The activation of CB2 enhances bone remodeling in periodontitis.

OBJECTIVES

The cannabinoid receptor 2 (CB2) is implicated in bone metabolism and reconstruction of periodontal tissues. However, its role in bone formation during periodontitis remains to be elucidated. This study aims to explore the impact of CB2 on alveolar bone in periodontitis, as well as the associated signaling pathways.

METHODS

Wild type (WT) and CB2 knockout (Cnr2) mice from the SPF C57BL/6J strain were utilized to establish periodontitis models via stainless steel wire ligation. Micro-CT, hematoxylin and eosin (HE) staining, and tartrate-resistant acid phosphatase (TRAP) staining were employed to assess morphological alterations in the periodontal tissues. Human primary periodontal ligament stem cells (PDLSCs) were obtained by tissue block culture method. Porphyromonas gingivalis lipopolysaccharide (P.g. LPS) was used to suppress PDLSCs. The study evaluated the influence of AM1241 on the osteogenic differentiation of PDLSCs under inflammatory conditions and the role of the ERK1/2 signaling pathway.

RESULTS

The absence of CB2 (Cnr2 knockout, Cnr2) exacerbated gingival inflammation and increased alveolar bone resorption by elevating osteoclast numbers. AM1241 was found to suppress inflammation in PDLSCs and to enhance their osteogenic differentiation under inflammatory conditions. Additionally, AM1241 could activate the ERK1/2 pathway.

CONCLUSIONS

The inhibition of CB2 facilitates osteoclast recruitment and exacerbates periodontitis. CB2 may promote the osteogenic differentiation of PDLSCs by activating ERK1/2 pathway.