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More informed discussions between physicians and older adults about the consequences of an initial osteoporotic fracture could encourage more patients to consider treatments that protect against future fracture.

The concept of compound fracture risk is redefined to combine the risk that an individual will sustain a fracture and the risk of mortality once the fracture has occurred.

Piezo1 functions as a key mechanotransducer for conferring mechanosensitivity to osteoblasts and determining mechanical-load-dependent bone formation, and represents a novel therapeutic target for treating osteoporosis or unloading-induced severe bone loss.

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.

Def6 functions as a novel immunoregulator in bone cells via endogenous type-I interferon response to regulate bone remodeling.

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

A systematic review and meta-analysis show that calcium supplementation significantly improves bone mass, implying that preventive calcium supplementation in young people (age ≤35 years) may be a shift in the window of intervention for osteoporosis.

miR-335-3p, which targets FOS and inhibits its activation of NFATC1 signaling, is an important regulator for osteoclast function and responsible for the psychological stress-induced osteoporosis.

A C-type lectin domain protein is an anabolic growth factor that promotes mesenchymal progenitors in the bone marrow to differentiate into bone cells to maintain skeletal bone mass throughout adult life.