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Metabolic dysfunction-associated fatty liver disease (MAFLD), as redefined by international consensus in 2020,1 represents a paradigm shift in hepatology. By moving away from a diagnosis of exclusion and instead anchoring the definition in metabolic dysfunction, MAFLD is now recognized as a systemic disorder with multisystem consequences. This reconceptualization has expanded clinical attention beyond hepatic steatosis and fibrosis to include extrahepatic complications such as cardiovascular disease, chronic kidney disease, and malignancy. Increasingly, skeletal health has emerged as another important, yet underappreciated, domain affected by metabolic liver disease. Osteoporosis, characterized by reduced bone mineral density (BMD) and increased fracture risk, may represent a hidden fragility within the MAFLD population, particularly among individuals who do not appear overtly obese. There is growing evidence that supports a connection between MAFLD and osteoporosis. Wang et al.2 demonstrated that patients with lean or normal-weight MAFLD (body mass index [BMI] <23 kg/m2 in an Asian cohort) had a significantly higher risk of osteoporosis compared with metabolically healthy controls. This observation is particularly compelling because it challenges the traditional perception that skeletal risk in fatty liver disease is primarily driven by obesity. Earlier investigations conducted during the nonalcoholic fatty liver disease (NAFLD) era similarly reported increased osteoporotic fracture rates among affected individuals.3 Population-based data further indicated that metabolic comorbidities commonly accompanying fatty liver disease, including diabetes and hypertension, independently increased osteoporosis risk.4 A comprehensive meta-analysis reinforced the complex and clinically relevant association between fatty liver disease and skeletal fragility.5 Taken together, these findings indicate that the metabolic abnormalities associated with MAFLD may disrupt bone remodeling processes, either directly or indirectly, increasing the risk of fractures. BMI serves as a critical factor in modulating the relationship between MAFLD and osteoporosis. The aforementioned study2 elucidated that higher BMI was associated with a lower prevalence of osteoporosis among patients with MAFLD. This apparent protective effect may reflect the mechanical loading advantage conferred by greater body mass, which can stimulate osteoblastic activity and preserve BMD. However, obesity exerts heterogeneous effects on bone. Although increased weight may enhance bone density, it is also associated with insulin resistance, chronic low-grade inflammation, and endocrine alterations, all of which can compromise bone health.6 Moreover, excess adiposity may increase fall risk and contribute to sarcopenic obesity, further complicating fracture outcomes. Thus, understanding of BMI's dual effects on bone health within the context of MAFLD is essential for developing effective management strategies. Therefore, it is crucial to understand how BMI has both positive and negative effects on bone health in the context of MAFLD when developing effective management strategies. Age and sex further influence the interplay between MAFLD and osteoporosis. Osteoporosis prevalence increases with older age, particularly among postmenopausal women who experience accelerated bone loss due to estrogen deficiency.7 Concurrently, older age has been identified as an independent risk factor for developing the lean MAFLD,8 amplifying the likelihood that older adults will experience overlapping hepatic and skeletal risks. Recent data2 indicate that male patients with MAFLD have a lower prevalence of osteoporosis compared with females, consistent with established sex differences in bone density and fracture incidence. Hormonal regulation, body composition, and inflammatory responses likely contribute to these disparities. In postmenopausal women, declining estrogen levels may exacerbate the adverse skeletal effects of metabolic inflammation. Although men generally experience a more gradual decline in BMD, metabolic disturbances associated with MAFLD may still meaningfully elevate fracture risk, particularly in the presence of additional comorbidities. These observations highlight the importance of age- and sex-specific risk stratification strategies in clinical practice. The relationship between MAFLD and osteoporosis is likely mediated by several interrelated biological mechanisms. Chronic inflammation, a hallmark of MAFLD, has been implicated in the dysregulation of bone metabolism. Proinflammatory cytokines promote osteoclastogenesis and inhibit osteoblast differentiation, leading to net bone resorption and declining BMD.9 In MAFLD, persistent inflammatory signaling may intensify skeletal remodeling imbalance and accelerate fragility. Endocrine factors also play a significant role. Vitamin D is essential for calcium absorption and bone mineralization, and deficiency is frequently observed in chronic liver disease. Impaired hepatic metabolism may influence vitamin D activation and bioavailability, thereby contributing to skeletal deterioration.10 Moreover, emerging evidence suggests that alterations in the gut microbiome may also influence the relationship between MAFLD and osteoporosis. Dysbiosis, characterized by alterations in intestinal microbiota composition, is commonly observed in MAFLD and may promote increased intestinal permeability and systemic inflammation.9 These changes can influence both hepatic steatosis and bone remodeling. Although mechanistic studies remain preliminary, the gut–liver–bone axis represents a promising framework for future translational research aimed at clarifying how metabolic liver disease affects bone health. The clinical implications of these findings are substantial. Bone health assessment should be integrated into the comprehensive management of MAFLD, particularly for lean or normal-weight individuals who may otherwise be perceived as lower risk. Consideration of BMD evaluation using dual-energy X-ray absorptiometry (DXA) in selected high-risk patients may facilitate early identification of osteopenia or osteoporosis. Preventive strategies should emphasize lifestyle modification, including adequate intake of calcium and vitamin D, sufficient dietary protein, and regular participation in weight-bearing and resistance exercises. Smoking cessation and moderation of alcohol consumption further benefit both hepatic and skeletal health. Patient education is essential, particularly for older adults and those with metabolic comorbidities, to promote awareness of fracture prevention and long-term monitoring. Pharmacologic therapy may be warranted in patients with established osteoporosis or high fracture risk. Anti-resorptive agents such as bisphosphonates should be considered when appropriate, with careful evaluation of hepatic status and comorbid conditions. An integrated, multidisciplinary approach involving hepatologists, endocrinologists, and primary care physicians is crucial to optimize outcomes. Future research should prioritize clarifying the causal relationship between MAFLD and osteoporosis. Most existing studies are observational and cannot definitively establish causation. Well-designed longitudinal cohorts are needed to track changes in BMD and fracture incidence across diverse MAFLD phenotypes, including lean individuals. Identification of clinical predictors and molecular biomarkers may enable more precise skeletal risk stratification. Randomized trials evaluating vitamin D supplementation, structured exercise interventions, and metabolic therapies could further elucidate modifiable pathways within the gut–liver–bone axis. Additionally, detailed investigation of dietary patterns and physical activity may inform public health strategies aimed at reducing the dual burden of metabolic liver disease and osteoporosis. The association between MAFLD and osteoporosis reflects a complex interplay of metabolic dysregulation, chronic inflammation, and hormonal imbalance. As the global prevalence of MAFLD continues to rise, recognizing its potential impact on skeletal health becomes increasingly important. Lean MAFLD, in particular, represents a hidden clinically significant source of fragility. A holistic approach that integrates bone health evaluation into MAFLD management may improve long-term outcomes and reduce fracture-related morbidity. Continued research will be essential to clarify underlying mechanisms and translate emerging insights into effective, evidence-based clinical practice. The author declares no conflicts of interest. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.