The regulation of bone homeostasis by the exercise-induced myokine irisin is in part potentiated by a direct action on osteoclast differentiation and resorption.

Simultaneous inhibition of two distinct kinase targets stimulates bone formation without concurrently increasing bone resorption, therefore representing a promising new treatment strategy for osteoporosis.

In vitro and in vivo studies highlight the dual regulatory effects that 7,8-dihydroxyflavone exerts on bone formation and resorption.

High-resolution multiphoton microscopy reveals coupling of blood vessel subtype with expanding osteoblasts at the bone regeneration interface, further highlighting the heterogeneity of oxygen microenvironment and its impact on cellular energy metabolism of bone and vessel forming cells.

The loss of miRNA-27a stimulates osteoclast-mediated bone resorption but does not affect osteoblast-mediated bone formation, leading to the development of osteoporosis in mice.

A mechanism is proposed that allows investigators to study interventions to delay onset of heart disease in patients suffering from chronic inflammatory disease with bone loss.

Transferrin receptor 1-mediated iron uptake plays a pivotal role in osteoclast energy metabolism and cytoskeleton and regulates bone remodeling in female mice.

MMnet is a conserved, trans-regulated gene network that controls skeletal homeostasis through osteoclast multinucleation and bone resorptive function.

Multiple levels of gene regulation in the TGFβ signaling pathway mediate the expression of Mmp13, establish species-specific domains of bone resorption, and likely generate evolutionary variation in jaw length.