GENETIC POLYMORPHISMS OF IL-1Β AND TNF-Α AS PREDICTORS OF PERIODONTAL DISEASE SEVERITY FOLLOWING NON-SURGICAL PERIODONTAL THERAPY

Abstract

Background: Periodontitis is a multifactorial inflammatory disease in which the host immune response plays an important role in determining the extent of periodontal tissue destruction and treatment response. Pro inflammatory cytokines such as interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) are involved in periodontal inflammation, connective-tissue breakdown, and alveolar bone resorption. Genetic polymorphisms affecting these cytokines may contribute to inter-individual differences in disease severity and response to periodontal therapy. Aim:To evaluate the association of selected IL-1β and TNF-α genetic polymorphisms with periodontal disease severity and clinical response following non-surgical periodontal therapy (NSPT). Materials and Methods: A prospective clinical observational study was conducted among 100 participants diagnosed with periodontitis. Clinical periodontal parameters, including plaque index (PI), gingival index (GI), probing pocket depth (PPD), clinical attachment level (CAL), and bleeding on probing (BOP), were recorded at baseline and 3 months following NSPT. Genomic DNA was obtained from biological samples and analyzed for selected IL-1β and TNF-α polymorphisms using a validated genotyping technique. Participants were categorized according to genotype and periodontal treatment response. Statistical analyses were performed to assess associations between genetic polymorphisms, periodontal severity, and treatment outcomes, with statistical significance established at p < 0.05. Results:The IL-1β genotype distribution consisted of 46% wild-type, 41% heterozygous, and 13% homozygous variant genotypes, whereas TNF-α genotypes comprised 52% wild-type, 37% heterozygous, and 11% homozygous variant genotypes. IL-1β variant-allele carriers demonstrated significantly greater baseline PPD (5.48 ± 0.79 mm) and CAL (6.02 ± 0.94 mm) than wild-type participants (5.10 ± 0.88 mm and 5.55 ± 1.03 mm, respectively; p = 0.031 and p = 0.028). TNF-α variant-allele carriers also demonstrated higher BOP (73.2 ± 10.6%) and PPD (5.51 ± 0.82 mm) compared with wild-type participants (65.7 ± 12.9% and 5.13 ± 0.87 mm; p = 0.018 and p = 0.026). NSPT significantly improved all clinical parameters at 3 months (p < 0.001). However, IL-1β and TNF-α variant carriers demonstrated significantly smaller reductions in PPD and other clinical parameters. A favorable response was observed in 72% of participants, while 28% demonstrated a limited response. IL-1β variant-allele carriage was associated with increased odds of limited treatment response (OR = 2.47; 95% CI: 1.08–5.64; p = 0.034), as was TNF-α variant-allele carriage (OR = 2.71; 95% CI: 1.14–6.42; p = 0.024). Conclusion: IL-1β and TNF-α genetic polymorphisms may influence periodontal disease severity and the magnitude of clinical response following NSPT. Variant-allele carriers demonstrated greater periodontal destruction at baseline and comparatively poorer treatment outcomes, suggesting that these polymorphisms may represent potential genetic modifiers of periodontal prognosis.