Sarcopenia is a progressive skeletal muscle disorder characterised by reduced muscle strength, impaired muscle quantity or quality, and declining physical performance, with important consequences for falls, fractures, disability, and loss of independence. Whether sarcopenia prevalence itself is rising remains difficult to quantify because diagnostic frameworks and surveillance methods vary, yet a growing burden is plausible. Population ageing, increasing multimorbidity, obesity, hospitalisation, surgery, and incomplete recovery after musculoskeletal events are likely to increase the absolute number of people living with low musculoskeletal reserve. Osteoarthritis (OA) and osteoporosis (OP) are central to this problem because they amplify the functional consequences of weakness and reduced loading. OA may lead to strength loss through pain, inflammation, altered movement, and activity restriction, while OP increases the likelihood that falls or loading errors will result in fracture and subsequent deconditioning. Shared mechanisms for sarcopenia include mechanical unloading, adiposity-related metabolic dysfunction, inflammageing, mitochondrial stress, endocrine change, and nutritional insufficiency, although the strength of evidence differs across pathways. New weight-loss approaches using glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may substantially affect sarcopenia risk and therefore require careful consideration. Current diagnostic frameworks increasingly prioritise muscle strength and performance over lean mass alone, supporting pragmatic case-finding in older adults with severe OA, fragility fracture, recurrent falls, poor postoperative recovery, or weight loss. Current management should focus on progressive resistance and balance training, adequate energy and protein intake, guideline-based OP care, optimised OA treatment, and protection of mobility during transitions of care. The most immediate clinical gains are likely to come from integrating existing rheumatology, orthopaedic, fracture-prevention, rehabilitation, and nutritional services rather than from any osteosarcopenia-specific drug therapy.
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Pan et al. (2026) studied this question.
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