Mice Lacking the Calcitonin Receptor Do Not Display Improved Bone Healing.

ABSTRACT: Despite significant advances in surgical techniques, treatment options for impaired bone healing are still limited. Inadequate bone regeneration is not only associated with pain, prolonged immobilization and often multiple revision surgeries, but also with high socioeconomic costs, underlining the importance of a detailed understanding of the bone healing process. In this regard, we previously showed that mice lacking the calcitonin receptor (CTR) display increased bone formation mediated through the increased osteoclastic secretion of sphingosine-1-phosphate (S1P), an osteoanabolic molecule promoting osteoblast function. Although strong evidence is now available for the crucial role of osteoclast-to-osteoblast coupling in normal bone hemostasis, the relevance of this paracrine crosstalk d

SUBMITTER: Appelt J 

PROVIDER: S-EPMC8471896 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature