Iron dysregulation, ferroptosis, and oxidative stress in diabetic osteoporosis: Mechanisms, bone metabolism disruption, and therapeutic strategies

Table 4 Current treatment strategies and future research directions

Treatment strategy/research direction	Mechanism of action	Clinical effect	Challenges and prospects
Bisphosphonates	Inhibit osteoclast activity, reduce bone resorption	Increase bone density, reduce fracture risk	Long-term use may lead to side effects such as osteonecrosis of the jaw; risks need to be balanced
Calcitonin	Inhibit osteoclasts, promote osteoblast activity	Relieve bone pain, increase bone density	Limited efficacy; long-term use may lead to drug resistance
Selective estrogen receptor modulators	Mimic estrogen effects, reduce bone resorption	Increase bone density, lower risk of spinal fractures	May increase risk of thrombosis; use with caution
Choice of anti-diabetic drugs	Different drugs have varying impacts on bone metabolism	Metformin may benefit bone health; thiazolidinediones may increase fracture risk	Need to select appropriate medications based on the patient's specific condition
Vitamin D and calcium supplementation	Provide raw materials for bone mineralization, promote calcium absorption	Improve bone density, prevent osteoporosis	Excessive supplementation may lead to hypercalcemia; dosage needs monitoring
New anti-osteoporosis drugs	Agents like denosumab inhibit RANKL, reducing osteoclast formation	Significantly increase bone density, reduce fracture risk	Long-term safety requires further research
Personalized treatment strategies	Develop comprehensive plans based on the patient's specific situation	Improve treatment effectiveness, reduce side effects	Requires multidisciplinary collaboration to formulate individualized plans
Traditional Chinese medicine therapy	Improve bone metabolism through multi-target regulation	Some herbal medicines show potential to enhance bone density	Lack of large-scale clinical research data; further validation needed
Gene therapy	Target specific genes to regulate bone metabolism pathways	Potentially curative treatment method	Technology is not yet mature; ethical and safety issues need to be addressed
Stem cell therapy	Use stem cells to differentiate into osteoblasts and repair bone tissue	Animal studies show some efficacy	Clinical application is still in early stages; more research is necessary

Bisphosphonates: Commonly used for treating osteoporosis by inhibiting osteoclast activity and reducing bone resorption; Calcitonin: A hormone-based medication that inhibits osteoclasts and promotes osteoblast activity; Gene therapy: Targets specific genes to regulate bone metabolism pathways; however, the technology remains immature; Personalized treatment strategies: Develop comprehensive treatment plans based on the patient's specific conditions to enhance effectiveness and reduce side effects; SERMs: Selective Estrogen Receptor Modulators, mimic estrogen effects to reduce bone resorption but may increase the risk of thrombosis; Stem cell therapy: Uses stem cells to differentiate into osteoblasts for bone tissue repair, though clinical applications are still in early stages; Traditional Chinese medicine therapy: Improves bone metabolism through multi-target regulation but lacks large-scale clinical research data; Vitamin D and calcium supplementation: Provide essential materials for bone mineralization, though excessive supplementation may lead to hypercalcemia; Choice of anti-diabetic drugs: Different anti-diabetic medications have varying effects on bone metabolism and should be selected based on the patient's specific needs; New anti-osteoporosis drugs: For example, denosumab reduces osteoclast formation by inhibiting receptor activator of nuclear factor-κB ligand; RANKL: Receptor activator of nuclear factor-κB ligand.