GAS5 is related to osteoporosis by regulating the differentiation of bone marrow stromal cells that acts as a promising treatment target for osteoporosis.

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

Transcriptomic comparison of inflammatory and steady-state osteoclasts reveals differences in their ability to sense their environment, which makes it possible to selectively inhibit inflammatory osteoclastogenesis and reduce bone loss in osteoporosis.

Impaired bone microstructure and bone strength are prominent characteristics of rats with hemizygous E10-16del mutation in PLS3, and treatment with alendronate or teriparatide can improve bone mineral density and bone microstructure of this novel rat model with PLS3-related early-onset osteoporosis.

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.

The lifespan of individuals who suffer from an osteoporotic fracture is reduced by between 1 and 7 years, depending on the location of the fracture and their risk profile, suggesting that their 'Skeletal Age' is higher than their chronological age.

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

rhPTH(1-34) and dimeric ^R25CPTH(1-34) significantly promoted bone regeneration and titanium implant osseointegration in an osteoporotic beagle model.

Peroxiredoxin 5 contributes to the maintenance of bone homeostasis by regulating osteoblast differentiation.

The first-in-class, humanized, epitope-specific FSH-blocking antibody MS-Hu6 is efficacious, durable, and manufacturable, and is therefore poised for further development towards future testing in human trials for osteoporosis, obesity, dyslipidemia and neurodegeneration.