Parathyroid hormone (PTH) has been used as a potent bone forming agent in the treatment of osteoporosis, and has been suggested to promote bone repair after fracture. We recently demonstrated that Tmem119, a crucial molecule for osteoblastic bone formation, participated in the bone anabolic effects of PTH through the stimulation of osteoblastic bone formation in mice. Therefore, we herein investigated the roles of Tmem119 in PTH-enhanced bone repair after a femoral bone defect using Tmem119-deficient female mice. Tmem119 deficiency significantly inhibited PTH-enhanced bone repair 7 days after the femoral bone defect. Tmem119 deficiency also significantly attenuated PTH-induced increases in the number of alkaline phosphatase-positive cells at damaged sites 7 days after the femoral bone defect. Moreover, Tmem119 deficiency seemed to suppress PTH-enhanced CD31- and endomucin-double positive type H vessel formation at damaged sites 7 days after the femoral bone defect in female mice without statistically significant differences. The present results indicate that Tmem119 is involved in PTH-enhanced bone repair after a femoral bone defect in female mice partly through the promotion of osteoblastic osteogenesis.
Yamada et al. (Mon,) studied this question.