Metabolic bone disease articles from across Nature Portfolio

The skeleton is a metabolically active organ, with bone formation and maintenance relying on highly anabolic, nutrient-consuming processes. Here, the authors describe the current understanding of fuel selection and intermediary metabolic pathways in bone cells during bone formation and discuss how metabolic dysfunction can contribute to skeletal disease.

In this Evidence-Based Guideline article, an international multidisciplinary working group of the European Society for Clinical and Economic Aspects of Osteoporosis, Osteoarthritis and Musculoskeletal Diseases presents recommendations for the diagnosis, monitoring and treatment of osteoporosis in men.

Bone resorption by osteoclasts requires tight control, as overactivation reduces bone mass and strength. Stegen et al. demonstrate that α-ketoglutarate produced during serine synthesis promotes osteoclast development via metabolic–epigenetic coupling and could be a therapeutic target.

New research shows that deficiency of the sulfation-related SLC26A2 affects osteocyte formation, and that targeting downstream mediators can ameliorate SLC26A2-deficient osteoporosis.

Nanoparticles consisting of long DNA molecules in association with Ca²⁺ and PPi⁴⁻ ions can modulate the pathological osteoporotic microenvironment and promote bone repair.

Magnesium ascorbyl phosphate is a stable derivative of ascorbic acid that has now been shown to promote bone formation via stimulation of the CAMKIIα pathway.