Current mechanisms of interaction between carbohydrate metabolism and periodontal disease. A review article

Abstract

Given the high global prevalence and significant impact on health, the relevance of complex and two-way interactions between atypical carbohydrate metabolism (especially in the context of diabetes mellitus) and the mechanism of producing periodontal disease is undeniable. A detailed understanding of this interconnection is crucial for the development of effective prevention strategies, early diagnosis, and integrated therapeutic management. The effects of chronic hyperglycemia, characteristics of diabetes mellitus, on the oral microbial ecosystem are multiple and profound. It favors a selection of pathogenic bacterial species, altering the structure and function of the subgingival biofilm and creating a pro-inflammatory environment. At the same time, hyperglycemia induces significant dysfunction of neutrophils, key cells of the innate immune system responsible for eliminating pathogens. This reduced capacity for local immune response allows uncontrolled bacterial proliferation and exacerbates inflammation. Furthermore, the crucial role of advanced glycation end products (AGEs) and their receptors (RAGE) in perpetuating chronic inflammation is well documented. The accumulation of AGEs in periodontal tissues and their interaction with RAGE triggers a proinflammatory signaling cascade, contributing to the destruction of tooth-supporting tissues and the progression of periodontal disease.