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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.

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