The global demographic shift toward aging populations has brought increasing attention to geriatric health challenges. Sarcopenia and osteoporosis, two prevalent geriatric syndromes, manifest as progressive declines in muscle mass and bone mineral density respectively. Epidemiological data indicate a sarcopenia prevalence of 10%–27% among individuals aged ≥60 years (1), while osteoporosis affects 30%–50% of this population (2). Emerging evidence reveals significant pathophysiological intersections and clinical synergies between these conditions, warranting systematic investigation.

From an etiological perspective, shared risk mediators include senescence-associated biological processes, hormonal alterations (particularly in estrogen, androgen, and growth hormone levels), nutritional insufficiencies (notably protein, vitamin D, and calcium deficiencies), chronic low-grade inflammation, and reduced physical activity (3). Clinically, these conditions exhibit bidirectional progression: sarcopenia-induced muscle weakness impairs osteogenic mechanical loading, accelerating bone density loss, while osteoporosis-related pain and fracture risk exacerbate mobility limitations, thereby perpetuating musculoskeletal deterioration.

Despite growing research interest, current understanding remains constrained by methodological heterogeneity across studies. Discrepancies in diagnostic criteria, population characteristics, and assessment protocols have yielded inconsistent findings regarding the magnitude and mechanisms of sarcopenia-osteoporosis associations. This knowledge gap underscores the imperative for rigorous evidence synthesis through systematic review and meta-analysis. Such methodology enables quantification of correlation strength, identification of heterogeneity sources, and elucidation of potential pathophysiological convergences.

This study intends to comprehensively collect studies on the correlation between sarcopenia and osteoporosis in older adults through systematic evaluation and meta-analysis. Literature was strictly screened, data were extracted and quality evaluated from studies that met the inclusion criteria, and meta-analysis was performed using appropriate statistical models, aiming at clarifying the degree of correlation between the two in the elderly population, further exploring their potential common pathogenic mechanisms and influencing factors, and providing a more reliable basis for early clinical diagnosis, prevention and comprehensive treatment, so as to improve the health status and quality of life of the elderly.

This meta-analysis of 14 studies (n = 182,307) provides the first systematic quantification of the sarcopenia-osteoporosis association, demonstrating a 3.16-fold increased osteoporosis risk in sarcopenic individuals compared to controls (OR = 3.16, 95% CI: 2.47–4.02). These findings underscore the pathophysiological synergy between these geriatric syndromes, likely mediated by shared mechanisms including hormonal dysregulation (e.g., IGF-1 deficiency, vitamin D insufficiency) and chronic inflammation (19).

Notably, subgroup analyses revealed sex-specific trends: males showed numerically higher risk (OR = 4.74) compared to females (OR = 3.46), though interaction testing was non-significant (P = 0.23), potentially reflecting estrogen’s protective effects on female bone health. Geographic disparities emerged, with European populations demonstrating numerically higher risk (OR = 4.74) than other subgroups (P = 0.07), possibly due to genetic predispositions and lifestyle factors (e.g., protein intake patterns). Community-dwelling individuals also exhibited greater osteoporosis risk (OR = 3.41) compared to inpatients (OR = 2.85) and outpatients (OR = 2.07), which may reflect earlier-stage sarcopenia where compensatory mechanisms preserve muscle function but fail to maintain bone integrity.

Based on our findings, we recommend that sarcopenia screening should be integrated into osteoporosis risk assessments. Since sarcopenia is significantly associated with an increased risk of osteoporosis, early identification of sarcopenia can help clinicians identify patients at high risk of osteoporosis. This can enable timely interventions such as exercise programs, nutritional supplements, and lifestyle modifications to prevent or delay the development of osteoporosis. Clinicians should also be aware of the differences in risk among different populations (such as gender, geographical regions) when assessing osteoporosis risk.

Importantly, consistent risk estimates across diagnostic criteria (e.g., EWGSOP vs. AWGS) highlight the cross-cultural stability of the muscle-bone density relationship. These findings reinforce the integrative bone-muscle axis, where mechanical loading, endocrine signaling, and paracrine networks coordinate mass homeostasis, and suggest that early sarcopenia intervention may mitigate osteoporosis risk in aging populations.

Sarcopenia and osteoporosis exhibit significant pathophysiological overlap, with accumulating evidence indicating shared regulatory pathways and bidirectional interactions (20). As integral components of the locomotor system, bone and muscle demonstrate coordinated mass changes across the lifespan, orchestrated by a triad of mechanical loading, endocrine regulation, and paracrine signaling networks (21). Notably, exercise deprivation, disuse atrophy, and aging-induced catabolism trigger synchronous bone-muscle degeneration, as posited by the Mechanical Homeostasis Theory, where reduced mechanical stimuli disrupt bone anabolic processes, leading to microarchitectural deterioration (22, 23). Within this framework, skeletal muscle serves as the primary transducer of mechanical loading, providing critical anabolic signals for bone maintenance.

While mechanical coupling is well-established, the systemic mechanisms governing bone-muscle mass equilibrium remain incompletely understood. Emerging evidence highlights secreted factors as key mediators: signaling molecules including myostatin, activin, and pro-inflammatory cytokines reciprocally regulate bone and muscle metabolism (24, 25). Skeletal muscle has recently been redefined as an endocrine organ, secreting myokines that not only modulate glucose metabolism but also form regulatory networks with osteokines, providing novel insights into integrated bone-muscle physiology.

At the molecular level, the Wnt/β-catenin signaling pathway emerges as a dual regulator, governing both bone mass homeostasis and skeletal muscle development (25). Osteocyte-derived sclerostin (encoded by SOST), a potent Wnt antagonist, acts as a pivotal node in this cross-talk, suggesting osteocytes establish biochemical dialogues with muscle tissues through secreted factors.

In summary, sarcopenia confers a significant osteoporosis risk, emphasizing the need for integrated screening strategies. Future longitudinal studies are required to clarify causal relationships and identify novel therapeutic targets within the bone-muscle metabolic axis.

In conclusion, sarcopenia is associated with an increased risk of osteoporosis, and early prevention of osteoporosis may focus on better identification and prevention of sarcopenia. In the future, more high-quality longitudinal studies are needed to provide insight into the correlation and potential mechanisms between sarcopenia and osteoporosis.