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Osteoblasts are one of the three cell types found in vertebrate bones. Osteoblasts synthesise the bone collagen matrix of the bone and also participate in matrix mineralisation, which provides strength. When osteoblasts are trapped into the matrix, they become osteocytes. While it is formed by osteoblasts, the bond matrix is degraded by osteoclasts.
Bone remodeling involves a switch between bone formation and resorption, but the mechanisms is unclear. Here, the authors show that intercellular communication via extracellular vesicles secreted by mature osteoblasts is a key factor for the switching, via a microRNA-mediated mechanism.
SP7 is a transcription factor required for osteoblast differentiation and bone formation. A neomorphic mutation in SP7 was found to alter DNA binding specificity, causing a complex skeletal disorder in both mice and humans.
Blood vessels perform vital roles in the skeletal system during development and homeostasis, and both participate in and are affected by inflammation. In this Review, the authors highlight the roles of endothelial cells during bone development, homeostasis and disease.
Genetic association signals for fractures have been reported at the RSPO3 locus, but the causal gene and the underlying mechanism are unknown. Here, the authors show that RSPO3 exerts an important role for vertebral trabecular bone mass and bone strength in mice and fracture risk in humans.
Activation of osteogenic cells is essential for bone regeneration. Here, the authors screen a peptide library and identify 2 compounds that promote osteogenic progenitor cell differentiation in vitro, and show that they increase bone formation and fracture repair in mice.
As the search for new faculty begins across many chemistry departments, Bruce Gibb takes the opportunity to assess his potential biases — and discusses how to address them.
