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This review highlights osteoclast activity and elevated CTX levels in thalassemia, suggesting VEGF's role in bone loss.
Thalassemia, a genetic hemoglobin disorder, is associated with numerous complications, including bone disorders such as osteoporosis. Osteoclast-mediated bone resorption plays a key role in the pathophysiology of thalassemia-associated bone loss. Biomarkers such as C-terminal telopeptide (CTX) are elevated in thalassemia, reflecting increased bone turnover. Vascular endothelial growth factor (VEGF), known for its role in angiogenesis, also contributes to the regulation of bone remodeling and is implicated in the pathogenesis of bone disorders in thalassemia. This review aims to explore the mechanisms of bone resorption in thalassemia, focusing on osteoclast biology, the significance of CTX levels, and VEGF's role in exacerbating bone loss.
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Rawat et al. (2025) studied this question.
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