Endoecology of the oral cavity and cytomorphological features of buccal epithelium in people with inflammatory periodontal diseases

Abstract

BACKGROUND: The state of endoecological homeostasis of the oral cavity is ensured based on the colonization resistance of the microbiota as well as the protective reactions on the part of immune and epithelial cells, including the buccal epithelium.
 AIM: To establish cytomorphological features of the buccal epithelium and the state of the microbiota that colonizes the biotopes of the oral cavity in individuals with periodontitis living in the Arctic Zone of the Russian Federation.
 MATERIAL AND METHODS: A cross-sectional clinical and laboratory examination of 91 people permanently residing under the conditions of the Arctic zone of the Russian Federation was conducted. Cytomorphological studies (index evaluation and detection of anomalies) of buccal epitheliocytes, molecular genetic studies (isolation of periodontopathogens by real-time PCR), and statistical analysis of the data obtained were conducted.
 RESULTS: The results of the index evaluation in the group with periodontitis were unsatisfactory: cell differentiation index 85%, p 0.001, keratinization index 88%, p 0.001. The frequency of detection of cytogenetic disorders, indicators of apoptosis, and proliferative processes also prevailed in the group of patients with periodontitis: micronuclei 88.0%, protrusions 71.6%, proliferation rates 89.5%, karyolysis 10.4% and karyorrhexis 26.8%. Most often (70.1%), the markers of P. gingivalis were detected, in 41.8% of cases T. forsythia, associations of periodontopathogens in 17.8%. Positive correlations of moderate and weak degree were identified between the presence of cells with cytomorphological disorders with the definition of P. gingivalis: cells with micronuclei (r=0.413; p 0.001), cells with protrusions (r=0.228; p=0.029), presence of binuclear cells (r=0.402; p 0.001), and indicators of apoptosis (r=0.283; p=0.006; r=0.383; p 0.001), as well as between all the studied cytomorphological disorders and the release of the periodontal pathogen T. forsythia. Direct correlations of the average degree were established between the isolation of periodontopathogens in associations and the presence of cells with protrusions and indicators of proliferation and apoptosis.
 CONCLUSION: Inflammation of periodontal tissues occurs as a result of a shift in the endoecological balance through the combined action of periodontal pathogenic microbes that trigger a cascade of immune responses, leading to damage of the tissue microenvironment, primarily the buccal epithelial cells.