Abstract
OBJECTIVES: This study aims to explore the mechanism of carvacrol (CV) in regulating alveolar bone repair in periodontal disease. METHODS: A rat model of periodontal disease (P group) was created by ligating the first molar and injecting lipopolysaccharide (LPS). A control model (C group) was also created. The treatment models received low (L group), medium (M group), and high (H group) doses of CV hydrogel. Hematoxylin-eosin (HE) staining was used to observe the pathological changes in periodontal tissues. Immunohistochemical staining was employed to analyze the expression of collagen typeⅠ(COL1) and Runt-related transcription factor 2 (Runx2). In vitro, the rat osteoblast cells were divided into C, P, L, M, H, CV and CV+LY294002 (CV+LY) groups. Western blot analysis detected the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase 3 beta (GSK-3β) pathway-related and osteoblastic proteins. Quantitative reverse-transcription po-lymerase chain reaction was used to measure the expression of inflammatory factors and osteoblastic proteins. The alkaline phosphatase (ALP) colorimetric kit and alizarin red S staining kit were utilized to assess osteogenic ability. Immunofluorescence (IF) was used to detect COL1 expression in osteoblasts. Transmission electron microscopy was applied to detect cell apoptosis. RESULTS: CV hydrogel alleviated periodontal symptoms, upregulated PI3K/AKT/GSK-3β pathway-related and osteoblastic proteins, and increased the expression of ALP and the number of calcified nodules. However, it decreased cell apoptosis and inflammatory factors. LY294002 inhibited the PI3K/AKT pathway and decreased osteoblastic protein expression, ALP coloration, and calcified nodule quantity. CONCLUSIONS: CV hydrogel promotes the proliferation and differentiation of alveolar bone osteoblasts by activating the PI3K pathway and inhibiting inflammation-induced bone resorption. This study emphasizes the potential of CV for the treatment of periodontal diseases.