Hasiuk N. V., Klitynska O. V., Pogoretska Kh. V., Gurando V. R.


About the author:

Hasiuk N. V., Klitynska O. V., Pogoretska Kh. V., Gurando V. R.



Type of article:

Scentific article


The prevalence of generalized periodontitis in different countries of the world is quite high. There are various systematizations and clinical and morphological forms of periodontitis, distinguished depending on the etiology, the nature of the process and the immune response. Polymorphic clinical manifestations of this nosology associated with different composition of subgingival microflora. A significant role is also played by factors that influence the antimicrobial response and the new metabolic status of adolescent organisms. The problem of early diagnosis of generalized periodontitis in adolescents, the development of effective measures for its prevention and treatment aimed at achieving positive long-term results, occupies one of the leading places among the priority areas of development of modern dentistry. Recent epidemiological and clinical studies show a relationship between pathology of the cardiovascular system and persistent bacterial infections or clinical conditions with generalized periodontitis. In addition, the current views and concepts do not fully explain the differences in identifying risk factors for the development and progression of periodontitis in adolescents, its course, and mixed results of treatment under the same conditions. The difference in the rate of progression of periodontitis known in the clinic in adolescents who received treatment according to standard generally accepted schemes suggests the biological heterogeneity of this disease and its possible complex causes. In this regard, studies are gaining particular importance, allowing to specify the effect on the possibility of developing periodontitis in healthy individuals and to predict the course in patients with this nosology. Therefore, the study of the relationship of this pathology with genetically determined factors should be attributed to a promising one. The latest data on the problem of metabolic disorders in the development of inflammation in periodontal tissues and, as a consequence, the etiopathogenesis of atherosclerosis demonstrate the main aspect of this leading form of pathology as an inflammatory disease. Recent large pathomorphological studies suggest that one of the places in atherogenesis is the inflammatory factor. High plasma cholesterol is an important factor in the development of atherosclerosis, makes it possible to consider it as a process associated with the accumulation of fats in the wall. According to some authors, granulocyte defects lead to a number of systemic diseases associated with periodontal tissue pathology: deficiency of adhesion of type 1 leukocytes; Chediak-Higashi syndrome; Down syndrome; PapillonLefebvre syndrome; diabetes; chronic granulomatosis; lazy white blood cell syndrome; Crohn’s disease. For the successful conduct of the surgical phase of treatment, a set of diagnostic methods is necessary, the results of which would allow predicting the final result of surgical interventions in periodontal tissues. However, traditional methods of diagnosing and predicting the development of various forms of rapidly progressive periodontitis in adolescents are not always effective and timely and do not completely solve the tasks set for clinicians due to the cyclical and unpredictable course of the pathological process, rapidly progressive destruction of periodontal tissues, toxic and allergic reactions. There are only a few achievements of foreign scientists regarding genetically determined prognostic risk factors and the clinical course of generalized periodontitis in adolescents. This necessitates the search for new, effective, highly specific techniques that would allow pathogenetic substantiation of the process from the standpoint of molecular genetics.


genotype, periodontitis, periodontal tissue, polymorphism, leukocytes.


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Publication of the article:

«Bulletin of problems biology and medicine» Issue 4 Part 1 (153), 2019 year, 17-22 pages, index UDK 616.311.2−018.7−02:616.379