Epidemiology and Pathogenesis of Periodontal Disease

Periodontal diseases include inflammatory diseases of the supporting structures around the teeth--the gingiva, periodontal ligament, alveolar bone, and cementum.^45,46 The two most common forms of periodontal disease are gingivitis and periodontitis.³¹ Gingivitis is a non-specific inflammatory disease associated with the accumulation of dysbiotic bacterial biofilm.⁴⁷ All patients are susceptible to gingivitis with cessation of oral hygiene measures. Further, for many patients, gingivitis is a precursor to more serious, irreversible forms of periodontal diseases.⁴⁷ Removal of biofilm and local etiologic factors results in the reversal of gingivitis symptoms and reduces local and systemic levels of inflammatory markers in patients with gingivitis.^47-49

Periodontitis is generally believed to be a bacterially-initiated disease in which the host immune-inflammatory response results in destruction of the alveolar bone and soft tissues supporting the teeth.^50,51 Periodontal disease progression is generally slow to moderate. Average clinical progression of periodontal disease is approximately 0.1mm of attachment loss and 0.2 teeth lost annually.⁵² In longitudinal investigations, groups with fastest and slowest disease progression differed considerably with regard to demographics and underlying health conditions.⁵² Increased rapidity of attachment loss is associated with decreased access to comprehensive dental care as well as certain local and/or systemic factors.⁵² In an updated classification system from the American Academy of Periodontitis (AAP) and European Federation of Periodontitis (EFP), individuals are classified with a Stage and Grade to characterize disease severity and risk of future disease progression.^51,53 Periodontitis Stages I-IV are determined based upon a patients’ current disease presentation, including attachment loss, alveolar bone levels, and tooth loss, and the Stage may be modified by case complexity.^51,53 Periodontitis Grades A-C are selected based upon risk factors and direct or indirect evidence of the pace of disease progression.^51,53 The prevalence of periodontitis has been estimated to be over 42% of U.S. adults over 30 years of age.³¹ Of those individuals, 7.8% had severe periodontitis.³¹ Further, severe periodontitis was most prevalent among adults 65 years or older, Mexican Americans, non-Hispanic blacks, and smokers. ³¹ In fact, periodontitis prevalence among US adults is nearly 4-fold greater than that of diabetes mellitus⁵⁴and over 6-fold greater than that of coronary artery disease.⁵⁵ Given the highly prevalent nature of periodontitis, identification of periodontal disease and consideration during assessment and therapy for systemic diseases is critical. Disease progression and tissue destruction occurs through host-mediated inflammatory pathways,⁵⁶ which may vary based upon genetic and other risk factors.^57-60 The result is a chronic immune-inflammatory disease that may pose a significant systemic burden for individuals.⁶¹