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A GWAS meta-analysis for OPLL identified fourteen significant genomic loci and a subsequent Mendelian randomization study provided genetic evidence for a causal effect of obesity on the pathogenesis of OPLL, especially one of its subtypes, thoracic OPLL.

Identification of bone marrow Adipoq-lineage progenitors as a novel and major cellular source of M-CSF in mice and humans, which controls bone marrow macrophage development, osteoclastogenesis, and bone mass in physiological and pathological conditions.

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.

Endocrine therapy after mastectomy may not be recommended for patients with hormone receptor positive ductal carcinoma in situ, even for those with high-risk factors.

Intracellular and interorgan skeletal crosstalk highlights integrative skeletal physiology.

Mitochondrial Cx43 hemichannels regulate ATP generation by mediating K+, H+, and ATP transfer across the mitochondrial inner membrane and the interaction with mitochondrial ATP synthase, contributing to maintenance of mitochondrial redox and cell protection under oxidative stress.

The targeted removal of legacy bisphosphonate from the jawbone by competitive equilibrium therapy not only elucidated the pathological mechanism of bisphosphonate-related osteonecrosis of the jaw (BRONJ) but also established a highly translatable therapeutic option for BRONJ.

Genetic and biochemical analyses uncover a dichotomy of ERK pathway functions in osteoblasts, whereby ERK activation promotes the early differentiation of osteoblast precursors, but inhibits the subsequent differentiation of committed osteoblasts via mTOR-mediated regulation of mitochondrial function and SGK1.

A mathematical model of osteoporosis explains why the sequence of osteoporosis medications matters for short-term and long-term treatment success.