Systemic Inflammation and Periodontal Disease
Periodontal diseases are both infectious and inflammatory diseases of the supporting structures around the teeth: the gingiva, periodontal ligament, alveolar bone, and cementum.2,9,10 The two most common forms of periodontal disease are gingivitis and periodontitis.1 Gingivitis is a non-specific inflammatory reaction to the accumulation of dysbiotic bacterial biofilm.11 All individuals are susceptible to developing gingivitis after oral hygiene procedures are stopped. Gingivitis is also a necessary precursor to periodontitis and, ultimately, a loss of hard and soft tissues around the teeth.11 Removal of biofilm and local etiologic factors results in the reversal of gingivitis symptoms and resolution of local and systemic levels of inflammatory markers is associated with reestablishment of gingival health.11-13
Periodontitis is initiated by dysbiotic biofilm accumulation in a susceptible host and this biofilm dysbiosis triggers an immune-inflammatory response that then leads to the destruction of hard and soft tissues supporting the teeth.14-15 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.15 In longitudinal investigations, groups with the fastest and slowest disease progression differed considerably with regard to demographics and underlying health conditions.16 In an updated classification system from the American Academy of Periodontology (AAP) and European Federation of Periodontology (EFP), individuals with periodontitis are classified with a Stage and Grade, which are meant to capture both the current state of disease severity and distribution and risk of future disease progression based upon the history of diease progression and patient-level risk factors.15,17 Periodontitis Stages I-IV are assigned based upon patients’ current clinical presentation of periodontitis, including attachment loss, alveolar bone levels, and tooth loss, and the Stage may be modified by case complexity and need for multidisciplinary care.15,17 In order to describe the risk of future disease progression, Periodontitis Grades A-C are determined based upon individualized patient risk factors (i.e. smoking status and glycemic control) and direct and/or indirect evidence of disease progression, including the calculation of alveolar bone loss/age.15,17 The prevalence of periodontitis has been estimated to be over 42% of U.S. adults over 30 years of age.1 Of those individuals, 7.8% were found to have severe periodontitis.1 Severe periodontitis was also most prevalent among US adults 65 years or older, Mexican Americans, non-Hispanic blacks, and current heavy (>10 cigarettes daily) smokers.1 Among US adults, periodontitis prevalence is nearly 4-fold greater than that of diabetes mellitus18 and over 6-fold greater than that of coronary artery disease,19 making it extremely common within the population. Periodontal disease progression and destruction of both hard and soft tissues occurs through host-mediated inflammatory pathways,20 which may vary based upon genetic and environmental risk factors, potentially including nutritional factors.2,20-23 It should also be noted that a number of systemic diseases that are influenced by diet and nutritional intake, including diabetes mellitus, cardiovascular disease, and obesity have been associated with periodontal disease development or progression.24-26
The process of periodontal tissue destruction is mediated by pro-inflammatory cytokines and mediators such as interleukin-1ß (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), receptor activator of nuclear factor kappa B ligand (RANKL), and matrix metalloproteinases (MMPs).2,9,10 These pro-inflammatory mediators drive the activation of osteoclastic functions and lead to alveolar bone loss. The heterogeneity of the immune-inflammatory response among individuals can influence disease susceptibility and severity.2 Additionally, periodontal disease severity is correlated to increased levels of pro-inflammatory mediators systemically.27-30 Because dietary intake can make a significant impact on systemic levels of inflammation, nutrition has the potential to influence the progression of periodontitis.