Osteoporosis

DXA bone density misses many people who go on to fracture, and in some fracture liaison services up to 30% report too little DXA access. This Nature Reviews Rheumatology review, written under a WHO Collaborating Centre, surveys the single-component tools that add to it or stand in for it: heel and pulse-echo ultrasound, REMS, trabecular bone score, finite element analysis, 3D shape modelling from DXA, and AI that reads bone density and vertebral fractures from routine X-rays and CT. Trabecular bone score and REMS are the best established. The harder questions now are validation across populations, calibration, equity of access and whether the tools relieve DXA services.

The British Society for Rheumatology has replaced its 2009 polymyalgia rheumatica guideline with nine overarching principles and eight graded recommendations. They start prednisolone at 12.5–15 mg, give bone protection to everyone, taper faster in people at risk of glucocorticoid toxicity, and add methotrexate or an IL-6 receptor antagonist in selected patients. Rheumatology should be consulted for advice at a first relapse, patients should be referred after a second relapse, and all patients after 18 months of glucocorticoids. Most recommendations rest on moderate or low-certainty evidence.

A common assumption is that controlling RA inflammation with a biologic or targeted synthetic DMARD also protects bone. In 797 Japanese patients followed for a median of 3.1 years, disease activity fell from high to low, yet femoral neck and radius T scores still fell in those not on osteoporosis treatment and held steady in those who were. Duration of b/tsDMARD use and cumulative CDAI did not predict bone maintenance. It is an uncontrolled real-world cohort, so it shows an association, not a cause.

Glucocorticoids remain the leading cause of secondary osteoporosis, and oral steroid use in rheumatic disease has risen over the last twenty years despite steroid-sparing agents. This review covers how quickly bone is lost, why DXA systematically underestimates fracture risk on steroids, how much the underlying rheumatic disease contributes, the steroid-sparing evidence in SLE, GCA, PMR and ANCA vasculitis, and what the trial data actually support.