Condition of periodontal tissues in experimental animals under the model of periodontitis combined with intestinal dysbiosis
 
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1
UZHHOROD NATIONAL UNIVERSITY, UZHHOROD, UKRAINE
 
2
POLISHCHUK DENTAL CENTER, KHMELNYTSKYI, UKRAINE
 
3
NATIONAL PIROGOV MEMORIAL MEDICAL UNIVERSITY, VINNYTSYA, UKRAINE
 
4
SHUPYK NATIONAL HEALTHCARE UNIVERSITY OF UKRAINE, KYIV, UKRAINE
 
 
Publication date: 2026-05-29
 
 
Wiadomości Lekarskie 2026;(5):918-928
 
KEYWORDS
ABSTRACT
Introduction:
Aim: To study the nature of clinical and morphological changes in periodontal tissues under combined modeling of periodontitis and intestinal dysbiosis in an animal experiment.

Material and Methods:
The study involved 30 rats (1 control and 2 experimental groups of 10 animals each). Histological changes in the gingiva were examined during periodontitis modeling in 10 animals over 30 days and its combination with intestinal dysbiosis in the remaining 10 animals over 30–35 days. The degree of alveolar bone ridge atrophy was assessed, and the composition of the intestinal microflora was analyzed to confirm intestinal dysbiosis.

Results:
It was established that the reproduction of experimental periodontitis in animals and its subsequent combination with intestinal dysbiosis contributed to the development of a pathological process in the periodontal tissues in 100% of rats, resembling an exacerbated course of human periodontitis, with increased severity and progression. In rats with simultaneous modeling of periodontitis and intestinal dysbiosis, more pronounced pathological changes were observed—compared to those without dysbiotic lesions—in the gingival epithelium, the connective tissue of the mucous membrane, and especially in the blood vessels of the microcirculatory bed and perivascular areas.

Conclusions:
Morphological studies confirmed that disturbances in the intestinal microecological system, accompanied by suppression of its saprophytic flora, aggravate the course of periodontitis, promote its generalization, and contribute to the development of abscess-forming inflammation.
eISSN:2719-342X
ISSN:0043-5147
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