**11. Conclusion**

A number of medications we use on a daily basis can negatively affect bone health and lead to bone loss. Collagen and other organic compounds of the matrix may also be affected, as well as mineral density, trabecular structure, and hydroxyapatite. Additionally, cellular turnover may be affected, leading to an imbalance between bone formation and resorption as well as between organic and inorganic matrix composition. Consequently, the biomechanical ability of bone is diminished, resulting in decreased bone density and an increased risk of fracture. Additionally, even in the presence of normal bone biomechanical competence, some drugs may increase the risk of falls and fractures.

A variety of drugs may cause bone loss by: 1. Lowering estrogen levels (e.g., aromatase inhibitors used in breast cancer, GnRH agonists used in prostate cancer). 2. Interfering with vitamin D levels (Enzyme-Inducing Anti-Seizure Medications), EIASM therapy has been proven to cause increased vitamin D metabolism, low vitamin D levels, impaired calcium absorption, and resultant hypocalcemia leading to secondary hyperparathyroidism and increased osteoclastic bone resorption. 3. Directly affecting bone cells (chemotherapy, phenytoin, or thiazolidinediones) which divert mesenchymal stem cells from osteoblastogenesis to adipocytogenesis, consequently, an imbalance occurs between bone formation and resorption, as well as between soft organic matrix and hard inorganic matrix. Besides effects on the mineralized matrix, interactions with collagen and other nonmineralized matrix components can decrease bone biomechanical competence without affecting bone mineral density (BMD). 4. Thyroid dysfunction caused by long-term use of (antiarrhythmic drug amiodarone) that can affect bone health might happen, though as follows: 1- Amiodarone-induced thyrotoxicosis (AIT) or 2- Amiodarone-induced hypothyroidism (AIH). 5. Strong inhibitors of stomach acid secretion (PPIs), which is thought to be important for calcium absorption by enhancing the solubility of calcium salts that are insoluble leading to decreases intestinal calcium absorption, and ultimately causing a decline in bone mineral density. 6. MTX treatment may reduce osteoblastic differentiation, which would then lead to a reduction in bone formation and an increased risk of osteopathy. To clarify the long-term effects of MTX on bone density of both axial and peripheral bones, a longitudinal investigation is consequently required. 7. Patients with IBD are more likely than general population to

experience bone loss due to malnutrition, vitamin D and calcium malabsorption and deficiency, vitamin K insufficiency, immobilization, underlying inflammatory state. 8. High blood pressure is linked to increased urinary calcium loss, which impairs the calcium balance necessary for bone remodeling. Furthermore, high levels of the parathyroid hormone are linked to hypertension and accelerated bone turnover, reducing bone mass and bone quality. Finally, high blood pressure may gradually harm brain regions involved in balance and gait regulation, which could increase the risk of falls and consequent fractures. 9. Psychotropic medications, especially selective serotonin reuptake inhibitors (SSRIs), can increase fracture risk. Gut-derived serotonin reduces osteoblast proliferation, which causes bone loss. 10. Thiazolidinediones (TZDs, Glitazones) enhance insulin sensitivity and beta cell response to a glucose load by acting as agonists of nuclear peroxisome proliferator-activated receptor gamma (PPAR-Ƴ), leading to enhanced adipogenesis and inhibited osteoblastogenesis.
