Abstract:Osteonecrosis of femoral head (ONFH), a kind of bone metabolic disease, is featured by reduced osteogenic activity of osteoblasts (OB), increased osteoclast activity of osteoclasts (OC), decreased bone marrow stromal cells (BMSCs) osteogenic differentiation with enhanced adipogenic differentiation, disrupted vascular endothelial cells, and dropped blood supply, resulting in a negative balance of bone metabolism in the femoral head. ONFH is closely related to the abnormal intercellular communication of bone tissue. Gap junction (GJ) is a membrane channel structure for intercellular communication between adjacent cells, and GJ plays an important regulatory role in substance exchange and signal transduction between bone tissue and cells. Communication of gap junction cell through GJ plays an important role to keep the dynamic balance of bone metabolism. Connexin 43 (Cx43) is an important component of GJ in bone tissue. Therefore, GJ-mediated intercellular communication is closely related to the occurrence of bone metabolic diseases such as ONFH. This paper reviews the research progress of GJ and Cx43 roles in the diseases of glucocorticoids-induced ONFH.
