Introduction: The relationship between periodontal diseases and atherosclerosis is addressed in this article. Both these diseases have an inflammatory basis. Because periodontal disease is a risk factor for developing atherosclerotic vascular disease, diagnosis of the former is important. Particular attention must be paid to patients who have periodontal disease with other risk factors for atherosclerotic vascular disease. Recommendations managing these patients have been made included. The aim: The paper is aimed at familiarization of broad medical public with the presence of the relationship between diseases of periodontal tissues and atherosclerosis. Materials and methods: A thorough comprehensive analysis and generalization of scientific achievements elucidated in the fundamental and periodical publications, relating to diseases of the periodontal tissues and atherosclerosis, has been carried out. Review: The article consists of many researchers regarding the prevalence and intensity of periodontal tissue diseases in people of all ages. Problems associated with the state of periodontal tissues in people under study as dentists and general practitioners. Proven role in the pathogenesis of inflammatory diseases of the periodontal tissues in people with atherosclerosis. In the modern concept of the etiology and pathogenesis of periodontal diseases in people is extremely important role for the immune system and resistance to periodontal bacterial invasion. Analyzed common changes important for pathogenesis of periodontal tissue diseases and atherosclerosis. Conclusions: Consequently, recent studies have shown a clear, directly proportional relationship between periodontal tissue diseases and atherosclerosis, but mechanisms for their development and interaction are not fully disclosed.

The aim of the work was a preclinical assessment of acute toxicity, skin resorptive, irritant effects, cumulative and catalase activity, as well as sensitizing properties of the local gel composition “Benzidaflaziverdine” (GCB) used for the treatment of periodontal diseases in orthodontic patients. Materials and methods. 119 animals were involved in the experiment, assigned to seven main and two control groups. GCB was administered intragastrically in doses of 300–600 mg/kg and intradermally of 200 μg into the outer surface of the ear. The native solution of GCB was applied to the skin and mucous membranes, administered orally by the method of “subchronic toxicity” and to the surface of the chorioallantoic membrane (CAM) of chicken embryos. The intensity of lipid peroxidation (LPO) was assessed by the level of diene conjugates (DCs) and malondialdehyde (MDA), and the antioxidant system by catalase activity. The specific leukocyte agglomeration reaction (SLAR), the specific leukocyte lysis reaction, and neutrophil damage indicators were used. Results. The median lethal dose LD50 for rats and mice of both sexes exceeded 5000 mg/kg. The irritant effect of GCB on the mucous membranes was manifested by hyperemia on the second day. Symptoms of irritation disappeared after 3–4 days without medical intervention. An analysis of the CAM blood vessels after exposure to GCB in two observations at the 120th second showed the beginning of hemorrhages. In one observation, GCB caused minor hemorrhages at the 300th second of the experiment. It was found that the coefficient of GCB irritant action was 5 (the mean score of Me (Q1; Q3) was 5 (4; 5)). The coefficient of cumulation (Kcum) exceeded 8.2. An insignificant increase in the median or mean values of catalase enzyme activity, DCs, and the amount of LPO end product such as MDA was observed compared to the control group animals. The SLAR test indicated the development of a delayed-type allergic reaction under the influence of GCB in a 1:10 dilution. One-hundred-fold dilution did not cause significant changes in the indicator in the main group compared to the control one. Conclusions. GCB belongs to the 4th class of toxicity – practically non-toxic substances, does not have sex- and species sensitivity, has weak cumulative activity, minimal effect on the system of LPO. GCB can be recommended for the use in clinical periodontology for medical support of orthodontic patients.

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