PERIODONTITIS IN PREGNANCY: ETIOLOGY, DIAGNOSIS, CLINICAL APPREANCE AND METHODS OF TREATMENT

ISSN: 2582-4686 SJIF 2021-3.261,SJIF 20222.889, 2024-6.875 ResearchBib IF: 9.948 / 2024 VOLUME-5, ISSUE-12 1301 PERIODONTITIS IN PREGNANCY: ETIOLOGY, DIAGNOSIS, CLINICAL APPREANCE AND METHODS OF TREATMENT Gulmuxamedov P.B. Tashkent State Medical University Abstract Chronic periodontitis is a multifactorial inflammatory disease in which host immune response plays a critical role in determining disease susceptibility and severity. Among host-related factors, genetic polymorphisms in pro-inflammatory cytokine genes may influence the progression of periodontal tissue destruction. The aim of this study was to investigate the association between polymorphic variants of the TNF-α and IL-1β genes and the risk and clinical severity of chronic periodontitis in an Uzbek population. A total of 141 patients with clinically diagnosed chronic periodontitis and 138 periodontally healthy controls were included. Patients were stratified into mild, moderate, and severe forms based on clinical and radiographic criteria. Periodontal examination included probing depth, bleeding on probing, clinical attachment loss, and alveolar bone resorption. Genotyping of TNF-α (rs1800629) and IL-1β (rs1143634, rs16944, rs1143627) polymorphisms was performed using polymerase chain reaction methods. Allele and genotype frequencies were compared, and associations were assessed using odds ratios (ORs) with 95% confidence intervals (CIs). The TNF-α rs1800629 A allele was significantly more frequent in patients with chronic periodontitis than in controls (5.1% vs. 1.4%; OR = 3.7; p < 0.05), with the highest prevalence observed in severe disease. The IL-1β rs16944 T allele was also associated with an increased risk of chronic periodontitis (OR = 1.9; p < 0.01) and correlated with disease severity. Combined unfavorable cytokine genotypes were linked to more pronounced clinical and radiographic tissue destruction. These findings indicate that TNF-α and IL-1β gene polymorphisms contribute to genetic susceptibility and severity of chronic periodontitis and may support personalized risk assessment in periodontal practice. Keywords chronic periodontitis; TNF-α; IL-1β; gene polymorphism; cytokines; genetic susceptibility; personalized dentistry 1. Introduction Chronic periodontitis is a highly prevalent inflammatory disease characterized by progressive destruction of periodontal connective tissue and alveolar bone, ultimately leading to tooth loss. Although dental plaque biofilm is the primary etiological factor, the severity and progression of periodontal destruction vary significantly among individuals exposed to similar microbial challenges. This variability suggests an important role of host-related factors, particularly genetic determinants of the immune-inflammatory response. Pro-inflammatory cytokines, including tumor necrosis factoralpha (TNF-α) and interleukin-1 beta (IL-1β), are central mediators in periodontal inflammation. These cytokines stimulate leukocyte recruitment, matrix metalloproteinase activation, and osteoclastmediated bone resorption. ISSN: 2582-4686 SJIF 2021-3.261,SJIF 20222.889, 2024-6.875 ResearchBib IF: 9.948 / 2024 VOLUME-5, ISSUE-12 1302 Single nucleotide polymorphisms (SNPs) in cytokine genes may influence cytokine expression levels and biological activity, thereby modulating individual susceptibility to periodontal diseases. Previous studies have demonstrated associations between TNF-α and IL-1β gene polymorphisms and periodontitis; however, results remain inconsistent and appear to be population-specific. Data regarding genetic risk factors for chronic periodontitis in Central Asian populations, particularly in Uzbekistan, are limited. Therefore, investigating cytokine gene polymorphisms in this population may contribute to improved understanding of disease pathogenesis and support the development of personalized preventive and therapeutic strategies. The present study aimed to evaluate the association between polymorphisms of the TNF-α and IL-1β genes and both the risk and clinical severity of chronic periodontitis in an Uzbek population. 2. Materials and Methods 2.1. Study Population This case–control study included 141 patients diagnosed with chronic periodontitis and 138 periodontally healthy individuals. All participants were ethnic Uzbeks. The study was conducted in accordance with the Declaration of Helsinki, and informed consent was obtained from all participants. 2.2. Clinical Periodontal Assessment Periodontal examination included assessment of gingival inflammation, bleeding on probing, probing pocket depth, clinical attachment loss, and tooth mobility. Radiographic analysis was performed to evaluate alveolar bone loss. Based on these findings, patients were classified into mild, moderate, and severe chronic periodontitis groups. 2.3. Microbiological Analysis Subgingival samples were collected from periodontal pockets for microbiological evaluation to identify aerobic and anaerobic bacterial species associated with periodontal inflammation. 2.4. Genetic Analysis Genomic DNA was extracted from venous blood and saliva samples. Genotyping of TNF-α (rs1800629) and IL-1β (rs1143634, rs16944, rs1143627) polymorphisms was performed using polymerase chain reaction (PCR). Genotype distributions were tested for Hardy–Weinberg equilibrium. 2.5. Statistical Analysis Allele and genotype frequencies were compared using chi-square tests. Associations between polymorphisms and chronic periodontitis were evaluated by calculating odds ratios (ORs) and 95% confidence intervals (CIs). A p-value < 0.05 was considered statistically significant. 3. Results The TNF-α rs1800629 A allele was significantly more frequent in patients with chronic periodontitis compared to controls. Carriage of the G/A genotype increased the risk of chronic periodontitis by approximately 3.8-fold. The prevalence of this allele increased with disease severity. For IL-1β, the rs16944 T allele showed a significant association with chronic periodontitis and was more common in moderate and severe cases. Other IL-1β polymorphisms demonstrated weaker associations but showed trends toward increased risk in severe disease. Patients carrying combined unfavorable TNF-α and IL-1β genotypes exhibited deeper periodontal pockets, greater attachment loss, and more pronounced radiographic bone resorption. 4. Discussion ISSN: 2582-4686 SJIF 2021-3.261,SJIF 20222.889, 2024-6.875 ResearchBib IF: 9.948 / 2024 VOLUME-5, ISSUE-12 1303 This study demonstrates that polymorphic variants of TNF-α and IL-1β genes are significantly associated with both susceptibility to and severity of chronic periodontitis in an Uzbek population. The findings support the hypothesis that genetic regulation of inflammatory responses contributes to interindividual differences in periodontal disease progression. The association between the TNF-α rs1800629 A allele and severe periodontitis highlights its role in osteoclastic activation and tissue destruction. Similarly, IL-1β rs16944 appears to be a key genetic marker influencing periodontal inflammation. Population-specific genetic studies such as this are essential for advancing personalized dentistry and may facilitate early identification of high-risk individuals. 5. Conclusions TNF-α and IL-1β gene polymorphisms are significantly associated with the risk and severity of chronic periodontitis in the Uzbek population. These genetic markers may be useful for personalized risk assessment and for optimizing preventive and therapeutic periodontal strategies. References 1. Budtz-Jørgensen, E.; Lombardi, T. Denture stomatitis revisited. Periodontology 2000 2018, 78, 254–261. 2. Felton, D.A. Complete edentulism and comorbid diseases: An update. Journal of Prosthodontics 2016, 25, 5–20. 3. Grigoriadou, M.E.; Koutayas, S.O.; Madianos, P.N.; Strub, J.R. Interleukin-1 as a genetic marker for periodontal disease. Journal of Clinical Periodontology 2010, 37, 517–523. 4. Napimoga, M.H.; Nunes, L.H.; Maciel, A.A.; et al. Possible involvement of IL-1β polymorphism in chronic periodontitis. Journal of Oral Science 2014, 56, 13–19. 5. Tian, Y.; Feng, P.; Wang, Y.; et al. Association between TNF-α gene polymorphism and chronic periodontitis: A meta-analysis. Journal of Periodontal Research 2013, 48, 298–305. 6. Ayazi, G.; Pirayesh, M. Genetic polymorphisms of cytokines and susceptibility to periodontal disease. Journal of Dental Research, Dental Clinics, Dental Prospects 2013, 7, 8–15. 7. Feng, P.; Tian, Y.; Chen, Z.; et al. Association of TNF-α polymorphisms with periodontal disease risk: Evidence from a population-based study. Inflammation Research 2014, 63, 901–908. 8. Casado, P.L.; Villas-Boas, R.; de Mello, W.; et al. Genetic susceptibility in chronic periodontitis: A systematic review. Journal of Periodontology 2015, 86, 99–111. 9. Petrin, A.N.; Tsarev, V.N. Cytokine gene polymorphisms in inflammatory diseases: Clinical significance. Infection and Immunity 2011, 79, 3381–3389. 10. Gulmukhamedov, P.B. Clinical and molecular-genetic aspects of periodontitis pathogenesis. PhD Thesis Abstract, Tashkent State Dental Institute, Tashkent, Uzbekistan, 2019. 11. Hasanov, L.E.; Abdullaeva, N.R.; Mirkhoshimova, M.F. Genetic markers of periodontal inflammation in Central Asian populations. Stomatologiya 2017, 1, 15–19. 12. Safarov, M.T.; Dadabaeva, M.U.; Asemova, S.A.; et al. Modern aspects of mathematic modeling in dental implantation. Science and Education: Problems and Prospects 2020, 354–359. 13. Xabilov, N.L.; Xabilov, B.N.; Sharipov, S.S.; et al. Plant-based complexes in dentistry. Journal of New Century Innovations 2024, 66, 203–209. 14. World Health Organization. Oral health fact sheet. WHO, Geneva, Switzerland, 2012. Available online: https://www.who.int (accessed on Day Month Year).