Abstract
BACKGROUND: Platelet-rich plasma (PRP) is utilized as an autologous blood product to encourage bone regeneration. The receptor activator of nuclear factor-NB ligand (RANKL) is a key and central regulator of osteoclast homeostasis. A rat model of experimentally generated periodontitis was used to assess the impact of PRP preparation on the expression of the osteoclastogenic and pro-inflammatory markers respectively; RANKL and IL-1β. MATERIAL AND METHODS: To induce periodontitis by silk ligature, thirty-six adult male Sprague Dawleys rats were used and they were allocated into three equal groups (n = 12): group I consisted of intact periodontal tissue, group II; rat-induced periodontitis without treatment by PRP, and group III of periodontitis + 10 µL PRP injection. The rats were sacrificed after both experiment durations (7 and 30 days), and the incisor teeth were fixed and decalcified in HCl for a day and in 10 % EDTA solution for eight weeks at room temperature then samples were processed for H&E stain for bone healing scores and bone cells counting, and the samples were utilized by IHC for detection of both RANKL and IL-1β expression. RESULTS: The PRP enhanced the process of healing on days 7 and 30 showed (Score 10) vs. the control positive group that had a delay in alveolar bone regarded as (Score 4) significantly (P ≤ 0.05). The PRP group attenuated significantly (P ≤ 0.05) the alveolar bone loss by increasing the number of osteoblasts and declining the proliferation of osteoclast vs. the control positive group that revealed bone destruction due to rising osteoclast proliferation and decreasing the osteoblast proliferation significantly (P ≤ 0.05). PRP inhibited the IL-1β expression (score = 0) vs. the control positive group that showed moderate staining of positive cells detected in both inflammatory cells and endothelium (score = 4). Regarding the RANKL expression, the PRP reduced its expression in vs. the control positive group (score = 4 vs. 12 respectively). CONCLUSION: PRP is an anabolic agent that enhances proliferation of osteoblast and inhibit the osteoclast differentiation by downregulation of IL-1β and RANKL.