Public Health Implications of Chronic Periodontal Infections in Adults

Genetic Aspects of Periodontal Diseases
Harvey A. Schenkein, DDS, PhD, Interim Chairman, Department of Periodontics, Virginia Commonwealth University School of Dentistry, Richmond, Virginia

Both clinical observation and experimental evidence indicate that there is a genetic component to risk for periodontitis in adults. Severe and aggressive forms of periodontitis are not common in the population, indicating that host susceptibility is important in determining such risk. Because all forms of periodontitis are associated with bacterial infections, defining the relative roles of genes and environmental factors in these complex diseases is a challenge. In the case of chronic periodontitis, studies of adult twins indicate that a substantial proportion of the population variance for periodontal measures—such as pocket depth, attachment loss, and bone loss—may be attributable to heritable factors. Aggressive periodontitis is often familial, and the likelihood of inheriting aggressive priodontitis is high, family studies indicate.

Current approaches to defining genetic risk factors for periodontitis include examination of genetic polymorphisms in candidate genes associated with the pathobiology of periodontitis. Linkage and association studies in families demonstrating disease also are being conducted. Some genetic polymorphisms that have thus far been shown to be associated with risk for various forms of periodontitis in various populations are in genes that code for inflammatory cytokines such as interleukin-1 and tumor necrosis factor, immunoglobulin receptors that are present on phagocytes, and the vitamin D receptor. In addition, genes associated with environmental risk factors such as smoking also may influence periodontitis.

There are many fundamental problems in studying genetic risk for these diseases. First, phenotype definition, is confounded by heterogeneity and overlapping clinical definitions. Second, clinical variability in disease presentation may include age-dependent criteria for diagnoses. Third, disease expression can vary substantially, depending on environmental etiologies such as bacterial flora and smoking. Fourth, systemic diseases can influence disease initiation. Finally, the severity of disease can change and the phenotype can be modified by intentional or inadvertent intervention.

Thus far, results of studies of genetic risk for periodontitis indicate that these diseases are etiologically complex. Although the ultimate utility of knowledge of genetic risk factors for periodontitis is not known, it is likely that in the future genetic tests could help clinicians and researchers to determine diagnoses based on etiology, better assess prognoses for symptomatic patients, predict future onset of disease, and tailor therapy based on this information. Genetic factors, once defined, will likely become one component of the overall risk profile for periodontitis.

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