Glucocorticoid-induced osteoporosis in children: emerging vascular and molecular targets.

PURPOSE OF REVIEW

Glucocorticoid-induced osteoporosis (GIO) poses a significant risk to pediatric patients undergoing chronic glucocorticoid therapy for inflammatory, autoimmune, and genetic conditions. This review highlights the pathophysiology of GIO in children and emerging insights into the role of bone vasculature in skeletal health during growth.

RECENT FINDINGS

GIO arises from a dual mechanism of increased bone resorption and decreased bone formation, leading to rapid declines in bone mineral density. Recent studies emphasize the importance of angiogenic-osteogenic coupling, particularly in the growing skeleton. Endothelial cells are now recognized as active participants in bone health and regeneration. Advances in the understanding of signaling pathways regulating skeletal angiogenesis could predict skeletal side effects during drug development. Therapies enhancing endothelial cell function or promoting skeletal angiogenesis could mitigate glucocorticoid-induced damage. Key signaling pathways, such as platelet-derived growth factor type BB and nuclear factor (NF)-κB play critical roles in recruiting osteoprogenitors and establishing a vascular niche for skeletal angiogenesis.

SUMMARY

GIO is uniquely concerning in children due to its impact on peak bone mass and lifelong fracture risk. Understanding how glucocorticoids impair bone vasculature and skeletal remodeling may reveal new therapeutic targets to preserve bone health and mitigate the osteotoxic effects of long-term glucocorticoid use in the growing skeleton.