Analytical epidemiology of periodontitis

• Published in: Journal of clinical periodontology Vol. 32; no. s6; pp. 132 - 158
• Main Authors: Borrell, Luisa N., Papapanou, Panos N.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Munksgaard International Publishers 01.01.2005
• Subjects: Aggregatibacter actinomycetemcomitans - pathogenicity; Bacteroides - pathogenicity; Diabetes Complications; Disease Progression; epidemiology; HIV Infections - complications; Humans; Obesity - complications; Osteoporosis - complications; periodontal disease; periodontitis; Periodontitis - classification; Periodontitis - epidemiology; Periodontitis - etiology; Porphyromonas gingivalis - pathogenicity; Risk Factors; Smoking - adverse effects; Stress, Psychological - complications; Terminology as Topic; Treponema denticola - pathogenicity
• ISSN: 0303-6979; 1600-051X
• DOI: 10.1111/j.1600-051X.2005.00799.x

Aims: To review the literature related to the analytical epidemiology of periodontitis generated over the past decade. This review does not deal with descriptive epidemiologic studies of the prevalence, extent and severity of periodontitis with respect to global geography, but focuses exclusively on analytical epidemiology issues, including the challenges posed by the use of different case definitions across studies, current theories and models of disease progression, and risk factors associated with the onset and progression of periodontitis. Methods: Relevant publications in the English language were identified after Medline and PubMed database searches. Findings and conclusions: There is a conspicuous lack of uniformity in the definition of periodontitis used in epidemiologic studies, and findings from different research groups are not readily interpretable. There is a lack of studies that specifically address the distinction between factors responsible for the onset of periodontitis versus those affecting its progression. Colonization by specific bacteria at high levels, smoking, and poorly controlled diabetes have been established as risk factors for periodontitis, while a number of putative factors, including specific gene polymorphisms, have been identified in association studies. There is a clear need for longitudinal prospective studies that address hypotheses emerging from the cross‐sectional data and include established risk factors as covariates along with new exposures of interest. Intervention studies, fulfilling the “targeting” step of the risk assessment process, are particularly warranted. Obvious candidates in this context are studies of the efficacy of elimination of specific bacterial species and of smoking cessation interventions as an alternative to the traditional broad anti‐plaque approach in the prevention and control of periodontitis. Ideally, such studies should have a randomized‐controlled trial design.