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Glucocorticoid-induced osteoporosis in children: emerging vascular and molecular targets
Sisir Kumar Barik1,2, Janet L Crane1,3,2
1Division of Endocrinology, Department of Pediatrics.
Insights
Glucocorticoid-induced osteoporosis (GIO) in children impairs bone density by increasing resorption and decreasing formation. Targeting bone vasculature offers new therapeutic strategies to prevent lifelong fracture risk.
Area of Science:
- Pediatric Endocrinology
- Bone Biology
- Vascular Biology
Background:
- Glucocorticoid-induced osteoporosis (GIO) is a significant risk for children on long-term glucocorticoid therapy.
- GIO impacts inflammatory, autoimmune, and genetic conditions, affecting skeletal development.
Purpose of the Study:
- Review the pathophysiology of GIO in pediatric patients.
- Explore the role of bone vasculature in GIO during skeletal growth.
- Identify emerging therapeutic targets for GIO.
Main Methods:
- Literature review focusing on GIO pathophysiology and bone vasculature.
- Analysis of recent studies on angiogenic-osteogenic coupling in pediatric bone.
- Examination of signaling pathways involved in skeletal angiogenesis.
Main Results:
- GIO involves increased bone resorption and decreased bone formation, leading to rapid bone mineral density loss.
- Angiogenic-osteogenic coupling is crucial in the growing skeleton, with endothelial cells playing an active role.
- Signaling pathways like PDGF-BB and NF-κB are key in recruiting osteoprogenitors and regulating skeletal angiogenesis.
Conclusions:
- GIO in children is concerning due to its impact on peak bone mass and lifelong fracture risk.
- Understanding glucocorticoid effects on bone vasculature may reveal new therapeutic targets.
- Preserving bone health and mitigating osteotoxic effects in the growing skeleton is critical.
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.
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