关键词: 雷公藤甲素, 具核梭杆菌, 牙周炎, 牙槽骨吸收

Abstract:

Objective To investigate the effects of triptolide on the secretion of inflammatory factors and alveolar bone resorption in rats with Fusobacterium nucleatum-related periodontitis, as well as its underlying mechanism. Methods Eighteen 6-week-old male SD rats were selected for periodontal ligation and randomly divided into three groups based on whether they were infected with Fusobacterium nucleatum and received triptolide gingival sulcus injection: The simple periodontal ligation control group (LC group), the periodontal ligation + Fusobacterium nucleatum group (FN group), and the periodontal ligation + Fusobacterium nucleatum + 30 μg/kg triptolide group (TPL group). The levels of liver and kidney function indicators in serum, including creatinine (Cr), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and blood urea nitrogen (BUN), were measured. The sulcus bleeding index (SBI) and probing depth (PD) of the upper left first molar in rats were recorded. Micro-CT was used to analyze the degree of alveolar bone resorption. Hematoxylin-eosin (HE) staining was employed to evaluate the inflammatory status of gingival tissue. Immunohistochemical staining was performed to detect the expression of interleukin-6 (IL-6), receptor activator of nuclear factor-κB ligand (RANKL), tumor necrosis factor-α (TNF-α), and osteoclastogenesis inhibitory factor (OPG). Alizarin red S staining and tartrate-resistant acid phosphatase (TRAP) staining were used to detect the precentage of alizarin red S-positive area and the number of osteoclasts in alveolar bone tissue, respectively. Results Gingival sulcus injection of 30 μg/kg triptolide had no significant impact on liver and kidney function-related indicators in rats. Compared with the LC group, the inflammatory response of periodontitis in the FN group was significantly aggravated, with significantly increased SBI, PD, the number of inflammatory cells and osteoclasts, the distance from the cementoenamel junction (CEJ) to the alveolar bone crest (ABC) (CEJ-ABC), and the levels of IL-6, TNF-α, and RANKL in gingival tissue (P<0.05). In contrast, the bone mineral density (BMD) and trabecular thickness (Tb.Th) of alveolar bone, the level of OPG in gingival tissue, and the percentage of alizarin red S-positive area were significantly decreased (P<0.01). Compared with the FN group, the TPL group exhibited reduced gingival inflammation, with significantly decreased SBI, PD, CEJ-ABC of alveolar bone, the number of inflammatory cells and osteoclasts, and the levels of IL-6, TNF-α, and RANKL in gingival tissue (P<0.05). Conversely, the BMD and Tb.Th of alveolar bone, the level of OPG in gingival tissue, and the percentage of alizarin red S-positive area were significantly increased (P<0.01). Conclusion Triptolide alleviates the inflammatory response in periodontal tissues and reduces alveolar bone resorption in rats with Fusobacterium nucleatum-related periodontitis by inhibiting the secretion of inflammatory cytokines and the formation of osteoclasts.

Key words: triptolide, Fusobacterium nucleatum, periodontitis, alveolar bone resorption