One of the urgent problems of modern medicine is to understand and explain the structural rearrangement of organs and tissues in the course of diabetes. The article presents the results of a comprehensive morphological study of the structural organization of micro- and macrovasculators, as well as some organs under conditions of diabetes mellitus in the experiment.  The study material constituted 52 adult outbred white male rats, with the average weight of 150-180 g, 4,5-6,5 months old. The following research methods were applied: histological, electron microscopic, biochemical, experimental modeling of streptozotocin-induced diabetes mellitus, morphometric and statistical. It was found that diabetic microangiopathy develops after 2 weeks of experimental diabetes, while after 4 weeks of the experiment there were some structural changes in the aorta observed. Furthermore, after 6 and 8 weeks, some profound destructive changes in the mandible and testis were revealed.  The obtained results may be used as fundamental data for the development of new methods for diagnosis, prevention and treatment of pathology of the cardiovascular system, oral cavity and male reproductive system caused by diabetes.

Introduction. To determine the primary events of gingival microvascular complex damage caused by inflammation (28 days) on an acidotic model of periodontitis in 36 white mongrel rats, and to clarify regulatory factors of the structural recovery after metabolic correction (14 days). Materials and methods. Expression and severity of gingival inflammation were visually analyzed with an ANOVA test. The gingival tissue specimens were examined (x 4000-6000) after 42 days with a transmission electron microscope JEM-100 CX II (JEOL, Japan). Results and discussion. Vacuolation of the endothelial cells' cytoplasm, thickening and loosening of the basal lamina, narrowing of the microvascular lumen, aggregation of the red blood cells and dilation of perivascular space were characteristic features of inflammatory derangement. A significantly lower severity of gingival inflammation (p < 0.05), thin condensed basal lamina …

ABSTRACT
The aim: of our work was investigation of dystrophy in periodontal tissues and an attempt to establish the correlation between dystrophy in the periodontium and presence of intestinal disbacteriosis.
Materials and methods: Clinical-radiological examination was carried out in 146 patients with generalized periodontal pathology at the age from 26 to 59 years old. Among them in 92 persons generalized periodontitis was diagnosed and in 54 – periodontosis. The rst stage of heaviness of the pathological process in the periodontium was revealed in 50 patients with generalized periodontitis and 28 persons with periodontosis. Other patients su ered from heavier forms of periodontal pathology (II and III stages), 42 persons with generalized periodontitis and 28 persons with periodontosis accordingly. Bacteriological analysis of feces for disbacteriosis was carried out in all patients.
Results: Changes in the physiological contour of the gums (that is macro relief of marginal periodontium) were found in the majority of examined patients. Because of the development of pathological gingival contour and recession of the gums, 72,5% of examined patients su ered from root denudation and di erent pathological conditions of roots cement structure – pigmentation, demineralization, wedge-shaped defects, caries. According to our clinical investigations it was found out that in majority of patients (83%) both in ammatory and dystophic changes were present, only 17% of patients had purely atrophic process in the periodontium without in ammation. In patients with GP and periodontosis, in whom dystrophic changes were accompanied by in ammation, clinical appearance was more expressed with redness, bleeding and suppuration from the pockets, thus hiding dystrophic signs.
Conclusions: According to clinical and radiological ndings numerous dystrophic changes were found in all structures of the periodontium and teeth of patients with periodontosis and generalized periodontitis. Changes intensify in disease progressing into the II-III stages. In patients with periodontosis clinical- radiological peculiarities of dystrophy were revealed in early stages of disease progression, while in generalized periodontitis dystrophic changes become apparent in late stages of disease. The presence of colon disbacteriosis was established in patients with periodontosis and generalized periodontitis. Disbacteriosis intensi es when diseases progress into II-III stages of heaviness. These data indicates to possible correlation between the development of dystrophic changes in periodontal tissues and the presence of intestinal disbacteriosis.
KEY WORDS: intestinal disbacteriosis, generalized periodontitis, periodontosis, dystrophy, gingival contour

Dystrophic changes of all periodontal structures and teeth in patients with periodontitis and generalized periodontitis were investigated in the study. Characteristic signs of the gums’ pathological contour, as well as other clinical and radiological features of dystrophy differ in patients with periodontitis and generalized periodontitis and contribute to the improvement of their differential diagnosis. Ultrastructural examination of the patients’ gums with periodontitis revealed disseminated microthrombosis, mucoid edema and fibrinoid transformation of intermediate connective tissue, and coagulation-dystrophic changes in periodontal tissues and cells.
Key words: periodontitis, parodontosis, gingival ultrastructure, coagulation dystrophy

Primary splenic cysts (SC) are rare in children and are registered with a frequency of 0.07% to 1.0% of all surgical diseases of the abdominal cavity [2, 7, 13]. Beginning in 1929, when the disease was first reported, the classification of SC changed. SC were classified based on the presence or absence of epithelial membrane, pathogenesis, etc. SC are divided into true cysts, which have an epithelial membrane (SC type 1), and false cysts (SC type 2), in which the epithelial lining is absent. A separate group consisted of pseudocysts. They are usually of post-traumatic origin and are formed in the parenchyma of the spleen or subcapsularly as a result of hematoma transformation, less often – due to an abscess or infarction of the spleen [9, 11]. Depending on the presence or absence of the pathogen, SC are divided into parasitic and non-parasitic [1, 4, 5]. Parasitic SC are usually observed in endemic areas and are caused mainly by Echinococcus granulosus[1, 6, 10]. Modern classification is based on the pathogenesis of cysts and divides non-parasitic SC into congenital, neoplastic, posttraumatic and degenerative [3]. Primary SC account for 10% of all non-parasitic SC and are observed in different pediatric age groups. Most SC are asymptomatic, so they are mostly detected by accident during examinations (ultrasound, CT or MRI). In addition, they can be detected due to complications: suppuration or splenic rupture with bleeding, which requires urgent surgery [10, 12].