LEVELS OF PRO-INFLAMMATORY CYTOKINES IN THE PERIODONTAL COMPLEX OF PARTIALLY EDENTULOUS PATIENTS DEPENDING ON BONE MINERAL DENSITY PRIOR TO DENTAL IMPLANTATION

Abstract

Dental implantation in patients with periodontal diseases is associated with an elevated risk of peri-implant complications. Generalized periodontitis, even in its initial stages (Stages I-II), maintains a persistent immune-inflammatory imbalance within the oral tissues Concurrently, a systemic reduction in bone mineral density (BMD) can further exacerbate local tissue reactivity. Elucidating the combined impact of these comorbid factors on the hyperproduction of pro-inflammatory mediators prior to surgical intervention is a crucial step for predicting and ensuring successful osseointegration. Objective. To investigate the profile of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) in the gingival crevicular fluid and periodontal pockets of partially edentulous patients with Stage I-II generalized periodontitis, depending on their systemic bone mineral density status during the pre-implantation phase. Materials and methods. An open controlled cross-sectional study was conducted. Out of 189 initially screened individuals, 99 patients were enrolled in the final stage. The main group consisted of 69 partially edentulous patients with periodontitis (Subgroup X: 10 individuals with Stage I; Subgroup Y: 59 individuals with Stage II). The control group comprised 30 somatically healthy individuals with an intact periodontium. Systemic bone mineral density was assessed using dual-energy X-ray absorptiometry (DXA). Cytokine concentrations in local fluids were determined via enzyme-linked immunosorbent assay (ELISA) using «Diaclone» reagents. Results. It was established that periodontal inflammation, in the presence of normal BMD, triggers moderate local immunoreactivity, with cytokine levels increasing by 1.4–2.6 times (p<0.01), and a non-significant elevation of TNF-α in Stage I (by 1.2 times, p>0.05). However, subclinical systemic bone loss (osteopenia) was associated with a pronounced exacerbation of local inflammation. A manifest surge in proinflammatory mediators was recorded in these patients: in Stage I periodontitis, IL-1β, IL-6, and TNF-α levels exceeded the control by 2.2–6.4 times, whereas in Stage II, the immune-inflammatory cascade reached an extreme peak, with IL-6 concentrations rising up to 9.1-fold, p<0.01. Conclusion. It has been proven that Stage I-II periodontitis induces a local hyperproduction of pro-inflammatory cytokines (exceeding the norm by 1.8–6.7 times). Concomitant osteopenia is associated with a marked aggravation of this inflammatory cascade, manifested by elevating the concentration of destructive mediators by 2.2–9.1 times. Such pronounced immunological hyperreactivity forms a potentially unfavorable biological profile for further osseointegration, thereby dictating the necessity for mandatory BMD screening and justifies the feasibility of developing algorithms for pharmacological preparation prior to dental implantation