 35 to 64 years 100.0 65 and older years 100.0 Insurance status unknown All ages 100.0 2 to 17 years 100.0 18to34years 100.0 35 to 64 years 100.0 65 and older years 100.0 Limitation of activity Unable to tarry on usual activity All ages 100.0 2 to 17 years 100.0 18 to 34 years 100.0 35 to 64 years 100.0 65 and older years 100.0 Limited in amount or kind of major activity All ages 100.0 2 to 17 years 100.0 18 to 34 years 100.0 35 to 64 years 100.0 65 years and older 100.0 Limited, but not in major activity All ages 100.0 2 to 17 years 100.0 18 to 34 years 100.0 35 to 64 years 100.0 65 years and older 100.0 Not limited in activity All ages 100.0 2 to 17 years 100.0 18 to 34years 100.0 35 to 64 years 100.0 65 and older years 100.0 Fear cost 5.9 6.8 1.1 5.8 7.0 9.2 7.8 6.0 "2.8 3.8 6.2 7.2 1.2 7.8 8.5 9.5 8.0 6.0 2.5 "1.6 4.0 18.5 1.6 20.5 5.5 26.7 5.4 18.9 2.3 4.9 1.6 3.9 "0.6 4.7 2.3 5.1 1.5 3.4 "1.4 "1.6 4.4 15.4 o 6.0 *27.6 7.4 25.3 5.4 18.3 "1.7 6.6 4.4 15.2 "1.7 18.9 6.9 30.2 6.1 17.6 2.4 5.1 4.4 12.4 `1.7 28.0 8.0 29.2 6.3 17.5 2.6 3.9 4.3 13.5 1.3 14.7 5.8 la.2 5.8 11.3 2.1 3.4 Access No Dental Problem Problem 2.6 52.3 2.0 56.8 3.6 55.4 2.3 49.1 "1.6 37.9 2.5 53.2 1.2 61.4 4.1 55.5 2.2 48.8 "1.1 39.3 1.5 48.7 1.7 60.1 1.9 56.3 1.3 45.1 1.2 31.9 0.7 23.8 `1.0 25.7 *0.9 28.2 "0.3 20.8 "0.6 19.8 1.7 33.2 "0.0 36.6 "1.9 47.1 o 1.2 34.5 2.4 26.0 `1.9 34.5 o 2.5 58.0 "3.9 44.3 1.7 31.2 o 1.2 26.3 0.9 34.3 *2.2 53.0 "1.9 50.5 "0.8 35.3 o 0.6 28.2 1.7 49.6 1.4 56.9 2.4 52.9 1.5 46.1 0.9 34.3 No Teeth 8.1 `0.6 o 0.6 13.2 41.6 10.1 "0.3 0.8 17.4 44.7 17.2 "0.2 0.7 19.9 52.5 9.3 *0.1 "0.3 9.2 36.8 31.9 "0.0 "1.9 28.9 49.9 29.7 o 0.3 o o.a 27.1 54.3 35.8 "0.0 "1.4 24.0 54.4 10.4 0.2 0.6 15.1 47.3 Not Other Important Reason 4.1 14.1 3.1 20.2 5.4 13.4 4.0 12.9 "2.0 4.4 3.4 15.2 2.4 18.8 5.1 16.3 3.1 13.7 *1.0 5.7 2.0 7.0 1.9 9.9 2.1 7.6 2.1 6.8 1.2 3.9 0.8 2.9 *0.6 3.6 1.1 3.5 "0.7 2.0 `0.6 2.6 1.1 6.2 "1.5 o 20.1 "1.9 6.1 "1.1 6.6 "0.7 4.6 1.7 7.5 "2.0 9.1 o ??? 10.4 2.2 9.3 "1.1 3.9 1.5 6.3 "1.7 "10.8 *1.7 10.3 *2.0 8.0 *1.2 3.9 2.4 9.2 1.9 11.9 3.3 9.6 2.4 8.6 1.2 3.7 dMSA = metropolitan statistical area. bPersons with unknown income not shown separately. Note: Data are based on household interviews of the civilian noninstitutionalized population. o = Figure does not meet the standard of reliability or precision (more than 30 percent relative standard error and numerator of percent or rate). Source: Bloom et al. 1992. 86 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem rABLE +.7 istimated number and percentage of people with unmet health care Wants, my selected characteristics, 1994 Medical or Number of People Dental Care Surgical Care (in millions) (percentage) (percentage) hll people 259.2 8.5 5.6 hge and sex Children, 1 to 18 years 73.5 5.9a 2.9" Adult men, 19 to 64 years 75.3 9.5 5.8 Adult women, 19 to 64 years 79.3 12.Y 9.3' Elderly people, 65 years and older 31.1 3.6' 2.46 Race/ethnic@ White 191.4 7.4 4.6 Black 32.2 15.0' 10.2a Hispanic 23.9 a.2 6.2 Other 11.7 9.9 8.6 Health status Fair or poor 24.6 16.1' 11.2' Good or excellent 233.5 7.7 5.0 Number of chronic conditions None 158.6 7.3 4.6 One or more 100.6 10.4 7.1 Geographical region Northeast 47.8 6.9 5.8 Midwest 65.8 6.9 4.5 South 92.6 11.2" 6.1 West 53.1 7.4 5.9 Rural/urban status Metropolitan statistical areas 208.2 8.6 5.6 Nonmetropolitan statistical areas 50.5 a.1 5.9 Education level of head of household High school or less 117.5 9.4 6.8 Some post-high school 141.2 7.9 4.7 Family income status Less than 150 percent of the poverty level 55.7 16.4a 9.1' 150 percent of the poverty level or more 174.3 6.3' 4.5 Health insurance status Private 166.6 5.9' 4.1 Medicare 36.0 5.6' 3.1" Medicaid 22.2 12.2 8.0 Uninsured 32.5 22.6' 14.9' Type of private health insurance Health maintenance organization/ independent practice association 45.1 5.5a 5.0 Preferred provider organization 30.7 4.6' 4.1 Fee-for-service 73.5 5.3' 3.1" d Rhe estimate differs from the percentage for the"all people"demographic at the 1 percent confidence level based on a two-tailed f-test of the difference in weighted estimates. Note: The standard error of each percentage is less than 30 percent of the percentage estimate. Source: Mueller et al. 1998. Access to dental care in the United States.JADA 1998 April; 129(4):429-37. Copyright 1998 by loumal ofthe American Dental Asrooation. Reprinted by permission of ADA Publishing Co. Inc. (2000). prophylaxis, and 29 percent had at least one tooth filled. Edentulism is virtually nonex- istent in the active duty military population. Also, active duty mili- tary personnel have a significantly lower proportion of their decayed, missing, and filled surfaces that are untreated; this is primarily due to dramatic improvements in the oral health of active duty blacks when compared to their civilian counter- parts. Active duty whites also have somewhat better oral health than white civilians of a similar age. The relative proportion of un- filled surfaces as a component of decayed and filled tooth surfaces in the military and civilian popula- tions is illustrated in Figure 4.25. ORAL HEALTH STATUS IN CHANGING TIMES The burden of oral diseases and conditions in the United States is extensive and affects persons throughout their life span. Birth defects such as cleft lip/palate, dental caries, and facial trauma are common in the young. Periodontal diseases, autoimmune disorders, and other chronic disabling condi- tions are seen in adults, while complete tooth loss and oral cavity and pharyngeal cancers are seen more often in older Americans. Because the most common oral disease, dental caries, is so wide- spread in the population, nearly every American has experienced oral disease. The effects of oral diseases and conditions on quality of life and well-being are discussed in Chapter 6. In sum, conditions such as cleft lip and palate and oral cancer not only involve costly and difficult surgeries and treatments, they also alter facial appearance and impair oral functioning. Pain disorders and pain as a conse- quence of dental disease are preva- lent in certain groups and can affect daily living. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 87 The Magnitudt of the Problctn The available trend data reveal improvements in dental health for most Americans; however, despite improvements in dental status, disparities remain. Diseases disproportionately affect some sex, income, and racial/ethnic groups, and the magnitude of the differences is striking. All the reasons for these dis- parities are not clear. Some of the most common den- tal diseases, such as dental caries, are preventable (prevention of oral diseases and conditions is pre- sented in Chapters 8 and 9). It appears, however, that not all individuals are benefiting from interventions that involve professional care, as represented by the data on dental visits. At the same time, as presented in Chapter 7, about 40 percent of the public does not receive the benefits of community water fluoridation. The emerging data on the effects of socioeconomic status on oral health are beginning to explain some, but not all, racial/ethnic differences. For other dis- eases, health disparities appear not to be related to professional services; a better understanding of the reasons for these differences is needed. This review of available data on oral diseases and conditions also reveals the lack or limitation of national or state data on oral diseases for many pop- ulation subgroups and for many conditions that affect the craniofacial structures. Information on the variables needed to explain health status differences, such as detailed utilization and expenditure data and data on services rendered, is limited as well. Data on specific services-self-care, services provided by pro- fessionals, and services that are commuhity-based- are needed to understand the dimensions of oral health. (Some of these services are described in Chapters 7 and 8.) Although some data on expendi- tures for care and health care personnel are available Available state data reveal variations within and among states in patterns of oral health and disease among population groups. Having state-specific and local data that augment national data is critical in identifying high-risk populations and areas and in addressing health disparities. These data also are vital in program evaluation, planning, and policy deci- sions. Yet state and local data are almost nonexistent. In recent years, the need for state and local data has intensified as more programs are funded by local authorities and responsibilities are shifted from national to state-based levels. The nation's health information system is under- going constant change to meet the current and future needs for health information. Consequently, many factors influence how and what data are collected and analyzed. These factors include emerging technolo- gies, legislation about how data are to be collected, and confidentiality and privacy concerns. The need for epidemiologic and surveillance data change as the understanding of specific diseases and conditions evolves and as society's goals and priori- ties change. The increasing focus on the long-term benefits of disease prevention and health promotion and the need to close the gap on disparities also affects how and what data are collected. For example, major initiatives such as the Department of Health and Human Services's Healthy People 2010 have pro- vided a framework for data collection and analysis tied to specific objectives and have helped identify needs for new health data systems. The Healthy People initiative now includes objectives for the nation's health status as well as for preven- tive interventions and objectives that would improve infrastructure and capacity building to provide the necessary services and moni- toring. FIGURE 4.25 The percentage of unfilled decayed surfaces is higher for civilian males than for males in the U.S. military 501 to (Chapter 9) complement the statistics needed to assess oral health in the United States, almost all these data come from cross-sectional surveys that do not allow for analysis of the outcomes of disease and related care. , I 18-19 20-24 25-29 30-34 35-39 40-44 Age group + Black civilian -+ White civilian - Black military x White military Source: York et al. 1995. This overview of the magni- tude of oral diseases and condi- tions in America raises many ques- tions still to be researched. If cer- tain oral diseases are preventable, why do we have populations with extensive and untreated disease? Once socioeconomic factors are controlled, why do we see differ- ences in services received? Why 38 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL are some conditions more prevalent in certain popu- lations than in others? How will the rapidly changing and projected demographics of America contribute to future trends in oral and craniofacial health and dis- ease? These and many other questions require more research, new databases, and an active and trained group of researchers. FINDINGS o Over the past five decades, major improve- ments in oral health have been seen nationally for most Americans. o Despite improvements in oral health status, profound disparities remain in some population groups as classified by sex, income, age, and race.feth- nicity. For some diseases and conditions, the magni- tude of the differences in oral health status among population groups is striking. 0 Oral diseases and conditions affect people throughout their life span. Nearly every American has experienced the most common oral disease, den- tal caries. o Conditions that severely affect the face and facial expression, such as birth defects, craniofacial injuries, and neoplastic diseases, are more common in the very young and in the elderly o Oral-facial pain can greatly reduce quality of life and restrict major functions. 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PR-9503. Connecticut and Denmark. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute; 1985. ORAL HEALTH IN AMERICA: .4 REPORT OF THE SURGEON GENERAL 93 What Is the Relationship Between Oral Health and General Health and Well-being? The next two chapters establish that oral health is essential to general health and well-being. Chapter 5 examines multiple linkages between oral and general health. The mouth and the face reflect signs and symptoms of health and disease that can serve as an adjunct for diagnosis for some conditions. Diagnostic tests using oral cells and fluids-especially saliva-are available to detect drug abuse, hormonal changes, and specific diseases; and more are being developed. The mouth is also a portal of entry for pathogens and toxins, which can affect the mouth and, if not cleared by the many defense mechanisms that have evolved to protect the oral cavity, may spread to the rest of the body Recent epidemiologic and experimental animal research provides evidence of possible associations between oral infections-particularly periodontal disease-and diabetes, cardiovascular disease, and adverse pregnancy outcomes, and this evidence is reviewed. The review highlights the need for an aggressive research agenda to better delineate the specific nature of these associations and the underlying mechanisms of action. Chapter 6 looks at the impact of oral health problems on the quality of life and includes examples of the kinds of questionnaires used to measure oral-health-related quality of life. Oral health is highly valued by society and individuals, and the chapter begins with a brief description of the reflections of those values in myth and folklore concerning facial appearance and the meaning of teeth. It then explores dimensions beyond the biological and the physical to examine how oral diseases and disorders can interfere with the functions of daily living, including participation in work or school, and what is known about their psychosocial impacts and economic costs. The deleterious effects of facial disfigurement and tooth loss may be magnified in a society such as ours that celebrates youth and beauty Self-reported impacts of oral conditions on social functions include limitations in communication, social interactions, and intimacy. Research on the oral-health-related quality of life is needed to permit further exploration of the dimensions of oral health and well-being. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 95 Linkages with General Health The mouth and face are highly accessible parts of the body, sensitive to and able to reflect changes occurring internally. The mouth is the major portal of entry to the body and is equipped with formidable mechanisms for sensing the environment and defending against toxins or invading pathogens. In the event that the integrity of the oral tissues is compromised, the mouth can become a source of disease or pathological processes affecting other parts of the body. It can also become a source of contagion by means of contaminated fluids or materials passed to others. This chapter explores what the mouth and face can reveal about general health, describes the role the mouth plays as a portal of entry for infection, and concludes with studies that are associating oral infections with serious systemic diseases and conditions. THE MOUTH AND FACE AS A MIRROR OF HEALTH AND DISEASE A physical examination of the mouth and face can reveal signs of disease, drug use, domestic physical abuse, harmful habits or addictions such as smoking, and general health status. Imaging (e.g., x-ray, MRI, SPECT) of the oral and craniofacial structures may provide early signs of skeletal changes such as those occurring with osteoporosis and musculoskeletal disorders, and may also reveal salivary, congenital, neoplastic, and developmental disorders. Oral cells and fluids, especially saliva, can be tested for a wide range of substances, and oral-based diagnostics are increasingly being developed and used as a means to assess health and disease without the limitations and difficulties of obtaining blood and urine. Physical Signs and Symptoms af Disease and Risk Factors A number of signs and symptoms of disease, lifestyle behaviors, and exposure to toxins can be detected in or around the craniofacial complex. Pathogens enter- ing the mouth may proliferate locally with oral and pharyngeal signs and symptoms; other pathogens may enter the bloodstream directly or through lym- phatic channels and cause generalized disease. Oral signs suspected to be indications of systemic illness may be confirmed by the presence of rash, fever, headache, malaise, enlarged lymph nodes, or lesions elsewhere on the body Swollen parotid glands are a cardinal sign of infection with the mumps virus and can also be seen in individuals with Sjogren's syndrome and HIV The salivary glands are also frequently involved in tuber- culosis and histoplasmosis infections. Oral signs of infectious mononucleosis, caused by Epstein-Barr virus, include sore throat, gingival bleeding, and multiple pinpoint-sized hemorrhagic spots (pettechi- ae) on the oral mucosa. The oral signs and symptoms associated with some viral, bacterial, and fungal infections are listed in Table 5.1. There can be a large overlap in the clinical appearance of oral manifesta- tions of various diseases with different etiologies, and the clinical diagnosis often involves ancillary proce- dures, which may include laboratory tests, diagnostic imaging, and biopsy. Oral tissues may also reflect immune deficiency. For example, nearly all HIV-infected individuals develop oral lesions at some time during their illness (Greenberg 1996, Greenspan and Greenspan 1996, Phelan 1997). Other immunosuppressed individuals may have the same lesions (Glick and Garfunkel 1992). However, the presentation and the extent, sev- erity, and management of some of these lesions may reflect nuances due to variation in the underlying ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 97 TABLE 5.1 Diseases and conditions causing lesions of the oral mucosa Condition Usual Location Clinical Features Course Viral Diseases Primary acute herpetic gingivostomatitis (herpes simplex virus type 1, rarely type 2) Recurrent herpes labialis Recurrent intraoral herpes simplex Chickenpox (varicella-zoster virus) Herpes zoster (reactivation of Cheek, tongue, gingiva, or varicella-zoster virus) palate Infectious mononucleosis (Epstein-Barr virus) Oral mucosa Warts (papillomavirus) Herpangina (coxsackievirus A; also possibly coxsackievirus Band echovirus) Hand, foot, and mouth disease (type A coxsackieviruses) Primary HIV infection tip and oral mucosa Mucocutaneous junction of lip, perioral skin Palate and gingiva Gingiva and oral mucosa Anywhere on skin and oral mucosa Oral mucosa, pharynx, tongue Oral mucosa, pharynx, palms, and soles Gingiva, palate, and pharynx Labial vesicles that rupture and crust, and intraoral vesicles that quickly ulcerate;extremely painful; acute gingivitis, fever, malaise, foul odor, and cervi- cal lymphadenopathy; occurs primarily in infants, thildren,and young adults Eruption of groups of vesicles that may coalesce, then rupture and crust; painful to pressure or spicy foods Small vesicles that rupture and coalesce; painful Skin lesions may be accompanied by small vesicles on oral mucosa that rupture to form shallow ulcers; may coalesce to form large bullous lesions that ulcerate; mucosa may have generalized erythema Unilateral vesicular eruption and ulceration in lin- ear pattern following sensory distribution of trigeminal nerve or one of its branches Fatigue, sore throat, malaise, low-grade fever, and enlarged cervical lymph nodes; numerous small ulcers usually appear several days before lym- phadenopathy;gingivaI bleeding and multiple petechiae at junction of hard and soft palates Single or multiple papillary lesions, with thick, white keratinized surfaces containing many point- ed projections; cauliflower lesions covered with normal-colored mucosa or multiple pink or pale bumps (focal epithelial hyperplasia) Sudden onset of fever, sore throat, and oropharyn- geal vesicles, usually in children under 4 years, during summer months;diffuse pharyngeal con- gestion and vesicles (1 to 2 mm),grayish-white surrounded by red areola;vesicles enlarge and ulcerate Fever, malaise, headache with oropharyngeal vesi- cles that become painful, shallow ulcers Acute gingivitis and oropharyngeal ulceration, associated with febrile illness resembling mononu- cleosis and including lymphadenopathy Healsspontaneously in 10 to 14 days unless secondarily infected lasts about 1 week, but condition may be prolonged if secondary infection occurs Healspontaneously in about 1 week Lesions heal spontaneously within 2 weeks Gradual healing without scarring; postherpetic neuralgia is common Oral lesions disappear during con- valescence Lesions grow rapidly and spread Incubation period 2 to 9 days;fever for 1 to 4 days; recovery uneventful Incubation period 2 to 18 days; lesions heal spontaneously in 2 to 4 weeks Followed by HIV seroconversion, asymptomatic HIV infection,and usually ultimately by HIV disease 98 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health Condition Usual Location Clinical Features Course Bacterial or fungal diseases Acute necrotizing ulcerative gingivitis ("trench mouth," Vincent's infection) Prenatal (congenital) syphilis Gingiva Palate, jaws, tongue, and teeth Painful. bleeding gingiva characterized by necrosis Continued destruction of tissue fol- and ulceration of gingival papillae and margins lowed by remission, but may recur plus lymphadenopathy and foul odor Gummatous involvement of palate, jaws, and facial Tooth deformities in permanent bones; Hutchinson's incisors, mulberry molars, dentition irreversible glossitis, mucous patches, and fissures of corners of mouth Primary syphilis (chancre) Lesion appears where organism enters body; may occur on lips, tongue, or tonsillar area Small papule developing rapidly into a large, Healing of chancre in 1 to 2 painless ulcer with indurated border;unliteral months, followed by secondary lymphadenopathy;chancre and lymph nodes con- syphilis in 6 to 8 weeks taining spirochetes;serologic tests positive by third to fourth week Secondary syphilis Oral mucosa frequently involved with mucous patches,primarily on palate, also at commissures of mouth Maculopapular lesions of oral mucosa,S to 10 mm in diameter with central ulceration covered by grayish membrane; eruptions occurring on various mucosal surfaces and skin accompanied by fever, malaise, and sore throat Lesions may persist from several week5 to 1 year Tertiary syphilis Palate and tongue Gummatous infiltration of palate or tongue fol- lowed by ulceration and fibrosis; atrophy of tongue papillae produces characteristic bald tongue and glossitis Gumma may destroy palate, caus- ing complete perforation Gonorrhea Tuberculosis Cervicofacial actinomycosis Lesions may occur in mouth at Earliest symptoms are burning or itching sensa- Lesions may resolve with appropri- site of inoculation or secondarily tion, dryness, or heat in mouth followed by acute ate antibiotic therapy by hematogenous spread from a pain on eating or speaking; tonsils and orophar- primary focus elsewhere ynx most frequently involved; oral tissues may be ' diffusely inflamed or ulcerated; saliva develops increased viscosity and fetid odor;submaxillary lymphadenopathy with fever in severe cases Tongue, tonsillar area,soft A solitary, irregular ulcer covered by a persistent Lesions may persist palate exudate; ulcer has an undermined, firm border Swellings in region of face, neck, Infection may be associated with an extraction, Acute form may last a few weeks; and floor of mouth jaw fracture, or eruption of molar tooth; in acute chronic form lasts months or form resembles an acute pyogenic abscess, but years; prognosis excellent; actin- contains yellow "sulfur granules" (gram-positive omycetes respond to antibiotics mycelia and their hyphae) (tetracyclines or penicillin) but not antifungal drugs Histoplasmosis Any area in mouth, particularly tongue, gingiva, or palate Numerous small nodules may ulcerate; hoarse- ness and dysphagia may occur because of lesions in larynx usually associated with fever and malaise May be fatal Candidiasis Any area of oral mucosa Pseudomembranous form has white patches that are easily wiped off leaving red, bleeding, sore surface; erythematous form is flat and red; rarely, candidai leukoplakia appears as white patch in tongue that does not rub off; angular cheilitis due to Candida involves sore cracks and redness at angle of mouth; Candida seen on KOH prepara- tion in all forms Responds to antifungals (confinuesJ ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 99 Linkages with General Health TABLE 3.1 continued Condition Usual Location Clinical Features Course Dermatologic diseases Mucous membrane pemphigoid Primarily mucous membranes of the oral cavity, but may also involve the eyes, urethra, vagi- na,and rectum Painful, grayish-white collapsed vesicles or bullae with peripheral erythematous zone; gingival lesions desquamate, leaving ulcerated area Protracted course with remissions and exacerbations; involvement of different sites occurs slowly;glu- cocorticoids may temporarily reduce symptoms but do not control the disease Erythema multiforme (Stevens-Johnson syndrome) Pemphigus vulgaris Primarily the oral mucosa and skin of hands and feet Oral mucosa and skin Intraoral ruptured bullae surrounded by an inflammatory area; lips may show hemorrhagic crusts; the "iris," or "target" lesion, on the skin is pathognomonic; patient may have severe signs of toxicity Ruptured bullae and ulcerated oral areas; mostly in older adults Onset very rapid; condition may last 1 to 2 weeks; may be fatal; acue episodes respond to steroids With repeated recurrence of bul- lae, toxicity may lead to cachexia, infection, and death within 2 years; often controllable with steroids Lichen planus Other conditions Oral mucosa and skin White striae in mouth; purplish nodules on skin at sites of friction;occasionally causes oral mucosal ulcers and erosive gingivitis Protracted course, may respond to topical steroids Recurrent aphthous ulcers Behcet's syndrome Traumatic ulcers Anywhere on nonkeratinized Single or clusters of painful ulcers with surround- Lesions heal in 1 to 2 weeks but oral mucosa (lips,tongue, buc- ing erythematous border; lesions may be 1 to 2 may recur monthly or several cat mucosa,floor of mouth, soft mm in diameter in crops (herpetiform), 1 to S times a year; topical steroids give palate, oropharynx) mm (minor),or 5 to 15 mm (major) symptomatic relief;systemic glu- cotorticoids may be needed in severe cases; a tetracycline oral suspension may decrease severity of herpetiform ulcers Oral mucosa,eyes,genitalia, Multiple aphthous ulcers in mouth; inflammatory Ulcers may persist for several gut,and central nervous system ocular changes; ulcerative lesions on genitalia; weeks and heal without scarring inflammatory bowel disease and CNS disease Anywhere on oral mucosa;den- Localized, discrete ulcerated lesion with red bor- Lesions usually heal in 7 to 10 tures frequently responsible for der; produced by accidental biting of mucosa, days when irritant is removed, ulcers in vestibule penetration by a foreign object, or chronic irrita- unless secondarily infected tion by a denture Source: Greenspan, in Fauci et al. 1998. Harrison's principles of internal medicine. Reprinted by permission from McGraw-Hill (2000). Copyright 2000 by McGraw-Hill. systemic condition. For example, the linear gingival erythema and necrotizing ulcerative periodontitis sometimes seen in HIV infection have been difficult to resolve with routine dental curettage and prophy- laxis (Glick et al. 1994b). The appearance of soft or hard tissue pigmentation is associated with a number of diseases and treatments. Malignant melanoma can appear in the mouth as brown or black flat or raised spots. Kaposi's sarcoma can appear as a flat or raised pig- mented lesion. Addison's disease causes blotches or spots of bluish-black or dark brown pigmentation to occur early in the disease. Congenital discrete brown or black patches (nevi) can appear in any part of the mouth. Pigmentation of the tooth crowns may be seen in children with cystic fibrosis and porphyria and those exposed to tetracycline during tooth development. The oral tissues can also reflect nutritional status and exposure to risk factors such as tobacco. The 100 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL tongue appears smooth in pernicious anemia. Group B vitamin deficiency is associated with oral mucositis and ulcers, glossitis, and burning sensations of the tongue. Scurvy, caused by severe vitamin C deficien- CY is associated with gingival swelling, bleeding, ulceration, and tooth loosening. Lack of vitamin D in utero or infancy impairs tooth development. Enamel hypoplasia may result from high levels of fluoride or from disturbances in calcium and phosphate metab- olism. which can occur in hypoparathyroidism, gas- troenteritis, and celiac disease. The mouth also can reflect the effects of tobacco use, perhaps providing the only visible evidence of its adverse effects. Oral Manifestations of HIV Infection and of Osteoporosis The mouth can serve as an early warning system, diagnostic of systemic infectious disease and predic- tive of its progression, such as with HIV infection. In the case where oral cells and tissues have counter- parts in other parts of the body, oral changes may indicate a common pathological process. During rou- tine oral examinations and perhaps in future screen- ing tests, radiographic or magnetic resonance imag- ing of oral bone may be diagnostic of early osteo- porotic changes in the skeleton. The following sec- tions provide details. HIV Infection The progressive destruction of the body`s immune system by HIV leads to a number of oral lesions, such as oral candidiasis and oral hairy leukoplakia, that have been used not only in diagnosis but also in determining specific stages of HIV infection (CDC 1992, 1994, Montaner et al. 1992, Redfield et al. 1986, Royce et al. 1991, Seage et al. 1997). Oral can- didiasis is rarely seen in previously healthy young adults who have not received prior medical therapy such as cancer chemotherapy or treatment with other immunosuppressive drugs (Klein et al. 1984). It was associated with AIDS as early as 1981 in the first report of the syndrome (CDC 1981a) and was fre- quently noted among otherwise asymptomatic HIV- positive populations (Duffy et al. 1992, Feigal et al. 1991). Oral candidiasis may be the first sign of HIV infection and often occurs as part of the initial phase of infection-the acute HIV syndrome (Tindall et al. 1995). It tends to increase in prevalence with pro- gression of HIV infection when CD4 lymphocyte counts fall (Glick et al. 1994a, Lifson et al. 1994). It also appears to be the most common oral manifesta- tion in pediatric HIV infection (Kline 1996, Leggott Linkages with General Health 1995, Ramos-Gomez et al. 1996) and has been demonstrated to proceed to esophageal candidiasis, a sign of overt AIDS (Saah et al. 1992). Both the pseudo- membranous and the erythematous forms of candidi- asis appear to be important predictors of progression of HIV infection (Dodd et al. 1991, Klein et al. 1984, 1992). Like oral candidiasis, oral hairy leukoplakia in HIV-positive persons heralds more rapid progression to AIDS (Glick et al. 1994a, Greenspan et al. 1987, Lifson et al. 1994, Morfeldt-Manson et al. 1989). Oral hairy leukoplakia is an oral lesion first reported in the early days of the AIDS epidemic (Greenspan D et al. 1984, Greenspan JS et al. 1985). Since its discov- ery, hairy leukoplakia has been found in HIV-negative persons with other forms of immunosuppression, such as organ or bone marrow recipients and those on long-term steroid therapy (Epstein et al. 1988, Greenspan et al. 1989, ltin et al. 1988, King et al. 1994, Zakrzewska et al. 1995), and less frequently among immunocompetent persons (Eisenberg et al. 1992, Felix et al. 1992). In a comprehensive review of periodontal condi- tions, Mealey (1996) noted that linear gingival ery- thema and necrotizing ulcerative periodontitis may be predictive of progression of HIV infection. Necrotizing ulcerative periodontitis, a more serious periodontal condition observed in HIV-infected per- sons, is a good predictor of CD4+ cell counts of under 200 per cubic millimeter, and in one study was a strong predictor of rapid progression to death (Glick et al. 1994a,b, Winkler and Robertson 1992, Winkler .et al. 1988). In addition, the numerous ulcerative and nonulcerative conditions that affect the oral cavity (Aldous and Aldous 1991, Coates et al. 1996, Cruz et al. 1996, Gandolfo et al. 1991, Itin et al. 1993, Mealey 1996) may affect the biologic activity of HIV and are affected by its treatments. Other oral conditions, unexpected in the oral cavity, have been noted in the early stages of HIV infection. The increased incidence of Kaposi's sarco- ma among young men in New York and California was one of the earliest signs of the AIDS epidemic (CDC 1981b). In addition, some conditions create a problem for differential diagnosis. For example, because involvement of the gingiva is common, early non-Hodgkin's lymphoma lesions are frequently mis- taken for common periodontal or dental infections (Epstein and Silverman 1992). The changing face of the HIV epidemic and changes in the therapies used to manage complica- tions are reflected in changes in the oral manifesta- tions, which warrant continued surveillance and research. The increasing resistance of microorganisms ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 101 Linkages with General Hdth to antibiotics and antifungals is challenging. On the other hand, the completion of the Candida albicans genome may yield better treatments for this oppor- tunistic infection. Osteoporosis and Oral Bone Loss With growing numbers of Americans living longer, there have been concomitant increases in the num- bers affected by age-related chronic degenerative dis- eases. Prominent among these conditions are bone and joint diseases. It is likely, for example, that some temporomandibular joint disorders are manifesta- tions of osteoarthritis, rheumatoid arthritis, or myofascial pain. Paget's disease, characterized by enlarged and deformed bone, can be particularly painful and debilitating when it affects the cranial and jaw bones. Osteoporosis, a degenerative disease character- ized by the loss of bone mineral and associated struc- tural changes, has long been suspected as a risk fac- tor for oral bone loss. In addition, measures of oral bone loss have been proposed as potential screening tests for osteoporosis (Jeffcoat 1998). Osteoporosis affects over 20 million people in the United States, most of whom are women, and results in nearly 2 million fractures per year (National Institute of Arthritis, Musculoskeletal and Skin Diseases 2000). The disease is more prevalent in white and Asian American women than in black women. Oral bone loss has been reported to be more prevalent in women than in men. Studies by,Ortman et al. (1989) found a higher percentage of women than men with severe alveolar ridge resorption. This finding parallels the findings of Humphries et al. (1989), who showed that loss of bone mineral densi- ty with age in edentulous adult mandibles was more significant in women than in men. Also, the associa- tion between estrogen status, alveolar bone density, and history of periodontitis in postmenopausal women has been studied (Payne et al. 1997). Most of the studies in this area have examined bone loss in women, and most investigators have reported a correlation between oral and skeletal bone loss measured in a variety of ways. Studies of non- osteoporotic women by Kribbs et al. (1990) showed that mandibular bone mass is significantly correlated with skeletal bone mass. Dual photon absorptiometry measurements of jawbone volume in women with osteoporosis have shown that reduction in mandibu- lar bone mass is directly related to the reduction in total skeletal mass density (Kribbs and Chesnut 1984, Kribbs et al. 1983, von Wowem 1985, 1988, von Wowern et al. 1994). Kribbs et al. (1989) further showed that mandibular mass is correlated with all skeletal measures in osteoporotic women and that the height of the edentulous ridge is correlated with total body calcium and mandibular bone mineral density. Hirai et al. (1993) found that the presence of skeletal osteoporosis strongly affects the reduction of the residual ridge in edentulous patients. A small case-control study comparing older female patients with osteoporotic fractures and non-osteoporotic women without fractures found greater periodontal attachment loss in the osteoporotic women than in the controls (von Wowern et al. 1994). Studies that have controlled for confounding fac- tors also have found correlations between oral bone loss and skeletal bone density. Controlling for pack- years of smoking, education, body mass, and years since menopause, Krall et al. (1994, 1996) found a significant positive relationship between number of teeth and bone mineral density of the spine and the radius. In a cohort of 70 postmenopausal women, Wactawski-Wende et al. (1996) measured skeletal bone mineral density at the Wards triangle area of the femur and compared it with periodontal disease assessed by attachment loss and the height of alveo- lar bone measured by radiographs. After adjusting for age, years since menopause, estrogen use, body mass index, and smoking, the investigators concluded that osteopenia (low bone mass) is related to alveolar cres- tal height and tooth loss in postmenopausal women. Methods used to measure oral and skeletal bone loss have varied among investigators and have shown different outcomes. Kribbs (1990) found that patients in an osteoporotic group had lost more teeth, had less mandibular bone, and had a thinner bone measured at a part of the jaw (cortex at the gonion) than a comparable non-osteoporotic group. However, using periodontal attachment loss as an indicator of mandibular bone loss, they found no differences between the osteoporotic and the non-osteoporotic group. Mohajery and Brooks (1992) compared non- osteoporotic postmenopausal women with women with mild to moderate osteoporosis and found no correlation between mandibular and skeletal bone mineral density This study raises questions about the quantification of mild and moderate osteoporosis. Defining healthy periodontal tissues as having no periodontal pockets deeper than 5 millimeters, Hildebolt et al. (1997) studied postmenopausal women with healthy periodontal tissues and found no relationship between periodontal attachment loss and postcranial bone mineral density. How- ever, preliminary studies from the oral ancillary study of the NIH Women's Health Initiative report signi- ficant correlations between mandibular basal bone mineral density and hip bone mineral density 102 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL (I- = 0.74, P -C ,001) (Jeffcoat et al. in press). In this study, digital subtraction radiography methods were used for mandibular bone measurements, and dual- energy X-ray absorptiometry (DXA) scans were used for the hip bone measurements. The authors of this study propose the possibility that high-quality intra- oral radiographs may be used in the future for screen- ing osteopenia. Larger cross-sectional studies, as well as longitu- dinal and mechanism studies, are needed to better define the relationship between osteoporosis. osteopenia. and oral bone loss, periodontal disease, and tooth loss. The role of factors involved in the reg- TABLE 3.2 Saliva/oral fluids: sampled analytes and current FDA-approved tests Category Drugs of abusea Analytes Alcohol Amphetamines Barbiturates Benzodiazepines Cocaine LSD Marijuana Nicotine Opiates PCP FDA-Approved Tests Cannabinoids Cocaine Cotinine Methamphetamine Opiates PCP Ethanol AntibodieG HIV HPV HHV-8/KSH C. parvum Helicobatter pylon' HIV antibodies Hormones Cortisol Progesterone Testosterone Substance P Met-enkephalin Estriol Environmental toxinsd Cadmium Lead Mercury Therapeutics? Antipyrine Carbamazepine Ciprofloxacin lrinotecan Lithium Methotrexate Phenytoin Phenobarbital Theophylline ~Coneetal.1993.1997. Yonrtantine et al. 1997. (Dabbr 1993,Ellison 1993. *Gonzalez et al.1997, Joselow et al.1968. eWilsOn 1993. Source:Constantme et al. 1997. Linkages with General Health ulation of bone mineral density in men as well as in postmenopausal women needs to be evaluated fur- ther with reference to oral bone loss, tooth loss, and periodontal disease. Variables such as sex, race, dietary calcium and phosphorus, vitamin D intake, exercise, body mass index, smoking, genetics, med- ication use, reproductive history, and psychosocial factors need to be assessed in depth. In addition, reli- able and valid criteria and imaging technologies for assessing osteoporosis and oral bone loss are needed to better elucidate the full relationship between skeletal and mandibular bone mineral density, peri- odontal disease, alveolar ridge resorption, and tooth loss. Oral-fluid-based Diagnostics: The Example of Saliva The diagnostic value of salivary secretions to detect systemic diseases has long been recognized (Mandel 1990), and oral fluids and tissues (buccal cells) are increasingly being used to diagnose a wide range of conditions. Saliva- and oral-based diagnostics use readily available samples and do not require invasive procedures. Researchers have detected antibodies in saliva that are directed against viral pathogens such as human immunodeficiency virus (Malamud 1997) and hepatitis A virus (O'Farrell et al. 1997) or B virus (Richards et al. 1996). Saliva is being used to detect antibodies, drugs, hormones, and environmental tox- ins (Malamud and Tabak 1993) (Table 5.2). The sim- plest tests are those that detect the presence or absence of a substance in the saliva, such as various drugs. Greater technical challenges are presented for tests that will be used for therapeutic monitoring since accurate levels of a substance and/or its metabolites are needed. In these instances the sali- va/plasma concentration ratio must be determined experimentally (Haeckel 1993). Tests beyond those listed in Table 5.2 are currently on the market, but do not yet have FDA approval. Saliva is also the fluid of choice to assess the integrity of the mucosal immune system (Mandel 1990). Most recently, oral fluids have been used as a source of microbial or host DNA. With the advent of polymerase chain reaction methods, the DNA con- tained within a single cell is sufficient for detection of viruses (e.g., Kaposi's sarcoma-associated herpes virus, Koelle et al. 1997; Epstein-Barr virus, Falk et al. 1997; mumps virus, Afzal et al. 1997) or bacteria (e.g., Helicobacter pylori, Reilly et al. 1997). Similarly, DNA extracted from sloughed buccal epithelial cells can be used to genotype persons. This has found application in forensics (Roy et al. 1997) and may be ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 103 Linkages with General Health used for diagnostic purposes in the future (van Schie and Wilson 1997). Saliva has the potential of replacing blood, the current standard for testing many diseases and conditions (e.g., diabetes, infectious disease, Parkinson's disease, alcoholic cirrhosis, Sjogren`s syndrome, and cystic fibrosis sarcoidosis). Important goals for the future are the development of new diagnostic tests for early disease detection, defining individual patient risk of adverse response to drugs, monitoring therapeutic progress, and determin- ing outcomes of treatment. Key issues in the development of a new generation of saliva diag- nostics include their selectivity, sensitivity, response time, dynamic range (values of interest), rep- resentative sampling, and, perhaps most important, their reliability or stability as well their ability to assess multiple substances simultaneously Conclusion For the clinician the mouth and face provide ready access to physical signs and symptoms of local and generalized disease and risk factor exposure. These signs and symptoms augment other clinical features of underlying conditions. Comprehensive care of the patient requires knowledge of these signs and symp- toms, their role in the clinical spectrum of general diseases and conditions, and their appropriate man- agement. Oral biomarkers and surrogate measures are also being explored as means of early diagnosis. With further development and refinement, oral- based diagnostics such as salivary tests can be- come widely used and acceptable tools for individu- als, health care professionals, researchers, and com- munity programs. The continued refinement of imaging techniques also has the potential of using oral imaging to identify early signs of skeletal bone degeneration. THE MOUTH AS A PORTAL OF ENTRY FOR INFECTION Chapter 3 provides an overview of the effects of oral microbial infections with viruses, bacteria, and fungi. More than 500 bacterial strains have been identified in dental biofilm, and more than 150 bacterial strains have been isolated from dental pulp infections. More recently, 37 unique and previously unknown strains of bacteria were identified in dental plaque (biofilm) (Kroes et al. 1999). Most oral lesions are opportunis- tic infections, that is, they are caused by microorgan- isms commonly found in the mouth, but normally kept in check by the body's defense mechanisms. These microorganisms can induce extensive local- ized infections that compromise general well-being in and of themselves. However, they also may spread to other parts of the body if normal barriers are breached. The oral mucosa is one such barrier that provides critical defense against pathogens and other challenges (Schubert et al. 1999). Salivary secretions are a second major line of defense. Damage to the oral mucosa from mechanical trauma, infection, or salivary dysfunction with resulting derangements in lubricatory and antimicrobial functions of saliva, as a result of chemotherapy, radiation, and medications causing hyposalivation, allows a portal of entry for invading pathogens. Oral Infections and Bacteremia Oral microorganisms and cytotoxic by-products associated with local infections can enter the blood- stream or lymphatic system and cause damage or potentiate an inappropriate immune response else- where in the body. Dissemination of oral bacteria into the bloodstream (bacteremia) can occur after most invasive dental procedures, including tooth extrac- tions, endodontic therapy, periodontal surgery, and scaling and root planing. Even routine oral hygiene procedures such as daily toothbrushing, subgingival irrigation, and flossing may cause bacteremia. However, these distant infections have been seen more often in high-risk patients such as those who are immunocompromised. Oral bacteria have several mechanisms by which they invade mucosal tissues, perhaps contributing to their ability to cause bacteremias. For example, oral bacteria and their products may invade the periodontal tissues directly. Actinobacillus actino- mycetemcomitans has been found in gingival connective tissue in patients with localized juvenile periodontitis (Christersson et al. 1987a,b, Meyer et al. 1991, Riviere et al. 1991). Invasion of tissue by Porphyromonas gingivalis has also been described in vivo (Saglie et al. 1988) and in vitro (Njoroge et al. 1997, Sandros et al. 1993, 1994, Weinberg et al. 1997). Although oral bacteria can enter the blood through injured or ulcerated tissue, bacterial invasion of periodontal tissues represents another possible mechanism. In the immunocompetent individual, bacteremia originating from the oral cavity is usually transient and harmless. However, if the individuals immune system is compromised, the normally harmless oral bacteria may pose a significant risk. The morbidity and mortality associated with oral foci of infections are hard to assess. This is due to the formidable task 104 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL of tracking the source of an infection unless the responsible pathogen is indigenous to a specific anatomic location. Viridans group streptococci (VGS) have a low degree of virulence but can be associated with mor- bidity and mortality under certain circumstances. Increased pathogenicity of Streptococcus viridans is most prominent in individuals with neutropenia (low blood counts of circulating white blood cells called neutrophils) and has been associated with a toxic- shock-like syndrome (TSLS) or viridans streptococ- cal shock syndrome (VSSS), as well as with adult res- piratory distress syndrome (ARDS) (Bochud et al. 1994). Although a high degree of morbidity is associat- ed with viridans streptococcal bacteremia, a low inci- dence of mortality has been reported (Heimdahl et al. 1989). Several studies have shown that under adverse circumstances oral flora and oral infections are associated with increased incidence of morbidity and even mortality (Engelhard et al. 1995, Lucas et al. 1998, Martin0 et al. 1995, Ruescher et al. 1998, Sparrelid et al. 1998, Sriskandan et al. 1995). Reduction of oral foci of infection decreases systemic complications, specifically in severely neutropenic patients undergoing chemotherapy (Heimdahl et al. 1984). In addition, hospital stays for patients with oral mucositis undergoing autologous bone marrow transplants were longer than for those without oral mucositis (Ruescher et al. 1998). Other cohorts identified at increased risk for sys- temic complications due to oral bacteria include hos- pitalized patients unable to perform adequate oral hygiene, those receiving saliva-reducing medications, and those taking antibiotics that alter the oral flora. A positive dental plaque culture for aerobic pathogens was significantly associated with the development of hospital-acquired pneumonia and bacteremia in a study of individuals in an intensive care unit (ICU) (Fourrier et al. 1998). In addition, several case reports have been pub- lished implicating indigenous oral flora in the devel- opment of brain abscesses (Andersen and Horton 1990, Andrews and Farnham 1990, Baker et al. 1999, Gallagher et al. 1981, Goteiner et al. 1982, Saal et al. 1988). This serious condition is associated with a mortality rate of almost 20 percent and full recovery in only slightly more than 50 percent of all patients (Goteiner et al. 1982). These data are based on single case reports and most probably represent rare events. However, they provide additional examples that point to the potential pathogenicity of the normal oral flora during special adverse circumstances. Linkages with General Health Oral Infections as a Result of Therapy Chemotherapy Oral mucositis can be a major dose-limiting problem during chemotherapy with some anticancer drugs, such as 5-fluorouracil, methotrexate, and doxoru- bicin. It is estimated that approximately 400,000 patients undergoing cancer therapy each year will develop oral complications (NIH 1990). Infection of ulcerated mucous membranes often occurs after chemotherapy, especially since patients are usually immunocompromised. Bacterial, fungal, and viral causes of mucositis have been identified (Feld 1997). The mechanism by which cancer-chemotherapy- induced mucositis occurs is likely associated with the rapid rate of turnover of oral epithelial cells. In addi- tion, other components likely include upregulation of pro-inflammatory cytokines and metabolic by- products of colonizing oral microflora (Sonis 1998). Chemotherapy alters the integrity of the mucosa and contributes to acute and chronic changes in oral tis- sue and physiologic processes (Carl 1995). The ulcerated mucosa is susceptible to infection by microbial flora that normally inhabit the oral cavity, as well as by exogenous organisms, and exacerbates the existing mucositis. Further, these microflora can disseminate systemically (Pizza et al. 1993, Rolston and Bodey 1993). Compromised salivary function can further elevate risk for systemic infection of oral origin. Both indigenous oral flora and hospital-acquired pathogens have been associated with bacteremias and systemic infection (Schubert et al. 1999). Changes in infection profiles in myelosuppressed (immunosup- pressed) cancer patients tend to occur in cyclic fash- ion over many years. This evolving epidemiology is caused by multiple factors including use of antibi- otics. Gram-positive organisms including viridans streptococci and enterococci are currently associated with systemic infection of oral origin in myelosup- pressed cancer patients. In addition, gram-negative pathogens including I? aeruginosa, Neisseria spp., and Escherichia coli remain of concern. Cancer patients undergoing bone marrow radia- tion who have chronic periodontal disease may also develop acute periodontal infections with systemic complications (Peterson et al. 1987). The extensive ulceration of gingival sulcular epithelium associated with periodontal disease is not directly observable clinically, yet may represent a source for disseminat- ed infection by an extensive array of organisms. Inflammatory signs may be masked due to the under- lying bone marrow suppression. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 105 Linkages with General Health Viruses are also associated with clinically impor- tant oral disease in patients receiving chemotherapy (Ralston and Bodey 1993, Pizzo et al. 1993). Infections caused by herpes simplex virus, varicella- zoster virus, and Epstein-Barr virus typically result from reactivation of a latent virus, whereas cytomegalovirus infections can result via reactivation of a latent virus or a newly acquired virus. The sever- ity of the infection, including fatal outcome, depends on the degree of immunocompromise. Many agents and protocols have been investigat- ed to manage or prevent mucositis (Peterson 1999, Schubert et al. 1998). For example, various biologic response modifiers, including transforming growth factor p3 or keratinocyte growth factor, have been under recent study in randomized clinical trials. Allopurinol mouthwash and vitamin E have been cited as agents that can decrease the severity of mucositis. although more extensive testing is neces- sary. Prostaglandin E2 was not shown to be effective in prophylaxis of oral mucositis following bone mar- row transplant; however, more recent studies indi- cate possible efficacy when administered via a differ- ent dosing protocol. Oral cryotherapy appears to be efficacious in reducing severity of oral mucositis caused by 54uorouracil and related compounds (Rocke et al. 1993). can require surgery to excise the dead tissue, which can in turn leave the face badly disfigured as well as functionally impaired (Field et al. 2000). The likeli- hood of ORN is increased with trauma to the bone, including that caused by tooth extraction (Murray et al. 1980a, b). The risk is especially marked when the trauma occurs near the time of radiation (Epstein et al. 1987). Management includes elimination of acute or potential dental and periodontal foci of disease, increased patient participation in oral hygiene, use of oral topical fluorides for caries prevention, and use of antiviral, antifungal, or antimicrobial therapy for management of infections associated with mucositis. Combined Cancer Therapies Local application of capsaicin preparations may be effective in controlling oral mucositis pain as dis- tinguished from tissue injury itself (Berger et al. 1995). Capsaicin and its analogs are the active ingre- dients in chili peppers. Capsaicin's clinical potential derives from the fact that it elevates the threshold for pain in areas to which it is applied. Rapid developments have occurred in the use of blood cell growth factors for treatment of various conditions, including the anemia of end-stage renal disease, the neutropenia occurring with cancer care, and the bone marrow toxicity and mucositis that can follow aggressive chemotherapy or radiation therapy (Sonis et al. 1997, Williams and Quesenberry 1992). Sonis et al. (1997) found that topical application of transforming growth factor beta (TGF-8) in the ham- ster model of oral mucositis significantly reduced basal cell proliferation and reduced the severity of mucositis associated with 5-fluorouracil treatment. Radiation Therapy Radiation therapy disrupts cell division in healthy tissue as well as in tumors and also affects the normal structure and function of craniofacial tissues, includ- ing the oral mucosa, salivary glands, and bone. Oral- facial complications are common after radiation ther- apy to the head and neck. The most frequent, and often the most distressing, complication is mucositis, but adverse reactions can affect all oral-facial tissues (Scully and Epstein 1996). Radiation can cause irreversible damage to the salivary glands, resulting in dramatic increases in dental caries. Oral mucosal alterations may become portals for invasion by pathogens, which may be life- threatening to immunosuppressed or bone-marrow- suppressed patients. A less common but very serious adverse consequence is destruction of bone cells and bone death, called osteoradionecrosis (ORN). ORN can result in infection of the bone and soft tissue and Other growth factors considered for use in reducing mucositis include granulocyte-monocyte colony-stimulating factor and granulocyte colony- stimulating factor. Bone morphogenetic proteins are also in development for alleviating the toxicity and mucositis that follow chemotherapy and radiation therapy Other approaches to reducing mucositis and adverse oral effects of chemotherapy and radiation therapy include fractionating the dose of radiation, and combining chemotherapy with growth factors or with less toxic oncostatic agents. Although the oral mucositis occurring in chemotherapy and in head and neck radiation patients shares many characteristics, distinct differences also exist (NIH 1990, Schubert et al. 1998, Wilkes 1998). For example, in contrast to chemotherapy-associated lesions, radiation damage is anatomically site- specific; toxicity is localized to irradiated tissue volumes. The degree of damage depends on treatment-regimen-related factors, including the type of radiation used, the total dose administered, the fractionation, and field size. Thus, research involving both cohorts of cancer patients remains essential to enhancing patient management. Development of new technologies to prevent cancer-therapy-induced oral mucositis could 106 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL substantially reduce the risk for oral and systemic infections, oral pain, and the number of hospital days. Improvement in quality of life and reduction in health costs are also likely and desirable outcomes. The new technologies could also provide a set- ting in which novel classes of chemotherapeutic drugs, utilized at increased doses, could be imple- mented. These advances in turn could lead to enhanced cancer patient survival and lengthen the duration of disease remission. Pharmaceuticals A number of medications used to treat systemic dis- eases can cause oral complications, ranging from xerostomic effects to alterations in the surface struc- ture of the enamel or mucosa. More than 400 over- the-counter and prescription drugs have xerostomic side effects (Sreebny and Schwartz 1997). These include tricyclic antidepressants, antihistamines, and diuretics. The dimensions and impact of these side effects vary depending on the response of the indi- vidual patient and the duration of medication use. Staining of the teeth or mucosa is associated with a variety of drugs, including tranquilizers, oral con- traceptives, and antimalarials. The antibiotic tetracy- cline can cause enamel hypoplasia when taken by the mother during pregnancy and by children during tooth development. The antimicrobial mouthrinse agent chlorhexidine also can stain the teeth, but this staining is external and can be removed by dental prophylaxis. Other drugs have been associated with gingival overgrowth, including cyclosporin, which has been used as an immunosuppressant in the United States since 1984 to prevent rejection of transplanted organs and bone marrow. This drug has also been used in other countries for treatment of type 2 dia- betes, rheumatoid arthritis, psoriasis, multiple sclero- sis, malaria, sarcoidosis, and several other diseases with an immunological basis (Adams and Davies 1984). Other drugs that cause gingival overgrowth include calcium ion channel blocking agents used in the treatment of angina pectoris and postmyocardial syndrome, such as nifedipine and verapamil (Lucas et al. 1985>, and phenytoin (sodium 5,5-phenylhy- dantoin), used in the treatment of epilepsy and also for management of other neurological disorders. Treatment often consists of using an alternate drug, although this is not always possible. Conservative periodontal therapy can reduce the inflammatory component of enlargement; however, surgery is often required. Oral candidiasis is typically caused by opportunistic overgrowth of Candida albicans. Drugs that cause systemic bone marrow suppression, oral Linkages with General Health mucosal injury, or salivary compromise collectively promote the risk for clinical infection. In addition, antibiotics and concurrent steroid therapy often alter oral flora, thereby creating an environment for fungal overgrowth. In high-risk cancer patients, fungal infection can cause severe morbidity and even death. Infective Endocarditis The purported connection between oral infection and a specific heart disease, infective endocarditis, has a long history. Endocarditis is caused by bacteria that adhere to damaged or otherwise receptive sur- faces of the tissue that lines heart valves (the endo- cardium) (Weinstein and Schlesinger f974). Dental and other surgical procedures may predispose sus- ceptible patients to infective endocarditis by induc- ing bacteremias (Lacassin et al. 1995). However, bac- teremias from oral infections that occur frequently during normal daily activities, coincidental even with chewing food, toothbrushing, and flossing, con- tribute more substantially to the risk of infective endocarditis (Bayliss et al. 1983, Dajani et al. 1997, Strom et al. 1998). Oral organisms are common etio- logic agents of infective endocarditis (Bayliss et al. 1983). For example, strains of S. sanguis, as well as gram-negative oral bacteria including Haemophilus aphrophilus, A. actinomycetemcomitans, E. cormdens, Capnocytophaga spp., and Fusobacterium nucleatum, have been associated with bacterial endocarditis (Barco 1991, Geraci and Wilson 1982, Kaye 1994, Moulsdale et al. 1980). Infective endocarditis occurs with different incu- bation periods, which differ in causative bacteria and signs and symptoms. For example, Staphylococcus aureus endocarditis may have a rapid onset and fatal course if it affects the left side of the heart. With a more indolent course, patients may often be unaware of infection and may experience fever, night chills, myalgia, and arthralgia for a considerable period of time before diagnosis. The infection is often curable if diagnosed and treated early The classic risk factors for endocarditis include cardiac valve disorders (valvulopathies) that include rheumatic and congenital heart disease, complex cyanotic heart disease in children, and mitral valve prolapse with regurgitation. Recent studies indicate that the use of certain diet drugs (fenfluramine and dexfenfluramine) has induced cardiac valvulopathy, which may in some cases be transient. Among at-risk persons, bacteremias are more likely to occur in those with periodontal disease (Silver et al. 1977). However, the oral pathogens causing periodontitis have only rarely been shown to cause endocarditis. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 107 Linkages Lvith General Health Prevention of infective endocarditis from oral bacteria depends on limiting the entry and dissemi- nation of bacteria through the bloodstream and lym- phatic circulation. Antibiotic prophylaxis for dental procedures that are likely to provoke bacteremia has historically been recommended (Dajani et al. 1997, Durack 1995). A recent study, however, suggests that receiving dental treatment does not significantly increase the risk of infective endocarditis, even in patients with valvular abnormalities (Strom at al. 1998). Further research is necessary to determine whether some heart or valvular conditions or certain dental procedures, such as surgery or scaling, would require coverage with pre-procedural antibiotics and others would be precluded. Oral Infections and Respiratory Disease Pathogens in the oral cavity can also gain access to the airway, sometimes with serious consequences. In adults, bacterial pneumonias are strongly associated with aspiration of bacteria into the lower respiratory tract, which is normally sterile. Common respiratory pathogens such as Streptococcus pneumoniae, Streptococcus pyogenes, Mycoplasma pneumoniae, and Haemophilus inf7uenzae can colonize the oropharynx and the lower airway. In addition, oral bacteria including A. actinomycetemcomitans (Yuan et al. 1992), Actinomyces israelii (Morris and Sewell 1994, Zijlstra et al. 1992), Capnocytophaga spp. (Lorenz and Weiss 1994), Eikenella corrodens Uoshi et al. 1991), Prevotella inter-media, and Streptococcus con- stellatus (Shinzato and Saito 1994) can be aspirated into the lower airways (Scannapieco 1998, 1999). Chronic obstructive pulmonary disease, charac- terized by obstruction of airflow due to chronic bron- chitis or emphysema and by recurrent episodes of respiratory infection, has been associated with poor oral health status (Hayes et al. 1998, Scannapieco et al. 1998). A positive relationship between periodon- tal disease and bacterial pneumonia has been shown by Scannapieco and Mylotte (1996). Although oral bacteria, including periodontal pathogens, have the potential for causing respiratory infections, the frequency and nature of such infec- tions are not known and merit further study. Oral Transmission of Infections Besides being a portal of entry for infections, the mouth is an important source of potentially patho- genic organisms and is often the vehicle by which infection is delivered to the bodies of others. Microorganisms were not discovered in the mouth until the seventeenth century, when van Leewenhoek examined dental plaque using a microscope he had constructed. In 1884, Koch demonstrated that tuberculosis could be transmitted by airborne droplets from the mouth and respiratory tract. Since that time, we have learned that many common respi- ratory infections, such as influenza, the common cold, pneumonia, and tuberculosis, can be transmit- ted from oral secretions. Before the development of effective vaccines, orally transmitted diseases such as chickenpox, measles, mumps, polio, and diphtheria were a major source of morbidity and mortality in childhood. Viral diseases such as hepatitis B, herpes labialis, acute herpetic gingivostomatitis, cyto- megalovirus, and infectious mononucleosis may also originate from oral contact. , Disease-causing microorganisms can be spread by direct contact (with saliva or blood from the mouth) or indirect contact (with saliva- or blood- contaminated surfaces, including hands or lips), droplet infection (from coughing, sneezing, or even normal speech), or by aerosolized organisms. These organisms can be inhaled, ingested, or taken in through mucous membranes in the eyes, nose, or mouth or through breaks in the skin. A number of diseases can be spread via oral sexual contact, includ- ing gonorrhea, syphilis, trichomoniasis, chlamydia, and mononucleosis. As mentioned earlier, the oral mucosa and saliva provide significant defense against disease transmis- sion. Epidemiological and animal studies are provid- ing evidence, however, that the oral cavity may be the site for transmission of serious systemic infections despite the protective factors in saliva (see Chapter 2). Infection with HIV provides a case in point (Baba et al. 1996, Dillon et al. 2000, Pope et al. 1997, Ruprecht et al. 1999, Stahl-Hennig et al. 1999, Baron et al. 2000). Early in the 198Os, when AIDS was first identi- fied in the United States, concern was expressed about casual (i.e., nonsexual) transmission of HIV (CDC 1983, 1985). Detailed household studies did not demonstrate transmission of HIV, even when family members shared eating utensils and tooth- brushes with an HIV-affected member (Fischl et al. 1987, Rogers et al. 1990, Sande 1986). Similarly, sur- veillance data collected over time showed no evi- dence of casual transmission (Ward and Duchin 1997). Only one nonoccupational episode of HIV trans- mission has been attributed to blood-contaminated saliva (CDC 1997); this incident involved intimate kissing between sexual partners. There have been a few cases of HIV transmission from performing oral 108 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL sex on a person infected with HIV, and it is also pos- sible to become infected with HIV by receiving oral sex. In the San Francisco Options Study of men who have sex with men identified within 12 months of HIV seroconversion, oral transmission represented 7.8 percent of primary HIV infections (Dillon et al. 2000). Rothenberg et al. (1998) reviewed epidemio- logic studies and reports of 38 cases of oral transmis- sion of HIV in the literature. They concluded that although oral-genital contact may be less efficient than needle-sharing or anal intercourse for the trans- mission of HIV, its increased use by men who have sex with men (Ostrow and DiFranceisco 1996, Schwartz et al. 1995) and in crack cocaine smokers (Faruque et al. 1996a,b) may increase its contribu- tion to HIV transmission over time. Several studies provide evidence that when the oral environment is compromised, the mouth can be a potential site of transmission of infectious microbes. Data from Faruque et al. (1996a,b) and Wallace et al. (1996) suggest that there is a positive association between the presence of oral lesions resulting from crack co- caine use, receptive oral intercourse, and HIV trans- mission. A case report has documented the passage of HIV from a partner who is HIV-positive to one who is HIV-negative in the presence of periodontal disease but in the absence of other risk factors (Padian and Glass 1997). Because the type, duration, and fre- quency of oral contact in past studies may not have been specified, the risk could be somewhat higher for oral transmission of HIV than previously reported. The risk might also vary depending on factors such as viral load, infectious dose, area of exposure, and presence or absence of oral lesions. Additional stud- ies are needed to evaluate the risk of oral-genital transmission of HIV; some are under way (J. Greenspan, K. Page-Schafer, personal communica- tion, 1999). Other sexually transmitted diseases (STDs) can occur through oral contact. For example, pharyngeal infection with Chlarnydia trachornatis has been found in 3 to 6 percent of men and women attending STD clinics. Most infections are asymptomatic (Holmes et al. 1999). Another common sexually transmitted infection, herpes simplex virus, commonly infects the pharynx and is seen in 20 percent of patients with primary genital herpes. The painless chancre of pri- mary syphilis can be found in the oral cavity; howev- er, there are no data on the prevalence of this site of infection for Treponema pallidurn. Among persons with gonorrhea, pharyngeal infection occurs in 3 to 7 percent of heterosexual men, 10 to 20 percent of het- erosexual women, and 10 to 25 percent of men who have sex with men (Holmes et al. 1999). Gonococcal Linkages with General Health infection can cause acute pharyngitis, but is usually asymptomatic. The transmission of pharyngeal gon- orrhea to sex partners had been thought to be rare. However, in one study, 17 of 66 men who had sex with men who had urethral gonorrhea reported insertive oral sex as their only risk factor in the past 2 months (Lafferty et al. 1997). Conclusion The role of the mouth as a portal of entry for infec- tion presents ever-new challenges for study. Although oral tissues and fluids normally provide significant barriers and protection against microbial infections, at times these infections can not only cause local dis- ease but, under certain circumstances, can dissemi- nate to cause infections in other parts of the body. The control of existing oral infections is clearly of intrinsic importance and a necessary precaution to prevent systemic complications. ASSOCIATIONS AMONG ORAL INFECTIONS AND DIABETES, HEART DISEASE/STROKE, AND ADVERSE PREGNANCY OUTCOMES Recent studies have reported associations between oral infections-primarily periodontal infections- and diabetes, heart disease and stroke, and adverse pregnancy outcomes, but sufficient evidence does not yet exist to conclude that one leads to the other. This section characterizes the nature of these associ- ations by describing the quality of the evidence sup- porting the reports. Both observational and experi- mental studies were accepted as admissible evidence. Table 5.3 presents the hierarchy of evidence used to interpret these associations. Where there are opera- tive mechanisms proposed that support an associa- tion between oral infectious agents and the systemic conditions in question, they are introduced at the outset. These are followed by animal studies and then by epidemiologic or population-based studies. The evidence for each association is presented in the table in rank order according to the rigor of the study design. The Periodontal Disease-Diabetes Connection There is growing acceptance that diabetes is associat- ed with increased occurrence and progression of peri- odontitis- so much so that periodontitis has been called the "sixth complication of diabetes" (L6e 1993). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 109 Linkages with General Health The risk is independent of whether the diabetes is type 1 or type 2. Type 1 diabetes is the condition in which the pancreas produces little or no insulin. It usually begins in childhood or adoles- cence. In type 2 diabetes, secretion and utilization of insulin are impaired; onset is typically after age 30. Together, these two types of diabetes affect an esti- mated 15.7 million people in the United States and represent the seventh leading cause of death (NIDDK 1999). The goal of diabetic care is to lower blood glu- cose levels to recommended levels. Some investiga- tors have reported a two-way connection between diabetes and periodontal disease, proposing that not only are diabetic patients more susceptible to peri- odontal disease, but the presence of periodontal dis- ease affects glycemic control. This section explores the bidirectional relationship, beginning with the effects of diabetes on periodontal disease. Effects of Diabetes on Periodontitis Prevalence and Severity Several reviews have described candidate mecha- nisms to explain why individuals with diabetes may be more susceptible to periodontitis (Grossi and Genco 1998, Manouchehr-Pour and Bissada 1983, Murrah 1985, Oliver and Tervonen 1994, Salvi et al. 1997, Wilton et al. 1988). These include vascular changes, alterations in gingival crevicular fluid, alter- ations in connective tissue metabolism, altered host immunological and inflammatory response, altered subgingival microflora, and hereditary patterns. Studies were classified by type of diabetes and age of study population (see Table 5.4). Tq'pe 1 Diabetes. Ten reports focused principally on children and adolescents with type 1 diabetes, com- paring them with groups of similar ages without dia- betes (Cianciola et al. 1982, de Pommereau et al. 1992, Faulconbridge et al. 1981, Firatli 1997, Firatli et al. 1996, Goteiner et al. 1986, Harrison and Bowen 1987, Novaes et al. 1991, Pinson et al. 1995, Ringelberg et al. 1977). All but one of the studies (Goteiner et al. 1986) reported greater prevalence, extent, or severity of at least one measure or index of periodontal disease (e.g., gingival inflammation, probing pocket depth, loss of periodontal attach- ment, or radiographic evidence of alveolar bone loss) among subjects with diabetes, even though these investigations were conducted in a variety of coun- tries across several continents. Another set of studies on the relationship between type 1 diabetes and periodontal disease included subjects with and without diabetes between the ages of 15 and 35 (Cohen et al. 1970, Galea et al. 1986, Guven et a1. 1996, Kjellman et al. 1970, Rylander et al. 1987, Sznajder et al. 1978). All six studies reported greater prevalence, extent, or sever- ity of at least one measure or index of periodontal disease. A third set of studies conducted in Scandinavia looked at the relationship between periodontal dis- ease and type 1 diabetes (or diabetes reported as requiring insulin therapy without specification of diabetes type) in adults between 20 and 70 years old. Three of the four studies were cross-sectional (Glavind et al. 1968, Hugoson et al. 1989, Thorstensson and Hugoson 1993), and one was a treatment follow-up study (Tervonen and TABLE 5.3 Hierarchy of evidence used in analyzing and interpreting results Quality of Evidence I: Evidence obtained from at least one properly randomized controlled trial. 11-l: Evidence obtained from well-designed controlled trials without randomization. 11-2: Evidence obtained from well-designed cohort or case-control analytic studies, preferably from more than one center or research group. 11-3: Evidence obtained from multiple time series with or without the intervention.Dramatic results in uncontrolled experiments (such as the results of the introduction of penicillin treatment in the 1940s) could also be regarded as this type of evidence. Ill: Opinions of respected authorities, based on clinical experience; descriptive studies and case reports; or reports of expert committees. Strength of Recommendation A: There is good evidence to support the recommendation. B: There is fair evidence to support the recommendation. C: There is insufficient evidence to recommend for or against, but recommendations may be made on other grounds. D: There is fair evidence to support the recommendation that the intervention be excluded. E: There is good evidence to support the recommendation that the intervention be excluded. I Source: Adapted from U.S.Preventive ServicesTask Force 1996. 110 ORAL HEAL-I-H IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health TABLE 5.4 Summary of studies of the association between diabetes and periodontal diseases, classified by strength of evidence, diabetes type, and age group Number of Measure of Subjects Agesb Periodontal Other Study Diabetes a. Diabetes a. Diabetes Disease Status: Diabetes-Related Evidence Country Design Type" b.Control b.Control Diabetes Effect Variables Considered Leveld Firatli 1997 Cohen et al. 1970 Tervonen and Karjalainen 1997 Novaes et al. 1996 Nelson et al. 1990 Taylor et al. 1998a Taylor et al. 1998b Goteiner et al.1986 Harrison and Bowen 1987 Novaes et al. 1991 Cianciola et al.1982 de Pommereau et al. 1992 Ringelberg et al. 1977 Firatli et al. 1996 Pinson et al. 1995 Faulconbridge et al. 1981 Kjellman et al.1970 Guven et al. 1996 Turkey USA Finland Brazil USA USA USA USA USA Brazil USA France USA Turkey USA England Sweden Turkey Prospective 1 Prospective 1" Prospective 1 Prospective 2 Prospective 2 Prospective 2 Prospective 2 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1 Cross-sectional 1" Cross-sectional 1 a.44 b. 20 a.21 b.18 a.36 b.10 a. 30 b.30 a.720 b. 1,553 a.24 b.338 a.21 b. 338 a.169 b. 80 a. 30 b.30 a.30 `b.30 a. 263 b. 208 a.85 b.38 a.56 b.41 a. 77 b. 77 a. 26 b.24 a.94 b.94 a. 105 b. 52 a.10 a. 12.2 (mean) b.12.3 (mean) a.18,35 b.18,35 a.24,36 b.24,36 a. 30,77 b. 30,67 a. 15,55+ b. l&55+ a. 1557 b.1557 a. 15,49 b. 15,49 a.school ages b.518 a.4,19 b.4,19 a.5,18 b.518 a.<10,>19 b.<10,>19 a.12,18 b.12,18 a.10,16 b.lO,lZ a. 12.5 (mean) b. 12.6 (mean) a.7-18 b.7-18 a.5,17 b.5,17 a.l5,24 b.1524 a.18,27 Ging: 0s Ppd:Os Lpa:ls Ging: 1s Lpa:lr,ls Ging:Oe Ppd:lr Lpa:le Ppd:ls,lr Lpa,ls,lr XRBL:li, lp XRBL: li, lr XRBL: li, lr Ging:Os Lpa: Op, OS PDI: OS Ging: 1s Lpa: lp Ging: 1s Ppd:Os XRBL: 1s Ging: lp Lpa: lp XRBL: lp, 1s JPS: lp,ls Ging:le Lpa: Oe, Op, OS XRBL: Oe, Op, OS Ging: 1s MGI: 1s Ging:Os Ppd: 1s Lpa: 1s Ging: 1s Ppd: OS Lpa: 0s Ging: 1s Ging: le Ppd: 0s XRBL: OS Ging: le Glycemic control Duration of diabetes None Glycemic control Duration of diabetes Diabetes complications Glycemic control None None Glycemic control None Glycemic control None Duration of diabetes Glycemic control Duration of diabetes None Duration of diabetes Glycemic control Duration of diabetes Duration of diabetes Glycemic control Diabetes complications None II-2 II-2 II-2 II-2 II-2 II-2 II-2 III Ill Ill Ill Ill Ill Ill Ill Ill Ill Ill (continues) ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 111 Linltagcs u-it11 General Health TABLE 5.4 continued Number of Measure of Subjects Age+ Periodontal Other Study Diabetes a.Diabetes a. Diabetes Disease Status: Diabetes-Related Evidence Country Design TYP@ b.Control b.Control Diabetes EffecF Variables Considered Leveld Rylander et al. 1987 Sweden Cross-sectional 1 a.46 a.18,26 Ging: le, 1 p Diabetes complications Ill b.41 b.19.25 Ppd: Oe Lpa:le,lp XRBL:Op Sznajder et al. 1978 Argentina Cross-sectional 1" a.20 a.9,29 Ging: 1s None Ill b.26 b.9,29 Lpa: 0s Galea et al. 1986 Malta Cross-sectional l* a.82 a. 5,29 Ppd:lp Glycemic control Ill b.unknown b.5,29 Duration of diabetes Diabetes complications Hugoson et al. 1989 Sweden Cross-sectional 1 a.154 a. 20,70 Ging: le Duration of diabetes Ill b. 77 b.20,70 Ppd:le,lp,ls XRBL: 1s Giavind et al. 1968 Denmark Cross-sectional lx a.51 b.51 a. 20,40 b. 20,4O Duration of diabetes Diabetes tomplications Ill Thorstensson and Hugoson 1993 Sweden Cross-sectional 1 a.117 b. 99 a.40,70 b. 40,70 Duration of diabetes Onset age III Morton et al. 1995 Shlossman et al. 1990 Emrich et al.1991 Wolf 1977 Benveniste et al.1967 Finestone and Boorujy 1967 Belting et al. 1964 Oliver and Tervonen 1993 Yavuzyilmaz et al. 1996 Bridges et al. 1996 Sandler and Stahl 1960 Bacic et al. 1988 Hove and Stallard 1970 Mauritius Cross-sectional 2 USA Cross-sectional 2 USA Cross-sectional 2 Finland Cross-sectional 1,2 USA Cross-sectional 1,2* USA Cross-sectional 1,2* USA Cross-sectional 1,2" USA Cross-sectional 1,2 Turkey Cross-sectional 1,2 USA Cross-sectional 1,2 USA Cross-sectional 1,2* Yugoslavia Cross-sectional 1,2 USA Cross-sectional 1,2" a. 24 b.24 a. 736 b. 2,483 a. 254 b. 1,088 a.186 b.156 a.53 b.71 a. 189 b.64 a.78 b. 79 a.114 b.15,132 a.17 b.17 a.118 b.115 a.100 b. 3,894 a.222 b.189 a. 28 b. 16 a.26,76 b. 25,73 a.5 45+ b.5,45+ a. 15,55+ b.15,55+ a.16,60 b.l6,60 a.5,72 b.5,72. a. 20,79 b. 20,79 a.20,79 b. 20,79 a.20,64 b.20,64 a.25,74 b. 19,29 a. 24,78 b. 24,78 a.20,69 b. 20,69 a. <20,6D+ b. <20,60+ a. 20,40+ b. 20,40+ Ging:Os Ppd: OS Lpa:ls XRBL: 1s Ging:Oe Ppd:le,ls XRBL: 1s Ging: lp Ppd: 1s Lpa: 1s Lpa: lp XRBL: 1 p Lpa:lp,ls XRBL: lp, 1s Ging: 1s Lpa: 1s XRBL: 1s Ging: 0s Ppd:Op,Os PI: `Is PI:ls Ppd:le,lp Lpa: le, Op,Os Ppd:ls Ging: OS Ppd: 0s Lpa: 1s PDR: le Ppd:le,lp,ls Ging:Os Ppd: OS XRBL:Os None None None Glycemic control Duration of diabetes Diabetes complications None Glycemic control Duration of diabetes Diabetes complications Diabetes severity None None Glycemic control Duration of diabetes None Glycemic control Duration of diabetes Diabetes complications Duration of diabetes Diabetes severity Ill III Ill III Ill Ill Ill III III ill Ill Ill III 112 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages \vith General Health Mackenzie and Millard 1963 Sznajder et al. 1978 Dolan et al. 1997 Grossi et al. 1994 Tervonen and Knuuttila 1986 Number of Measure of Subjects Age+ Periodontal Other Study Diabetes a. Diabetes a. Diabetes Disease Status: Diabetes-Related Evidence Country Design TYP@ b.Control b.Control Diabetes Effect< Variables Considered Leveld USA Cross-sectional 9 a. 124 a. 32,78 XRBL:Os None Ill b.92 b.32,78 Argentina Cross-sectional 9 a.63 a. 30,49 Ging: 1s None Ill b. 39 b. 30,50 Lpa: 1s USA Cross-sectional 9 Weighted a.45,75+ Lpa:le,lp,ls None Ill a. 107 b.45,75+ b.554 USA Cross-sectional 9 a. 1,426 All: 25,74; Lpa: Is, lp None Ill b. 69 unknown for diabetes Finland Cross-sectional 9 a.50 a. <30,40+ Ging: le Glycemic control Ill b.53 b.<30,40+ Ppd:le, lp XRBL: OS Campbell 1972 Australia Cross-sectional 9 a. 70 a.17,39 PI:lp,ls None Ill b.102 b.17,39 Albrecht et al. 1988 Hungary Cross-sectional 9 a. 1,360 a. 15,65+ Ging: 1s None Ill b. 625 b. 15,65+ PI: OS Szpunar et al. USA Cross-sectional 9 a.474 a. 6,65+ PI: 1s None Ill 1989 (NHANES I) b. 15,174 b.6,65+ Szpunar et al. USA Cross-sectional 9 a. 322 a. 15,65+ PI: 1s None III 1989 (HHANES) b. 8,040 b. 12,65+ `Diabetes type: 1 = type 1 diabetes mellitus; 2 = type 2 diabetes mellitur; 1,2 = both type 1 and type 2 diabetes mellitus;9 = diabetes type not specified and not clearly ascertaina- ble from other information in the report; o = diabetes type not specified but ascertained by reviewer from other information in the report. bAges:subjects'ages presented as minimum, maximum reported for those with diabetes and controls unless otherwise specified. (Measure of periodontal disease status. Measures used include Ging = girigivitis or gingival bleeding; Ppd = probing pocket depth; Lpa = loss of periodontal attachment; XRBt = radiographic bone loss;JPS = juvenile periodontal score; MGI = modified gingival index; PI = Russell's periodontal index; PDR = periodontal disease rate (proportion of teeth affected by periodontal disease).The number following the measure corresponds to greater disease in those with diabetes (1) or no difference between those with diabetes and controls (0). The letter followmg the number corresponds to the parameter(s) assessed in the study:e = extent;i = incidence; p = prevalence; s = severity; r = progression. dlevels of evidence are delineated in Table 5.3. Karjalainen 1997). All four studies reported greater prevalence, extent, or severity of at least one measure of periodontal disease. Type 2 Diabetes. There are fewer reports on the rela- tionship between type 2 diabetes and periodontal dis- ease, particularly where type 2 diabetes is explicitly identified or discernible from the ages of subjects. Seven studies limited to subjects with type 2 diabetes included a comparison group without diabetes. Two of these studies included only adult subjects (Morton et al. 1995, Novaes et al. 1996); the remaining five were large population-based studies of diabetes and periodontal disease in Pima Indians, a group with the highest known prevalence of type 2 diabetes in the world. The Pima Indian studies included subjects aged 5 years and older (Shlossman et al. 1990) or 15 and older (Emrich et al. 1991, Nelson et al. 1990, Taylor et al. 1998a,b). All seven studies reported greater prevalence, extent, or severity of periodontal disease among subjects with diabetes for at least one measure of periodontal disease. Three of these stud- ies were longitudinal (Nelson et al. 1990, Taylor et al. 1998a,b) and showed that the progression of peri- odontal disease was greater in diabetes patients than in individuals without diabetes. In addition to finding significant differences in various measures of periodontal status between sub- jects with and without type 2 diabetes, a number of these reports also provide estimates of association and risk. Using periodontal attachment loss as the measure, Emrich et al. (1991) estimated that people with type 2 diabetes were 2.8 times more likely to have destructive periodontal disease (odds ratio, 2.8; 95 percent CI, 1.9 to 4.1). When they used radi- ographic bone loss as the measure and controlled for ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 113 Linkages with General Health other important covariates, the estimate rose to 3.4 (odds ratio. 3.4; 95 percent CI, 2.3 to 5.2). Nelson et al. (1990) quantified the increased risk of advanced periodontal disease in Pima Indians with and without type 2 diabetes, finding the prevalence of periodontal disease in subjects with diabetes to be 2.6 times greater (95 percent CI, 1.0 to 6.6) than that of sub- jects without diabetes. Taylor et al. (1996), in anoth- er analysis of data from the Pima Indians, reported that type 2 diabetes was a significant risk factor for more severe alveolar bone loss progression (odds ratio, 4.2; 95 percent CI, 1.8 to 9.9), in addition to being a significant risk factor for the prevalence of alveolar bone loss. Studies of individuals with Type 1 or Type 2 Diabetes. Twelve reports included analyses in which subjects with type 1 and type 2 diabetes were not separated. All of these studies were cross-sectional and included adults; two studies included children or adolescents as well (Benveniste et al. 1967, Wolf 1977). Nine of the 12 studies reported greater prevalence, extent, or severity of periodontal disease among the diabetic subjects for at least one measure or index of peri- odontal disease (Bacic et al. 1988, Belting et al. 1964, Bridges et al. 1996, Finestone and Boorujy 1967, Hove and Stallard 1970, Oliver and Tervonen 1993, Sandler and Stahl 1960, Yavuzyilmaz et al. 1996, Wolf 1977). Hove and Stallard (1970) and Benveniste et al. (1967) did not find significant differences in peri- odontal disease between subjects with and without diabetes. The Hove and Stallard report included 28 subjects with diabetes and 16 without diabetes and may not have had enough statistical power to detect clinical differences, although they were able to detect a significantly higher prevalence of gingival vascular changes in subjects with diabetes. Benveniste et al. (1967) commented that their results may have been influenced by use of relatives without diabetes as the comparison group and that the subjects with diabetes were all under reasonably good control with either insulin or dietary regulation. Both factors may have minimized differences between the groups. Diabetes Type Not Specified. The final set of reports on the association between diabetes and periodontal dis- eases consists of seven cross-sectional studies in which the type of diabetes was not specified and was not easily determined from other information pro- vided. Four of the seven studies included only adults (Dolan et al. 1997, Grossi et al. 1994, Mackenzie and Millard 1963, Tervonen and Knuuttila 1986). In the other three studies, subjects ranged in age from childhood to older adulthood (Albrecht et al. 1988, Campbell 1972, Szpunar et al. 1989). Szpunar et al. (1989) presented analyses of two separate national surveys (the National Health and Nutrition Examination Survey, NHANES I, conducted between 1971 and 1974, and the Hispanic Health and Nutrition Examination Survey, HHANES, conducted between 1982 and 1984). All seven studies found subjects with diabetes to have increased prevalence, extent, and severity of periodontal disease. The statistical significance of the diabetes effect was markedly diminished in the final linear regression model used by Szpunar et al. (1989) in analysis of the NHANES I data: Two of the popu- lation-based surveys, Grossi et al. (1994) and Dolan et al. (1997), provided epidemiologic estimates of the association of diabetes and attachment loss severity with odds ratios of 2.3 (95 percent CI, 1.2 to 4.6) and 1.9 (95 percent CI, 1.3 to 3.0), respectively, while controlling for other covariates. Conclusion. Diabetes is a risk factor for the occur- rence and prevalence of periodontal diseases. Although there is insufficient evidence of a causal association, the findings of greater prevalence, sever- ity, or extent of at least one manifestation of peri- odontal disease in individuals with diabetes is remarkably consistent in the overwhelming majority of studies. Furthermore, there are no studies with superior design features in the literature to refute this assessment. The studies were conducted in distinctly different settings, with subjects from different ethnic populations and of different ages, and with a variety of measures of periodontal status. This inevitable variation in methodology and study populations lim- its the possibility that the same biases apply in all the studies. There is a need for further research using stronger designs that also control for confounding variables such as socioeconomic status. Glycemic Control Several lines of evidence support the plausibility that periodontal infections contribute to problems with glycemic control, thus compromising the health of diabetic patients. It has been reported that the chron- ic release of tumor necrosis factor alpha (TNF-o) and other cytokines such as those associated with peri- odontitis interferes with the action of insulin and leads to metabolic alterations (Hotamisligil et al. 1993, Flier 1993). Other studies have noted relation- ships between insulin resistance and active inflam- matory connective tissue diseases (Hallgren and Lundquist 1983, Svenson et al. 1987), other clinical diseases (Beck-Nielsen 1992, Beisel 1975), acute 114 ORAL HEALTH IN AMERIC4: .4 REPORT OF THE SURGEON GENERAL infection (Drobny et al. 1984, Sammalkorpi 1989), and periodontal disease (Grossi et al. 1999). Grossi and Genco (1998) have proposed a model whereby periodontal infection contributes to hyperglycemia and complicates metabolic control in diabetes. Clinical Studies. The effects of periodontal infection on glycemic control have been investigated in a small number of clinical studies that looked at metabolic control at baseline and following various periodontal treatments (see Table 5.5; Aldridge et al. 1995, Christgau et al. 1998, Grossi et al. 1996, 1997, Miller et al. 1992, Seppala and Ainamo 1994, Seppala et al. 1993, Smith et al. 1996, Westfelt et al. 1996, Williams and Mahan 1960, Wolf 1977). One report is based on an epidemiological cohort study (Taylor et al. 1996). The randomized controlled trials of Grossi et al. (1997) involving populations with type 2 diabetes found that use of the systemic antibiotic doxycycline to treat periodontitis patients with diabetes resulted in a transient (3 to 6 months) improvement in glycemic control. On the other hand, the two con- trolled trials conducted in London by Aldridge et al. (1995) involving patients with type 1 diabetes found no effect. Taken together, these three studies provide inconsistent results and are limited in how well they generalize to broader populations. A small uncon- trolled study of 10 patients by Miller et al. (1992) also reported an improvement in glycemic control of diabetic patients whose periodontal disease was treated with mechanical therapy and systemic doxy- cycline. Five of the above-mentioned studies did not include control groups (Miller et al. 1992, Seppala et al. 1993, Smith et al. 1996, Williams and Mahan 1960, Wolf 1977), and four were not specifically designed to address the relationship between peri- odontal therapy and glycemic control (Grossi et al. 1996, Seppala et al. 1993, Smith et al. 1996, Westfelt et al. 1996), although the data collected allowed the investigators to address the issue. One nonrandom- ized but controlled clinical trial of nonsurgical peri- odontal therapy found no significant influence on medical data for the diabetic patients (Christgau et al. 1998). A clear relationship between improvement in periodontal health and glycemic control has not been shown. The studies seem to suggest that antibiotic treatments may help in glycemic control. A recent longitudinal study indicates inflammation may be a precursor to the onset of type 2 diabetes (Schmidt et al. 1999). Thus periodontal infection may contribute to that inflammation. Conclusion. The body of literature concerning the relationship between periodontal infection and Linkages with General Health impaired glycemic control is varied in the strength, quantity, breadth, and consistency of evidence pre- sented. The preliminary evidence, while encourag- ing, does not support a clear-cut conclusion that treating periodontal infection can contribute to man- agement of glycemic control in type 1 or type 2 dia- betes. As the table indicates, only studies using sys- temic antibiotic treatment affected glycemic control favorably. The results suggest that infections other than periodontitis may be implicated or that inten- sive treatment of periodontal infections with sys- temic antibiotics is necessary to affect glycemic con- trol favorably. Further rigorous controlled studies in diverse populations are warranted. The Oral Infection-Heart Disease and Stroke Connection During the past decade, infectious agents have become recognized as causes of systemic diseases, without fever or other traditional signs of infection. Helicobacter pylori is associated with peptic ulcers and, along with Chlamydia pneumoniae and cytomegalovirus, is now thought to be associated with increased risk for cardiovascular disease as well as malignancies (Wu et al. 2000). Studies investigating the relationship between oral and dental infections and the risk for cardiovascular disease suggest that there is potential for oral microorganisms, such as periodontopathic bacteria, and their effects to be linked with heart disease. Mechanisms of Action Infectious agents are thought to affect the risk of heart disease through several possible mechanisms. Bacteria or viruses originating in tissues such as the lungs or oral mucosa may directly infect blood vessel walls. Such infection may be largely asymptomatic, but may cause local vascular inflammation and injury, which would contribute to the development of lipid-rich plaques and atherosclerosis. Bacteria or viruses may also interact with white blood cells or platelets, both of which integrate into the developing atherosclerotic plaque. Cells of the blood vessel wall and white blood cells and platelets can release prostaglandins (especially PGE,), interleukins (espe- cially IL-l), thromboxane B2 (TBX,), and tumor necrosis factor alpha (TNF-ok). Bacterial products in the blood may also stimulate liver production of other pro-inflammatory or pro-coagulant molecules such as C-reactive protein and fibrinogen. Microbes may also stimulate expression of tissue factor, which would activate coagulation. During the process of ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 115 Linkages with General Health TABLE 5.5 Effects of periodontal disease and its treatment on glycemic control: clinical and epidemiological evidence Study Diabetes Designa Type Number of subjects Metabolic a.Treatment (ages) Follow-up Control Evidence b.Control (ages) Time Periodontal Therapy Outcome Effects on Metabolic Control Levelb Aldridge RCT et al. 1995, Study 1 Type 1 a.16(16-40) b.15 (16-40) 2 months Experimental group: oral Glycated Periodontal treatment had no I hygiene instruction, scaling, hemoglobin, effect on change in glycated adjustment of restoration fructosamine hemoglobin. margins, and reinforcement after 1 month;control group: no treatment Aldridge RCT et al.1995, Study 2 Grossi et RCT al. 1996, 1997 Type 1 Type 2 a. 12 (20-60) b. 10 (20-60) a.89 (25-65) b.24 (25-65) 2 months Experimental group: oral Glycated Periodontal treatwnt had no I hygiene instruction, scaling hemoglobin effect on change in glycated and root planing, extractions, hemoglobin. root canal therapy; control group: no treatment 12 months Experimental groups received Glycated The three groups receiving I either systemic doxycycline or hemoglobin doxycycline and ultrasonic placebo and ultrasonic bacterial curettage showed bactericidal curettage with significant reductions irrigation using either water, (P < 0.04) in mean glycated chlorhexidine, or povidone- hemoglobin at 3 months. iodine Christgau Treatment Type 1 a.20 (30-66) 2 months Scaling/root planing; Glycated No effect on glycated hemoglobin. II-1 et al. 1998 study, non- and type 2 b.20 (30-66) subgingival irrigation with hemoglobin RCT chlorhexidine; oral hygiene instruction; and extractions Westfelt Treatment Type 1 a. 20 (45-65) 5 years Baseline oral hygiene Glycated "The mean value of HbAlc II-1 et al. 1996 study, non- and type 2 b. 20 (45-65) instruction,scaling and root hemoglobin between baseline and 24 months RCT planing followed by periodic was not significantly different from prophylaxis,oral hygiene that between 24 and 60 months." instruction, localized sub- gingival plaque removal,and surgery at sites with bleeding on probing and a periodontal probing depth of >5 mm Smith Treatment Type 1 a. 18 (26-57) 2 months Scaling and root planing with Glycated Found no statistically or clinically II-1 et al. 1996 study,non- b.0 ultrasonics and curets; oral hemoglobin significant change in glycated RCT hygiene instruction hemoglobin. Taylor Historical Type 2 No treatment or 24 years Not applicable Glycated Those with severe periodontitis II-2 et al. 1996 prospective control subjects hemoglobin were -6 times more likely to have cohort 49 (severe poor glycemic control at follow-up. periodontitis) 56 (less severe periodontitis) Miller Treatment Type 1 a. 10 (not given) 8 weeks Scaling and root planing, Glycated Found decrease in glycated Ill et al. 1992 study, non- b.0 systemic doxycycline hemoglobin, hemoglobin and glycated albumin RCT glycated in patients with improvement in albumin gingival inflammation (P < 0.01). Patients with no improvement in gingival inflammation had either no change or increase in glycated hemoglobin post treatment. coagulation, platelets would become trapped in the growing clot or thrombus. Microthrombus formation is one of the key factors in the development of ather- osclerotic plaques. As atherosclerotic plaques enlarge, the lumen of the coronary blood vessels narrows and the blood supply to the heart muscle becomes reduced. A frank heart attack or myocardial infarc- tion results when a larger part of the coronary artery !!6 OR4L HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health Study Diabetes DesigV Type Number of subjects a.Treatment (ages) Follow-up b.Control (ages) Time Periodontal Therapy Metabolic Control Outcome Effects on Metabolic Control Evidence Levelb Seppala Treatment Type 1 et al. 1993, study, non- Seppala and RCT Ainamo 1994 a. 38 for 1 year; 2 years Scaling and root planing, Medical Reported an improvement of the 22 for 2 years' periodontal surgery,and history for HBAl levels of the PIDD and CIDD 26 PIDD-ly (48 + 6) extractions baseline subjects (P < 0.068, r-test). 12 CIDD-lv (43 k 51 control status; 16 PIDD-2; 6 CIDD-2y b.0 glycosylated hemoglobin Al and blood glucose for assessing response to treatment Williams Descriptive Not speci- and Mahan clinical fied a.9 (20-32) 1960 study b.0 Wolf 1977 Treatment Type 1 and study, non- type 2 a. 117 (16-60) RCT b.0 3-7 Extractions, scaling and months curettage, gingivectomy, systemic antibiotics B-12 Scaling and home care months instruction, periodontal surgery, extractions,endodontic treatment, restorations, denture replacement or repair Insulin requirement; diabetes control (not operationally defined) Blood glucose, 24-h urinary glucose, insulin dose 7 of 9 subjects had'kignificant" reduction in insulin requirements. 2 RCT = randomized controlled trial. b Levels of evidence are delineated in Table 5.3. Note that because this body of literature is small, this review does not distinguish between"well-designed"studies and otherwise in assigning the evidence levels. ( PIDD = poorly controlled insulin-dependent diabetes;ClDD = controlled insulin-dependent diabetes. Compared 23 subjects with improved oral infections with 23 who had no improvement after treatment for oral infection and inflammation.The subjects with improved oral inflammation and infection tended to demonstrate diabetes control improvement (P < O.l).However,Wolf states in discussion,"treatment of periodon- tal inflammation and periapical lesions . . does little to improve the control of diabetes." lumen becomes occluded. Failing to receive enough blood, the heart muscle dies, resulting in an infarct. Animal Studies Bacteria originating in the oral cavity may also con- tribute to platelet clotting or thrombosis, as proposed by Herzberg et al. (1983, 1994). These investigators have suggested that the association between peri- odontal disease and cardiovascular disease may be due in part to the potential for oral bacteria such as S. sanguis and F? gingivalis to induce platelet aggrega- tion. Platelets aggregate in response to these bacteria as a result of mistaken identity: a protein structure on the surface of certain common strains of S. sanguis and I? gingivalis mimics the platelet-interactive regions of collagen molecules (Erickson and Herzberg 1993, Herzberg et al. 1994). Exposure of flowing blood to collagen triggers clotting, the cen- tral event in stopping blood flow. When an experi- mental bacteremia was created with a strain of S. san- guis that carried the collagen-like protein, rabbits showed changes in blood pressure, electrocardio- gram readings, heart rate, and cardiac contractility (Herzberg and Meyer 1996, 1998). Platelets also aggregated in the circulation, resulting in significant declines in platelet counts. From the electrocardio- graphic tracings, rabbit heart muscle also appeared co have suffered ischemic damage. The investigators concluded that oral bacteria carrying the collagen- like protein induced platelet aggregation or clotting in the bloodstream. These clots were of sufficient size to obstruct coronary arteries and produce ischemic heart damage, an early warning sign of a heart attack or an infarction. Because S. sanguis is present in large numbers in dental plaque and is a causative agent in infective endocarditis, it is likely that these bacteria ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 117 Linkages with Gencrnl Health have an opportunity to induce platelet clotting dur- ing human bacteremias from oral sources. Bacteria- induced platelet clotting could contribute to microthrombosis during the development of athero- sclerotic plaques and occlusive thrombus formation with occasional myocardial infarction. Population-based Studies Any study investigating the possibility of a unique role for oral pathogens as risk factors for cardiovascu- lar disease, including atherosclerosis and the forma- tion of a blood clot in a coronary artery of the heart, which typically precedes myocardial infarction, must take into consideration such known risk factors as smoking, hypertension, obesity, diabetes, genetic sus- ceptibility, and elevated cholesterol. Genco (1998) and Beck et al. (1998) have recently reviewed studies examining the associations between oral conditions (including pe d rro ontitis) and atherosclerosis and coronary heart disease, the latter of which affects 12 million people in the United States and is the leading cause of death. These are summarized in Table 5.6. Of the ten studies cited in the table, six are prospective cohort studies, in which oral health sta- tus was established at the outset (baseline) of the study period and the subjects were followed at peri- odic intervals to a previously defined endpoint, for example, diagnosis of coronary heart disease or an acute myocardial infarction, or death. Beck et al. (1996) combined data from the \ieterans Administration Dental Longitudinal Study and its parent longitudinal study, the Normative Aging Study, for a total of 203 cases and 891 noncases, to determine whether periodontal disease, judged by measuring alveolar crestal bone, is a risk factor for cardiovascular disease. After adjusting for age, blood pressure, cholesterol, and body mass index, the investigators found that subjects with periodontal disease were 1.5 times more likely to develop coro- nary heart disease over a 2%year period than controls (odds ratio of 1.5). Similarly, after adjusting for age, smoking, and blood pressure, the investigators found that veterans with periodontal disease were I.9 times more likely to develop fatal coronary heart disease (odds ratio of 1.9). In a longitudinal study to eliminate the potential confounding effects of smoking, Genco et al. (1997) measured the incidence of periodontal disease and cardiovascular disease in 1,372 American Indians of the Gila River Indian Reservation. Although diabetes is prevalent in this population, cigarette smoking is rare in these individuals (a fact confirmed in this study), so it was considered not to be a risk factor for either cardiovascular disease or periodontal disease in this study. Periodontal disease was measured at baseline, and the incidence of cardiovascular disease was followed over the next 10 years. When the analy- sis was restricted to individuals under age 60, the risk of cardiovascular disease was 2.7 times higher in sub- jects with periodontal disease than in those with lit- tle or no periodontal infection. This association was seen even after adjusting for other risk factors for cardiovascular disease or periodontal disease such as age, sex, cholesterol, weight, high blood pressure, diabetes, and insulin use. The investigators conclud- ed that periodontal disease is an important risk fac- tor for cardiovascular disease for individuals under 60 in this group, second only to the presence of long-term diabetes. Further analysis of death due to cardiovascular disease is needed in this population to complete the study. Mattila and coworkers have conducted both prospective and retrospective studies. A prospective study (Mattila et al. 1995) showed that new episodes of myocardial infarction occurred more frequently in subjects with more extensive "dental" disease. The authors used a measure of dental disease that includ- ed a composite index that assessed caries, periodon- titis, pericoronitis, and periapical lesions. The com- posite index estimates the combined infectious load that contributes to many possible oral infections. After combining the prospective study data with data from an earlier retrospective study (Mattila et al. 1989) and adjusting for age, triglyceride levels, cho- lesterol, C-reactive protein, smoking, social class, diabetes, and hypertension, the investigators found a significant association between dental infections and acute myocardial infarction in men under age 50 (P < 0.01). A more recent study (Mattila et al. 2000) com- pared 85 patients with proven coronary heart disease and 53 matched controls. This case-control study showed that dental indices were higher among coro- nary heart disease patients than controls, but the dif- ferences were not statistically significant. Participants in the study were older, which the authors believed was the most likely reason for the results. In the first National Health and Nutrition Examination Survey, 9,670 subjects were followed for over 14 years. DeStefano et al. (1993) found that there was a 25 per- cent increased risk of cardiovascular disease in indi- viduals with periodontitis compared with those with minimal periodontal disease. The strongest associa- tion was seen in men under 50 (relative risk, 1.7). A limitation of this study, which the authors acknowl- edge, was the lack of baseiine data on smoking, a major risk factor for both periodontal and cardiovas- cular disease. Morrison et al. (1999) evaluated a ret- rospective cohort study using participants in the 118 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages uTith General Health TABLE 5.6 Summary of studies assessing the association between oral conditions, atherosclerosis, and coronary heart disease Study Designd Subjects (cases/ controls) Oral Condition Cardiovascular Outcome Adjustment+ Association (odds ratio or relative risk) Evidence Level< OeStefano et al. 1993 Prospective 1,786/7,974 Mattila Prospective 521162 et al. 1995 Joshiputa Prospective 757/44,119 et al. 1996 Beck Prospective 203/891 et al. 1996 Genco Prospective 68/1,304 et al. 1997 Morrison Retrospective 10,000 et al. 1999 Joshiputa Prospective 42,151 et al. 1999 Mattila Case-Control 100/102 et al. 1989 Gtau Case-Control 166/166 et al. 1997 Mattila et al. 2000 Case-control 85153 Russell's periodontal Coronary heart disease index (admission to hospital or death) Dental index (caries, New acute myocatdial periodontal disease, infarction or death pulpal infection) Periodontal disease (self-reported), tooth loss due to self-repotted periodontal disease Alveolar ctestal bone 10% Alveolar crestal bone New coronary heart IO% disease Severe gingivitis; petiodontitis; edentulousness New coronary heart disease;tetebrovasculat deaths New coronary heart disease New coronary heart disease,fatal coronary heart disease,stroke Number of teeth lost lschemic stroke Dental index (caries, periodontal disease, Acute myocatdial pulpal infections) infarctions Dental index (caries, periodontal disease, Stroke petiapical infections) Dental index (caries, periodontal disease, New coronary heart pulpal infections) disease Age, sex, race, education, poverty, marital status, cholesterol, BMI, diabetes,smoking Smoking, hypertension, age, sex, triglycerides, socioeconomic status, diabetes, lipids, BMI, previous Ml Age, BMI, exercise, smoking, alcohol,vitamin C,family history, Ml Age, BMI, total cholesterol, socioeconomic status, DBP, LDL, smoking, cholesterol Age, sex, smoking, BMI, diabetes, cholesterol, hypertension Age,sex,setum total cholesterol, smoking,diabetes, hypertension Age, smoking, obesity, alcohol, exercise, aspirin, family history, profession, hypertension, hypetcholesterolemia HDL, smoking, C-reactive protein, hypertension, age, cholesterol, diabetes, social class Diabetes, preexisting vascular disease, socioeconomic status, smoking Age, sex, smoking, socioeconomic class, hypertension, number of teeth, serum lipid levels 1.72 (1.1-2.68) (only for men under age 50) Yes,P -c 0.01 1.67 (1.03-2.71) . 1.5 (1.04-2.14) 1.9 (1.0-3.43) 2.8 (1.45-5.48) 2.68 (1.35-5.60) 1.37 (0.80-2.35) for petiodontitis 1.90 (1.17-3.10) for edentulousness for fatal CHD 210 teeth 1.75 (1.03-2.99) ll-15reeth 1.95 (1.07-3.64) 17-24 teeth 1.48 (1.02-2.13) Yes, P < 0.01 Odds ratio 2.6 (1.18-5.70) II-2 II-2 II-2 II-2 II-2 II-2 II-2 II-2 II-2 it-2 "Far the prospective studies, the total number of rubjects in the cohort is the sum of the two numbers given,the first number of which represents the subjects followed to the endpoint. For the case-control studies, the first number represents the cases, and the second the controls. bBMl = body mass index; MI = myotardial infarction; LOL = low-density lipoproteins; HDL = high-density lipoproteins. [Levels of evidence are delineated in Table 5.3. 1970-72 National Canada Survey. In the younger dence. This pattern of higher risk observed among cohort, those under age 69, they found that gingivi- tis, periodontitis, and edentulousness were related to fatal coronary heart disease in a statistically signifi- cant manner. However, in analyzing those over age 70, none of these dental conditions was associated with fatal heart disease. These results were adjusted for age, sex, serum total cholesterol, smoking status, diabetes SWUS, hypertension status. and province of resi- younger subjects may, to some extent, reflect the rel- ative instability of risk estimates. However, it is also possible that periodontal disease, like other co-mor- bid relative risks for coronary heart disease, general- ly declines with age (Semenciw et al. 1988). Wu et al. (1999) found periodontal disease to be a potential factor for coronary heart disease and stroke based on an analysis of the first National ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 119 Linkages 11.ith Gencrd Health Health and Nutrition Examination Survey and its 21- year follow-up. In this analysis, periodontitis was found to be a significant risk factor for cerebrovascu- lar disease, in particular nonhemorrhagic stroke. Compared with no periodontal disease, relative risk (95 percent CI) for incident nonhemorrhagic stroke was 2.11 (1.30 to 3.42) for periodontitis. There was no significant relationship for gingivitis or edentu- lousness, which were 1.24 (0.74 to 2.08) and 1.41 (0.96 to 2.06), respectively. The increased relative risk for total cerebrovascular disease and nonhemor- rhagic stroke was not seen for hemorrhagic stroke. Similar relative risks for total cerebrovascular disease and nonhemorrhagic stroke associated with peri- odontitis were seen in white men and women and African Americans. A conclusive statement about a cause-and-effect relationship between periodontitis and the risk of developing cerebrovascular disease, in particular nonhemorrhagic stroke, cannot be made at this time. The consistency of the findings in different racial groups and the strength of the association war- rant further examination of the potentially important association between these two clinical conditions, which are highly prevalent in the adult population. cular disease or stroke. The methods used to measure or identify periodontal disease ranged widely from self-report, to composite indices that included dental caries experience, to precise measures of periodonti- tis severity. Nevertheless, there were consistent find- ings of increased odds ratios and significant proba- bility (P) values pointing to an association of peri- odontal and other oral infections with an increased risk for cardiovascular disease. Further studies are needed to determine whether periodontal disease alone or in the presence of other oral infections is an independent risk factor for cardiovascular or cere- brovascular disease. Research to elucidate the under- lying pathological mechanisms is also essential. Studies must also clarify the potentially confounding effects of sex, age, socioeconomic level, and race/ ethnicity. Periodontal Disease and Adverse Pregnancy Outcomes In the largest cohort studied, Joshipura et al. (1996) found that among a group of male health pro- fessionals who were relatively homogeneous socio- economically and who self-reported preexisting peri- odontal disease, those with 10 or fewer teeth were at increased risk of new coronary heart disease, com- pared with those with 25 or more teeth (relative risk, 1.67). These results were adjusted for sta'ndard car- diovascular disease risk factors. Preterm birth and low birth weight are considered the leading perinatal problems in the United States (Gibbs et al. 1992). Although infant mortality rates have decreased substantially over the past genera- tion, the incidence of low birth weight (just under 300,000 cases in 1995) has not shown a comparable decline (Institute of Medicine 1985, USDHHS 1984). Over 60 percent of the mortality of infants without structural or chromosomal congenital defects can be attributed to low birth weight (Shapiro et al. 1980). Mechanisms of Action In a case-control study of 166 patients with acute cerebrovascular disease and I66 age- and sex- matched controls, Grau et al. (1997) found that "poor dental status" was independently associated with cerebrovascular ischemia. These results were based on a subgroup of patients and controls who completed the dental examination. A modified form of the Total Dental Index was used to measure dental status. In an 8-year follow-up of 42,151 male health professionals who were free of cardiovascular disease at baseline, Joshipura et al. (1999) reported that edentulousness was associated with an increased risk of ischemic stroke after adjusting for age, smoking, obesity, alcohol, exercise, aspirin, family history of cardiovascular disease, profession, hypertension, and hypercholesterolemia. Periodontal disease may contribute to adverse out- comes of pregnancy as a consequence of a chronic oral inflammatory bacterial infection. Toxins or other products generated by periodontal bacteria in the mother may reach the general circulation, cross the placenta, and harm the fetus. In addition, the response of the maternal immune system to the infection elicits the continued release of inflammato- ry mediators, growth factors, and other potent cytokines, which may directly or indirectly interfere with fetal growth and delivery Conclusion None of the studies reviewed to date achieves the level of rigor that can unequivocally establish peri- odontitis as an independent risk factor for cardiovas- Evidence of increased rates of amniotic fluid infection, chorioamnion infection, and histologic chorioamnionitis supports an association between preterm birth, low birth weight, and general infection during pregnancy It is noteworthy that the largest proportion of such infections occurred during the pregnancies of the most premature births (Hillier et al. 1988, 1995). The biological mechanisms involve bacteria-induced activation of cell-mediated immuni- ty leading to cytokine production and the synthesis 120 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and release of prostaglandins, which may trigger preterm labor (Hillier et al. 1988). Elevated levels of prostaglandin as well as cytokines (interleukin-1 (IL- I), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-a)) have been found in the amniotic fluid of patients in preterm labor with amniotic fluid infection (Romero et al. 1993), compared with levels in patients with preterm labor without infection. r\nimal Models ;\ variety of studies have used the pregnant hamster model. Some investigators have examined the effects of lipopolysaccharide, produced by oral gram-neg- ative pathogens, on cytokine production (Collins et al. I994a). In other studies, hamsters have been infected with I? gingivalis, with or without prior immunization. Collins et al. (1994b) challenged the animals with nondisseminating, low levels of P gingi- \aaIis, introduced in a subcutaneous chamber at a dorsolumbar site. Although the doses were insuffi- cient to induce fever or wasting, the hamster litters of the infected animals showed a significant reduction in fetal weight (24 percent) in comparison with con- trol animals (P < 0.0001). This suppressive effect on fetal weight was accompanied by a proportional intrachamber rise in tumor necrosis factor alpha (TNF-(-w) and prostaglandin E2 (PGE,) (P < 0.0001). Immunization prior to mating did not provide pro- tection from a challenge during pregnancy, but rather potentiated the effects, indicating the potential strength of a chronic infection. In another series of hamster studies, researchers observed the effects of experimental periodontitis on pregnancy outcomes and amniotic fluid mediators (Offenbacher et al. 1998). The investigators noted a 20 percent decrease in fetal weight (P = 0.002). Periodontal infection in the pregnant hamster also was associated with a significant rise in intra-amniotic PGEz from 3.31 + 1.1 to 13.5 f 4.1 micrograms per milliliter (P = 0.03). These data suggest a link be- tween oral infection and changes in the fetal envi- ronment. Epidemiologic Studies Human case-control studies have demonstrated that mothers of low-birth-weight infants born as a result of either preterm labor or premature rupture of membranes tend to have more severe periodontal dis- ease than mothers with normal-birth-weight infants (Offenbacher et al. 1996, 1998). A case was defined as a mother whose baby weighed less than 2,500 grams and who had one or more of the following fac- tors: gestational age of infant of less than 37 weeks; Linkages with General Health preterm labor; or preterm, premature rupture of membranes. Controls were all normal-birth-weight, full-term infants. In a case-control study of 124 sub- jects, the mean clinical periodontal attachment level for the mothers of low-birth-weight babies was 3.10 + 0.74 (SD) millimeters (mm) per site (93 subjects) versus 2.80 + 0.61 (SD) mm per site (31 subjects) for mothers of normal-weight infants (P = 0.038 for all cases and controls). For a subset of mothers for whom this was the first child, the mean clinical peri- odontal attachment level for those with low-birth- weight babies was 2.98 + 0.84 (SD) mm per site (46 subjects) versus 2.56 + 0.54 (SD) mm per site for controls (20 subjects) at P = 0.041 (Offenbacher et al. 1996). This subset was analyzed separately to avoid the confounding effects of mothers %ith periodontal disease who had previously given birth to low-birth- weight infants but who later had normal-weight infants. Logistic regression models demonstrated that severe periodontal disease was associated with a sev- enfold increase in risk of low birth weight, after con- trolling for known risk factors such as smoking, race, alcohol use, age, nutrition, and genitourinary tract infection. This study suggests an association between periodontal disease and prematurity In a subsequent case-control study of 44 sub- jects, additional biochemical and microbial parame- ters of periodontal disease status were studied to assess the relationship of current periodontal status to current pregnancy outcome (Offenbacher et al. 1998). Results indicate that PGE, levels in gingival crevicular fluid were significantly higher in mothers of low-birth-weight infants than in controls (131.4 + 21.8 (SE) versus 62.6 + 10.3 (SE) nanograms per mil- liliter), respectively (at P = 0.02). Furthermore, with- in the group of mothers of low-birth-weight infants there was a significant inverse association between birth weight, gestational age, and gingival crevicular fluid PGE, levels (at P = 0.023 for current births). These data suggest that the level of PGE, in gingival crevicular fluid, serving as a marker of current peri- odontal disease activity, varies inversely with birth weight; that is, the higher the PGE, level, the lower the birth weights. In this study the periodontal dis- ease was more severe in mothers with adverse preg- nancy outcomes, as determined by biochemical and microbial biomarkers, but the difference in clinical attachment levels did not reach statistical signifi- cance (P = 0.11). Studies also have been reported in other coun- tries. In the United Kingdom a preliminary analysis of 167 cases and 323 controls did not show an asso- ciation between periodontal disease and pregnancy ORAL HEALTH 1N AMERICA: A REPORT OF THE SURGEON GENERAL 121 Linkages with General Health outcomes (Davenport et al. 1998); however, the investigators did not control for confounding factors. Dasayanake (1998) conducted a matched case-con- trol study with 55 cases in Thailand. Gingivitis was associated with a higher risk of having a growth- restricted infant (odds ratio = 0.3; 95 percent CI, 0.12 to 0.72), controlling for mothers height, prenatal care, dental caries status, and the infant's gender. Smoking was not controlled for in this study. Conclusion As a remote gram-negative infection, periodontal dis- ease may have the potential to affect pregnancy out- come. Not all the obstetric risk factors that result in babies being born too soon and too small have been fully identified (Gibbs et al. 1992, McCormick 1985). Oral infections have been investigated as a potential risk factor for preterm labor or premature rupture of membranes, which are major obstetric antecedents to spontaneous preterm births. .4lthough the findings from animal research and case-control studies are promising, additional work, including longitudinal studies, research on mechanisms, and intervention trials, is needed to determine whether periodontitis is a risk factor and what the mechanisms of action may be for adverse pregnancy outcomes. In the United States, longitudinal and intervention studies are under way. Conclusion This critical look at the emerging associations among oral infections and specific conditions establishes the need for an aggressive research agenda to better understand the specific aspects of these associations and the underlying mechanisms. Prospective and intervention studies are under way and should pro- vide additional and stronger evidence of the presence and direction of an association. It is essential for such studies to include populations at known risk for the underlying conditions as well as the general popula- tion. Of the conditions reviewed, the relationship of periodontal disease and diabetes has the strongest evidence, demonstrating that the risk of periodontitis is higher in individuals with diabetes. However, the effect of periodontitis on glycemic control is less clear, a reflection of the difficulty of controlling for the effect of systemic antibiotic treatments used to manage periodontal disease in diabetic patients in clinical trials. IMPLICATIONS OF THE LINKAGES This review of oral health linkages with general health reveals implications for the clinical practice of both medicine and dentistry The recognition of well- known and established signs and symptoms of oral diseases may assist in the early diagnosis and prompt treatment of some systemic diseases and disorders, The presence of these signs also may lead to the insti- tution of enhanced disease prevention and health promotion procedures. All health professionals, and the public, should be aware of these signs and symp- toms. Individuals, practitioners, and community pro- grams may also benefit from the accelerated develop- ment and testing of readily accessible, acceptable, and simple oral-based diagnostics. A better understanding of the role of the oral cav- ity and its components in protecting against infection is needed. This information should permit the devel- opment of interventions to enhance these compo- nents. For example, research is under way investigat- ing how to augment some of the natural antimicro- bial molecules that are present in saliva and how to use oral and nasal vaccination routes to enhance immunity Also, host susceptibility factors contribut- ing to the dissemination of oral infections to other parts of the body should be investigated, especially in populations at high risk for disease and infection. In addition, further studies are needed to elucidate the role of the mouth as a means of transmitting infec- tious microbes. This in turn will allow the develop- ment of interventions to prevent transmission and curb .the progression of infections once established. The associations between oral infections and dia- betes, heart disease and stroke, and adverse pregnan- cy outcomes warrant a comprehensive and targeted research effort. If any of these associations prove to be causal, major changes in care delivery and in the training of health professionals will be needed. Awareness of the oral complications of medica- tions and other therapies for disease management and for health promotion needs to be enhanced among health care professionals, the public, drug manufacturers, and the research community. For some of these therapies, known interventions exist and should be followed before initiating the therapy to minimize or modulate its side effects. To prevent the oral complications of other therapies, new approaches are needed. Ultimately, and ideally, the side effects of therapies should be considered in the development of new drugs and biologics. 122 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL FINDINGS o Many systemic diseases and conditions have oral manifestations. These manifestations may be the initial sign of clinical disease and as such serve to inform clinicians and individuals of the need for fur- ther assessment. o The oral cavity is a portal of entry as well as the site of disease for microbial infections that affect general health status. o The oral cavity and its functions can be adversely affected by many pharmaceuticals and other therapies commonly used in treating systemic conditions. The oral complications of these therapies can compromise patient compliance with treatment. o Individuals such as immunocompromised and hospitalized patients are at greater risk for gen- eral morbidity due to oral infections. o Individuals with diabetes are at greater risk for periodontal diseases. o Animal and population-based studies have demonstrated an association between periodontal diseases and diabetes, cardiovascular disease, stroke, and adverse pregnancy outcomes. 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ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Effects on Well-being and Quality of Life Fifty years ago the World Health Organization (WHO) defined health as the "complete state of physical, mental, and social well-being and not mere- ly the absence of infirmity" (WHO 1948). In its defi- nition the WHO acknowledged that an individual who is technically "cured" of disease may not neces- sarily be "well" and went on to indicate three dimen- sions of well-being. Physical well-being assumes the ability to function normally in activities such as bathing, dressing, eating, and moving around. Mental well-being implies that cognitive faculties are intact and that there is no burden of fear, anxiety, stress, depression, or other negative emotions. Social well- being relates to ones ability to participate in society, fulfilling roles as family member, friend, worker, or citizen or in other ways engaging in interactions with others. The WHO declaration resonated with ongoing developments in the social sciences as theoreticians recognized the need for multiple indicators in assess- ing health and treatment outcomes (Bergner et al. 1981, Fries et al. 1982, Hunt et al. 1985, Meenan et al. 1980). These efforts led to definitions of "health- related quality of life" (Guyatt et al. 1993) as well as explanatory models. The model proposed by Wilson and Cleary (1995), for example, posits five dimen- sions by which to measure treatment outcomes: bio- logical and physiological variables, symptom status, functional status, general health perceptions, and overall quality of life. These factors are not inde- pendent but may be reciprocally connected. For example, a diabetic patient with symptoms of depres- sion may experience a rise in serum glucose as a result of less vigilant glucose monitoring; the depres- sion may then lead to a deterioration in physical and social activities. Most importantly, measures of bio- logical and physiological factors are often inconsis- tent with patients' own reports of symptoms, ability to function, general health perceptions, and overall quality of life. In the wake of these developments in general medicine, researchers began to elaborate multidimensional models of "oral-health-related" quality of life. The efforts to understand these relationships are particularly relevant given the aging of the popula- tion. As Gift and Atchison (1995) stated, measuring health-related quality of life allows assessment of "the trade-off between how long and how well peo- ple live." Diseases and disorders that result in dental and craniofacial defects can thwart that goal, disturb- ing self-image, self-esteem, and well-being. Oral- facial pain and loss of sensorimotor functions limit food choices and the pleasures of eating, restrict social contact, and inhibit intimacy Oral complications of many systemic diseases also compromise the quality of life. Problems with speaking, chewing, taste, smell, and swallowing are common in neurodegenerative conditions such as Parkinson's disease; oral complications of AIDS include pain, dry mouth, mucosal infections, and Kaposi's sarcoma; cancer therapy can result in painful ulcers, mucositis, and rampant dental caries; and periodontal disease is a complication of diabetes and osteoporosis. Prescription and nonprescription drugs often have the side effect of dry mouth. The ability to measure the quality of life has the practical value of guiding policymakers, health serv- ice researchers, epidemiologists, program evaluators, and clinicians interested in the effects of interven- tions. The measures can also provide useful informa- tion to patients and family members, third-party pay- ers, and employers. For example, measures of the ability to perform activities of daily living may inch- cate areas where the patient is able and competent, as well as areas where further therapy may be helpful. This chapter reviews oral-health-related quality of life findings along functional, psychosocial, and economic dimensions, taking into consideration the ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 133 Effects on Well-being and Quality of Life influence of cultural and spiritual values. The results of studies in which investigators asked adults how they value their oral health and whether they are sat- isfied with their oral health care are included. The study of the association between oral health and quality of life is a relatively new but rapidly growing field. A variety of questionnaires have been designed to assess oral-health-related quality of life, and the chapter concludes with a discussion of their use in surveys and analytic studies, and their potential importance in outcome research. THE CULTURAL CONTEXT The determination of the health-related quality of life of an individual is implicitly made against a cultural background that includes a set of values, standards, customs, and traditions associated with a particular society. Decisions about whether to seek care from a den- tist, a physician, or other care provider may be influ- enced by cultural or ethnic perspectives and under- standing (Aday and Forthofer 1992, Andersen and Davidson 1997, Davidson and Andersen 1997, Diehnelt et al. 1990, Kiyak 1993, Lee and Kiyak 1992). Different population groups differ in the way they think about health, and in how they define a health problem, determine its seriousness, and decide whether to seek care. In one cultural setting a painful tooth may be enough to motivate care seek- ing. In another, bleeding, swelling, or fever may be necessary before care is sought. Similarly, decisions about whether to comply with a suggested treatment regimen, whether to engage in self-care, and whether to return for a follow-up appointment are also cul- turally influenced. The anthropology and ethnography literature is rich in references to the ways in which different cul- tures at different times and places have regarded the human body (Hufford 1992, Kleinman 1979). Cultural beliefs regarding the body, health, and dis- ease are often embedded in religious or spiritual traditions, which in turn may govern how diseases and disorders are regarded and treated. A brief des- cription of Western and non-Western perspectives follows. Cultural Models In the medical model typical of Western society the body is partitioned into organs and systems, each with identifiable functions. The body is seen as func- tioning well unless disease disrupts it. Diseases in themselves are understood to be invariable across cultures. The medical model has traditionally dichotomized body and mind/soul/spirit-science and magic. Such a perspective sees the body as rela- tively objective and value-free, immune to nonso- matic influences. That perspective began to change with the pio- neering work of Hans Selye in the 1930s on the importance of stress in health and disease (McEwen 1999). Research in the intervening half century has confirmed the reciprocal connections of the nervous, endocrine, and immune systems, not only in relation to stress, but also in terms of the effects of emotions and cognitive processes on health status. The model that has emergkd as a new paradigm in the study of health and disease incorporates bio- logical with psychological and social factors. This biopsychosocial model is defining agendas for research in such fields as behavioral medicine and psychoneuroimmunology Social and psychological factors are routinely incorporated into health assess- ments, the better to describe the quality of life. Other societies hold views of the body strikingly different from the medical model. In some cultures, individu- als and their care providers conceive of the body as the union of soul and soma. Illness may occur as a result of a "failure in harmony" or "an imbalance of forces." Schools of medicine in China, India, and other non-western societies incorporate such princi- ples into their teaching and practice (Hufford 1992). Combining Perspectives All Americans hold culturally influenced perspec- tives on healing and illness (Henderson et al. 1997), some of which come from more traditional beliefs. Some people accept pain as an inevitable part of ill- ness, a necessary evil, or even punishment for past iniquities or shortcomings and may shun pain-reliev- ing drugs (Zborowski 1952). Many pragmatically combine cultural, folk, complementary, and altema- tive healing practices with participation in conven- tional care delivery systems. A recent survey indi- cates that over 50 percent of Americans sought non- traditional therapies for a number of ailments (Eisenberg et al. 1998). Traditional beliefs are often comforting and satis- fying to individuals (Selikowitz 1994). Certainly, Western culture and science have not always improved the quality of people's lives (Harris et al. 1993). Dietary changes to refined foods have been associated with dental caries (Godson and Williams 1996, Navia 1994), obesity, and other deleterious health changes (Selikowitz 1994). The marketing of tobacco products has added to the burden of cancer 134 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and heart and lung problems worldwide. Migrations from traditional community rural life to urban cen- ters have been associated with family disruption and Iiolence, drug abuse, sexually transmitted diseases. and hypertension in developing countries. On the other hand, Western science may inform some cultural groups that certain traditional child- rearing practices can be detrimental to oral health (Kolasa 1978, Scheper-Hughes 1990). Early child- hood caries is a form of tooth decay with complex etiologies. Researchers studying high rates of infant caries among some cultural groups are exploring the extent to which traditional means of soothing crying babies or handling bedtime routines play a role, as xvell as investigating prenatal nutrition and transmis- sion of infection from caregiver to child (Febres et al. 1997, Kelly and Bruerd 1987, Ripa 1988, Tinanoff and O'Sullivan 1997). People who hold different cultural perspectives may distance themselves from Western, scientific worldviews (Lee et al. 1993), a behavior that must be addressed in any program of health promotion and disease prevention. Health professionals who under- stand indigenous or local healing practices and con- cepts are better able to motivate patients and thereby enable them to integrate elements from various heal- ing systems (Kleinman 1979). America is undergoing major demographic changes, with the expectation that at some point before 2050 the white population will no longer represent the majority (Henderson et al. 1997). As these changes occur, cultural elements that now reflect minority groups may become more accepted and dominant. However, cultural values are neither static nor omnipotent in shaping people's lives. Furthermore, individuals within a culture manifest their cultural identity in different ways. Therefore, both the direction of these changes and their effects may be hard to predict. ORAL-HEALTH-RELATED QUALITY OF LIFE DIMENSIONS Multiple factors act and interact in determining one's quality of life, as Wilson and Cleary (1995) and others have observed. Thus the idea of assessing quality of life along multiple "dimensions" implies a departure from a simple linear scale with excellent quality of life at one end and greatly diminished quality of life at the other. The following sections explore several dimensions, beginning with effects along functional and psychosocial dimensions and concluding with a discussion of economic effects on quality of life. Effects on Well-being and Quality of Life Functional Dimensions Investigators have reported on the effects of dental and craniofacial diseases on the ability to eat and enjoy the full range of dietary choices. The impact of less-than-optimal oral health also has been studied in relation to sleep problems, primarily in relation to oral-facial pain. Eating Both dental and systemic diseases can profoundly affect appetite and the ability to eat, and hence can compromise overall health and well-being. Because chronic illness and medications increase in aging populations, these effects may be particularly evident among the frail elderly (Ship et al. 1996). Undernutrition was observed in 50 percent of geri- atric residents in a U.S. long-term care facility; in many cases, it was linked to eating and swallowing problems (Keller 1993). Less severe oral disorders have more subtle effects on functions relating to eating, although the high prevalence of those disorders elevates their rela- tive importance among health problems. For exam- ple, data from the National Health and Nutrition Examination Survey III indicate that 33.1 percent of people aged 65 and older have no teeth (Marcus et al. 1996). Furthermore, clinical studies indicate that the masticator-y efficiency of replacement teeth is at least 30 to 40 percent lower than that of natural teeth (Idowu et al. 1986). Consistent with these findings, surveys of elderly populations in the United States indicate that self-reported chewing problems affect significant proportions of people. For example, in California 1 percent of Medicare enrollees were unable to swallow comfortably, whereas 37 percent of senior center residents reported trouble biting or chewing foods (Table 6.1). A number of studies have indicated that having missing teeth is linked to a qualitatively poorer diet. For example, in studies of U.S. veterans (Chauncey et al. 1984), Canadians (Brodeur et al. 1993), and Finns (Ranta et al. 1987), people with impaired dentitions preferred soft, easily chewed foods that were lower in fiber and had lower nutrient density than foods eaten by people with intact dentitions. Quality of life clear- ly suffers when individuals are forced to limit food choices and the foods chosen do not provide optimal nutrition. For example, they would be hard put to comply with the healthful diet recommendation of "five-a-day" helpings of fiber-rich fruits and vegeta- bles. In the elderly, edentulousness and poor oral health may contribute to significant weight loss, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 135 Effects on IYell-being and Quality of Life TABLE 6.1 Prevalence of self-reported eating dysfunction in surveys of elderly Americans Dysfunction Attributed to Oral Condition(s) Percentage of Population Group Reporting Dysfunction Elderly Persons in Californiaa Senior Center Residents Medicare Enrollees Had trouble biting or chewing 37 13 Limited the kinds of foods eaten 23 10 Unable to swallow comfortably 10 1 Elderly Persons in Floridab Mouth sometimes dry 39 Noticed an unpleasant taste in mouth 23 Unable to chew hard things 19 Experienced change in sense of taste 9 Difficulty tasting some foods 6 Noticed change in sense of smell 5 Elderly Persons in North Carolina< African Americans Whites Difficulty chewing any foods 18 6 Felt sense of taste had worsened 13 3 Uncomfortable eating foods 13 6 Had to avoid eating some foods 10 4 Felt digestion had worsened 8