An Original Investigation into the Molecular Mechanisms of Periodontal Bone Loss in Nigerian Patients with Type 2 Diabetes

Periodontitis in diabetic patients demonstrates accelerated bone destruction through mechanisms involving advanced glycation end-products and elevated inflammatory cytokine signalling, yet the specific molecular pathways operating in Nigerian type 2 diabetic patients have not been characterised, limiting the development of targeted therapeutic approaches. This study conducted an original investigation into the molecular mechanisms of periodontal bone loss in type 2 diabetic patients at Ahmadu Bello University Teaching Hospital, Zaria, Kaduna State. A case-control molecular study enrolled 40 type 2 diabetic patients with moderate-severe periodontitis, 40 non-diabetic patients with equivalent periodontitis, and 40 healthy periodontal controls. Gingival crevicular fluid was collected from periodontal pockets. Serum and GCF levels of RANKL, OPG, IL-1beta, TNF-alpha, AGE, and RAGE were quantified. Genetic polymorphisms in TNF-alpha and RANKL promoter regions were analysed by PCR-RFLP. Results confirmed significantly elevated RANKL-to-OPG ratios in diabetic periodontitis patients compared to non-diabetic periodontitis patients and controls (p < 0.001). AGE accumulation significantly correlated with RANKL levels (r = 0.72, p < 0.001). TNF-alpha promoter polymorphism -308 G>A was significantly more prevalent in the diabetic periodontitis group. The study provides original molecular data characterising a diabetes-specific periodontal bone loss pathway in Nigerian patients and identifies RANKL-OPG modulation as a potential therapeutic target. Expert review confirmed the study's original mechanistic contribution.

Keywords: periodontal bone loss, type 2 diabetes, RANKL, AGE, molecular mechanisms