Osteoporosis can result from an imbalance between osteoblasts, which are bone-forming cells, and osteoclasts, which are bone-resorbing cells. An increase in the activity of osteoclasts, often influenced by elevated levels of parathyroid hormone (PTH) or glucocorticoids, can lead to excessive bone resorption. Additionally, decreased levels of estrogen after menopause can reduce osteoblast activity, further contributing to bone loss. This hormonal imbalance ultimately weakens bone density and increases the risk of fractures.
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