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.