Effects of initial periodontal treatment on heat shock protein 90 and Interleukin-1β levels in gingival crevicular fluid of stage III periodontitis patients

Abstract

Aim: This study aimed to evaluate the effect of phase I periodontal therapy on interleukin-1β (IL-1β) and heat shock protein 90 (HSP90) levels in gingival crevicular fluid (GCF) of patients with stage III, grade C periodontitis.

Materials and methods: Nineteen systemically and periodontally healthy individuals and nineteen patients with stage III, grade C periodontitis were enrolled. Clinical parameters including plaque index (PI), gingival index (GI), probing depth (PD), bleeding on probing (BOP), and clinical attachment level (CAL) were recorded. Three site-specific GCF samples (shallow, moderate, and deep pockets) were collected from maxillary anterior teeth of periodontitis patients. IL-1β and HSP90 levels were quantified using enzyme-linked immunosorbent assay (ELISA). Clinical measurements and GCF samples were obtained at baseline and 6 weeks after baseline following initial periodontal therapy.

Results: Periodontal therapy significantly improved clinical parameters and reduced GCF IL-1β and HSP90 levels (p < 0.05). Baseline HSP90 levels were significantly higher in moderate and deep pockets compared with healthy controls (p < 0.05). HSP90 levels in deep pockets remained significantly higher than in shallow pockets both before and after treatment (p < 0.05). A positive correlation was found between PD and IL-1β levels in moderate pockets prior to treatment (p < 0.05), and between CAL and HSP90 levels in moderate pockets both before and after treatment (p < 0.05).

Conclusion: Within the limitations of this study, GCF IL-1β and HSP90 levels were elevated in patients with stage III, grade C periodontitis compared with healthy controls, but decreased following periodontal treatment in parallel with clinical improvements. Further studies are warranted to elucidate the role of HSP90 and other heat shock proteins in periodontal disease activity and pathogenesis.