Relevance. Among many comorbid pathologies, it is of considerable interest to study and compare the pathogenetic mechanisms of neurological and mental disorders that combine the clinical manifestations of multiple sclerosis (MS) and affective disorders. The high MS prevalence, economic and social significance of the disease, heterogeneity of clinical symptoms, an unfavorable progressive course, as well as the frequent combination of this pathology with various forms of hypothymic disorders determine the relevance of studying the common pathogenetic mechanisms for the development of this comorbid pathology, which is necessary for the development of effective and safe preventive medical activities. The purpose of the review is to determine the common immunopathological mechanisms of affective disorders and multiple sclerosis, to analyze the role of cytokine status imbalance in the mutual increase in the severity of clinical symptoms in comorbid pathology, and to identify prognostic markers of disease progression. Materials and methods. On the basis of electronic Russian and foreign databases for the period 2017–2022, a theoretical analysis of the pathophysiological mechanisms of autoimmune CNS damage in MS and affective disorders was carried out. In order to search for literary sources, the following resources were used: https://elibrary.ru/, https://www.ncbi.nlm.nih.gov/pubmed/, https://cyberleninka.ru/. 10 Russian and 25 foreign sources were cited. Results. The mechanisms of development of mental affective disorders and multiple sclerosis have common pathogenetic features and are characterized by a violation of pro-inflammatory cytokine reactions and autoimmune nature of changes in the structures of the central nervous system (CNS). The similarity of immunological disorders underlying the pathogenesis of various forms of multiple sclerosis and affective disorders is of undoubted interest in terms of developing common approaches to the prevention and treatment of detectable interleukin status imbalance in neurological and mental diseases. Conclusion. Identification of mutually reinforcing changes in interleukin status and determination of the features of the course of immune imbalance in multiple sclerosis and hypothymic disorders in various pathologies of the mental sphere are necessary for a deeper understanding of neuroimmune interactions.

Relevance. The study of bioradical processes in periodontitis in the dynamics of the disease and the establishment of the role of predictors of periodontal tissue damage will provide a deeper understanding of the links of pathogenesis and, on this basis, introduce new therapeutic and diagnostic technologies into practice. The purpose of the study: Assessment of the level of markers of oxidative stress in experimental periodontitis in the dynamics of the study. Materials and methods. The study was conducted on white non-linear rats, reproducing the model of periodontitis proposed by Shkolnaya K. D., Atrushkevich V. G. (Patent RU No. 2625295 of 12.07.2017). The total activity of free radical oxidation and the body's antioxidant potential were evaluated by biochemiluminescence, the intensity of lipoperoxidation processes, and the enzyme antioxidant potential. Results. A comprehensive analysis of the overall oxidative and antioxidant capacity of the body was carried out, during which it was revealed that progressive experimental periodontitis causes inhibition of the antioxidant potential and is characterized by a violation of the processes of neutralization of reactive oxygen species and the inability to inhibit the launched reactions of free radical oxidation, as evidenced by the dynamics of an increased level of markers of oxidative stress. Conclusion. Thus, in periodontitis, oxidative stress develops, which contributes to the progression of destructive processes of periodontal tissues, which substantiates the feasibility of using markers of the intensity of free radical oxidation as diagnostic and prognostic criteria for the course of the disease and the introduction of antioxidant-type drugs in complex therapy.

Involutional hormonal processes characteristic of the postmenopause are accompanied by disorders that deteriorate the quality of life in the female population and lead to an increased risk of developing metabolic diseases of the bones and cardiovascular system. In modern medicine, it is extremely important to understand the pathogenesis of postmenopausal osteoporosis (PMO) in association with cardiovascular diseases, which are the main causes of mortality in the population.This review is devoted to determining the key aspects of the pathogenesis of PMO and identifying their relationships with cardiovascular pathology. Epidemiological data are assessed, the main mechanisms of PMO and vascular pathology development are considered, the fundamental role of hormone deficiency, immune dysregulation disorders, and disorders of macrophage polarization is described, and data on the association between the pathogenesis links of the studied pathological processes are analyzed.The obtained data will form a unified approach to reducing the growing prevalence of cardiovascular diseases and complications of PMO and contribute to the development of new research areas in disease prevention.