What impact does Hyperparathyroidism have on bone mineral density (BMD)?

What impact does Hyperparathyroidism have on bone mineral density (BMD)?

• A. Increases BMD in cortical bone
• B. Decreases BMD in more cortical bone
• C. No impact on BMD
• D. Primarily affects trabecular bone density

Answer: (B)

Hyperparathyroidism significantly influences bone mineral density (BMD) primarily through its effects on the skeletal system. In cases of hyperparathyroidism, there is an overproduction of parathyroid hormone (PTH), which leads to increased osteoclastic activity, subsequently resulting in bone resorption. This process typically causes a decrease in bone density, particularly impacting more cortical bone structures. Cortical bone is dense and forms the outer shell of long bones, while trabecular bone is more spongy and located within the interior of bones. The excessive resorption associated with hyperparathyroidism can manifest substantially in cortical areas, where the density tends to decrease more prominently compared to trabecular bone. Thus, the statement indicating that hyperparathyroidism decreases BMD specifically in more cortical bone accurately reflects the pathophysiological effects of elevated PTH levels. While trabecular bone is indeed affected, the more pronounced impact of hyperparathyroidism is observed in the cortical bone, making the choice that emphasizes this decrease in cortical density the most appropriate response.

Hyperparathyroidism significantly influences bone mineral density (BMD) primarily through its effects on the skeletal system. In cases of hyperparathyroidism, there is an overproduction of parathyroid hormone (PTH), which leads to increased osteoclastic activity, subsequently resulting in bone resorption. This process typically causes a decrease in bone density, particularly impacting more cortical bone structures.

Cortical bone is dense and forms the outer shell of long bones, while trabecular bone is more spongy and located within the interior of bones. The excessive resorption associated with hyperparathyroidism can manifest substantially in cortical areas, where the density tends to decrease more prominently compared to trabecular bone. Thus, the statement indicating that hyperparathyroidism decreases BMD specifically in more cortical bone accurately reflects the pathophysiological effects of elevated PTH levels.

While trabecular bone is indeed affected, the more pronounced impact of hyperparathyroidism is observed in the cortical bone, making the choice that emphasizes this decrease in cortical density the most appropriate response.