CD226 Deficiency Attenuates Periodontal Bone Destruction in a Murine Ligature-Induced Periodontitis Model.

Periodontal disease is widely recognised as a chronic infectious-inflammatory disorder, leading to the destruction of alveolar bone. Osteoclasts and their progenitors have been demonstrated to play pivotal roles in the process of periodontitis-induced bone damage. The mechanisms that govern the differentiation of osteoclasts in the context of periodontitis remain to be elucidated. In this study, we assessed the expression of CD226 on osteoclasts and their progenitors, as well as the function of CD226 in experimental periodontitis mice. Periodontitis was induced in C57BL/6 wild-type and CD226 knockout (CD226-KO) mice. Micro-CT was used to analyse bone loss. Haematoxylin-eosin (HE) or tartrate-resistant acid phosphatase (TRAP) staining was conducted to examine osteoclast differentiation. Flow cytometric analysis and quantitative real-time PCR (qRT-PCR) were used to identify the expression of CD226 and related molecules. The expression of CD226 on osteoclasts was found to decrease gradually during the process of osteoclastogenesis. In addition, the study revealed that the knockout of CD226 inhibited osteoclast differentiation in vitro. Furthermore, the knockout of CD226 has been demonstrated to attenuate inflammatory responses and alleviate bone damage in a murine periodontitis model. The present study suggests that CD226 plays an important role in regulating the function and differentiation of osteoclasts and their progenitors. The targeting of CD226 has the potential to be developed as a potent therapy for bone loss caused by periodontitis.