Background: Disturbances in the differentiation of cells and the processes of cellular renewal of the buccal epithelium, which occur when the functional activity of cells change, or with aging of the organism, in general can show the functioning of the body's homeostasis system. The high prevalence of chronic periodontitis, low effectiveness of treatment, especially in elderly and senior age people, indicates the urgency of the problem. The aim of the study: To reveal molecular-cellular mechanisms of dysfunction of the buccal epithelium in patients of mature, elderly and senior age with chronic generalized periodontitis. Materials and methods: The object of study was the buccal epithelium of people of different ages. The sample for the study was 90 patients with chronic generalized periodontitis of moderate severity: 34 patients of middle age (45-59 years), 32 elderly patients (60-74 years) and 24 senior age patients (75-89 years). The study used the material of 77 people without signs of inflammatory periodontal pathology: 27 middle-aged people, 25 elderly people and 20 senior age people. An immunocytochemical study was carried out of a number of signal molecules – markers of the functional state of the mucous membrane of the cheek and the homeostasis of the organism as a whole. The method of immunofluorescence confocal microscopy was used to study the buccal epithelium. All the data obtained were subjected to morphometric analysis. Results: In the buccal epithelium of patients with chronic generalized periodontitis of middle, elderly and senior age, the area of expression of caspase-dependent apoptosis markers p16, p21, p53 increased 2-7 times compared with healthy donors of the corresponding age. The area of expression of these proteins increases on average 2-5 times in elderly and senior age patients compared with middle-aged donors in norm and in pathology. Conclusion: An increase in the expression of proteins p16, p21, p53 in chronic periodontitis, which increases with age, indicates a predominance of death of buccal epithelial cells and accelerated aging.