Abstract
Periodontal disease is a chronic inflammatory condition that results in the destruction of the teeth supporting tissues, eventually leading to the loss of teeth and reduced quality of life. In severe cases, periodontal disease can limit proper nutritional intake, cause acute pain and infection, and cause a withdrawal from social situations due to esthetic and phonetic concerns. Similar to other chronic inflammatory conditions, periodontal disease increases in prevalence with age. Research into what drives periodontal disease pathogenesis in older adults is contributing to our general understanding of age-related chronic inflammation. This review will present periodontal disease as an age-related chronic inflammatory disease and as an effective geroscience model to study mechanisms of age-related inflammatory dysregulation. The current understanding of the cellular and molecular mechanisms that drive inflammatory dysregulation as a function of age will be discussed with a focus on the major pathogenic immune cells in periodontal disease, which include neutrophils, macrophages, and T cells. Research in the aging biology field has shown that the age-related changes in these immune cells result in the cells becoming less effective in the clearance of microbial pathogens, expansion of pathogenic subpopulations, or an increase in pro-inflammatory cytokine secretions. Such changes can be pathogenic and contribute to inflammatory dysregulation that is associated with a myriad of age-related disease including periodontal disease. An improved understanding is needed to develop better interventions that target the molecules or pathways that are perturbed with age in order to improve treatment of chronic inflammatory conditions, including periodontal disease, in older adult populations.