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Public Health Implications of Chronic Periodontal Infections in Adults
Introduction to Periodontal Diseases: Clinical Presentations, Etiology,
and Pathogenesis
Roy Page, DDS, PhD,
Director of Periodontics, School of
Dentistry, University of Washington, Seattle, Washington
Periodontitis is a chronic infectious disease that affects approximately
34% of the United States population over age 30 (about 36 million persons),
and it a major cause of tooth loss in about 13% of adults. The
disease begins as an acute inflammation of the gingival tissue known as
gingivitis, manifested by bleeding, especially during tooth brushing. In
susceptible individuals, gingivitis progresses to periodontitis, in which
the destructive inflammatory process extends into the deeper periodontal
tissues. Clinical signs of periodontitis are gingival bleeding, loss
of periodontal attachment as detected by increasing probing depth around
the necks of the teeth, and radiographic loss of alveolar bone. As the
disease advances, the teeth may become loose, periodontal abscesses may
form, and the affected teeth may be lost.
Periodontitis is caused by a small group of predominantly gram-negative
anaerobic bacteria among which Porphyromonas gingivalis is
especially important. Biofilms containing these pathogenic bacteria form on
the tooth surfaces and extend apically between the surface of the tooth
root and gingiva to cause a destructive inflammation that destroys the
attachment of gingival tissue to the tooth. Consequently, periodontal
pockets form and collagenous fibers of the periodontal ligament and the
bony housing of the tooth roots are destroyed.
Lipopolysaccharide, antigenic bacterial components, and intact bacteria
have ready access through the ulcerated pocket wall into the inflamed
tissue, where they may enter the circulation and become systemically
disseminated. Bacteria and their components stimulate a dense infiltrate of
inflammatory cells including neutrophilic granulocytes, macrophages, and
lymphoid cells. Bacterial substances activate macrophages and neutrophilic
granulocytes to produce and release large quantities of proinflammatory
cytokines and prostanoids especially interleukin-1 (IL-1), tumor necrosis
factor-alpha (TNF-alpha), prostaglandin E2 (PGE2) and matrix metalloproteinases. Resident connective tissue fibroblasts also
are involved
in this process. Binding of the C1 component of complement and cytokines
such as IL-1 and TNF-alpha causes the fibroblasts to contribute to the
growing concentrations of proinflammatory cytokines, prostaglandins, and
matrix metalloproteinases. PGE2 mediates alveolar bone
destruction, and the matrix metalloproteinases destroy the collagens and
other connective tissue components of the gingiva and periodontal ligament.
A growing body of evidence suggests that periodontitis, in addition to
being a major cause of tooth loss in adults, also enhances risk for several
potentially deadly systemic diseases and conditions. This enhanced
risk may be related to the systemic dissemination of gram-negative
anaerobic bacteria and their components present in subgingival biofilms as
well as inflammatory mediators that reach very high levels in the diseased
periodontal tissues.
Back to Chronic Periodontal Infections Conference
Historical Document
Page last reviewed: February 2, 2005
Content source:
Division of Oral Health,
National Center for Chronic Disease Prevention and
Health Promotion |
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