Generalized periodontitis and gout: a comparison of pathogenetic mechanisms of development
(literature review)
DOI:
https://doi.org/10.11603/2311-9624.2021.1.12040Keywords:
pathogenesisAbstract
Summary. The article presents a review of the literature on the modern vision of pathophysiological mechanisms that are formed in gout and their comparison with those of generalized periodontitis. Gout is a chronic progressive disease associated with impaired purine metabolism, characterized by increased levels of uric acid in the blood (hyperuricemia) and deposition in the tissues of the musculoskeletal system and internal organs of sodium uric acid (urate) with the development of acute arthritis and gout. nodules (tofus). The occurrence of primary gout is associated with hereditary defects in the structure and activity of enzymes that control purine metabolism; hereditary disorders of excretory renal function. Secondary gout can occur as one of the paraneoplastic syndromes and as a negative side effect of chemotherapy, in which there is a massive decay of nuclear substances. Factors that provoke exacerbation of gout are a diet high in purines, alcohol, physical activity A characteristic feature of gout is its polymorbidity: each patient has a history of 3 to 6 comorbid diseases, among which the most common and most serious are chronic cardiovascular and chronic renal failure. Systemic disorders in gout, including chronic autoimmune inflammation, oxidative stress, endothelial dysfunction and a high risk of atherosclerosis can create preconditions for both the development and aggravation of destructive inflammatory lesions of the periodontium, which determines the relevance of the study of periodontal status in these patients. for them treatment and prevention complexes.
The aim of the study – based on the analysis of literature data to analyze and compare the pathogenetic mechanisms of generalized periodontitis and gout.
Conclusions. According to the literature, gout as a metabolic disease associated with impaired protein metabolism, develops chronic autoimmune inflammation and oxidative stress, which causes a high risk of atherosclerosis; conditions are formed that can affect bone metabolism. Thus, the pathogenetic mechanisms formed in gout create conditions for both the development and aggravation of destructive-inflammatory lesions of the periodontium.
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