Background/Objectives: Malnutrition and frailty are independent risk factors of prolonged hospitalization and mortality, respectively. However, the combined association of these conditions with the risk of prolonged hospitalization and mortality in hospitalized elderly patients remains unclear. Our object was to investigate the combined association of malnutrition and frailty on the risk of prolonged hospitalization and mortality in hospitalized elderly patients. Methods: The current study was a retrospective analysis of 470 patients admitted to the geriatric care unit of a tertiary hospital in Taiwan between 01 August 2019 and 31 March 2023. The Mini Nutritional Assessment-short form and Clinical Frailty Scale were used as evaluation tools for nutritional and frailty status, respectively. Patients were divided into four groups based on nutritional and frailty status. The association between these conditions and the risk of prolonged hospitalization and mortality was investigated using multivariate logistic and Cox proportional hazard models and adjusting for potential confounders. Results: Among 470 patients, 144 (31%) exhibited no malnutrition risk or frailty, 146 (31%) exhibited malnutrition risk but no frailty, 46 (10%) exhibited frailty but no malnutrition risk, and 134 (28%) exhibited both malnutrition risk and frailty. Compared to patients with neither condition, those with both conditions had higher risks of prolonged hospitalization (odds ratio 3.23, 95% confidence interval [CI] 1.68–6.12) and mortality (hazard ratio 4.33; 95% CI 2.01–9.34). Conclusion:: The co-occurrence of malnutrition and frailty has significant detrimental impacts on the risk of prolonged hospitalization and mortality in hospitalized older adults. The findings of this study emphasize the importance of early screening and intervention for malnutrition and frailty among hospitalized elderly patients.

Osteoporosis is a prevalent metabolic bone disorder characterized by reduced bone mass, compromised microarchitecture, and increased fracture risk. Its pathogenesis extends beyond simple bone mineral density (BMD) loss and reflects complex disruptions in bone remodeling governed by osteoblast–osteoclast coupling and systemic metabolic factors. This review lays particular emphasis on diabetes mellitus-related osteoporosis (DOP) and estrogen deficiency-induced osteoporosis (EDOP), discussing bone remodeling between osteoclastogenesis and osteoblast differentiation regulated by key signaling pathways, including the RANKL/RANK/OPG, Wnt/β-catenin, BMP–Smad, Hedgehog, and inflammatory cytokine networks. This review then explores how chronic hyperglycemia, insulin deficiency or resistance, oxidative stress, ferroptosis, advanced glycation end products, and low-grade inflammation disrupt bone homeostasis in diabetes, resulting in impaired bone quality and elevated fracture risk, particularly in type 2 diabetes. In parallel, we discuss the genomic and non-genomic actions of estrogen in maintaining skeletal integrity and elucidate how estrogen deficiency accelerates bone resorption and suppresses bone formation through altered cytokine signaling, oxidative stress, and impaired mechanotransduction. Advances in diagnostic strategies beyond BMD, including trabecular bone score, high-resolution peripheral quantitative computed tomography, and emerging biomarkers, are reviewed. Finally, this review summarizes current and emerging therapeutic approaches tailored to DOP and EDOP, emphasizing the need for mechanism-based, individualized management. A deeper understanding of these shared and distinct pathways may facilitate improved risk stratification and the development of targeted interventions for osteoporosis.