ABSTRACT
Introduction
Inflammatory bowel disease (IBD) is a chronic disease characterized by the presence of systemic inflammation, manifesting not only as gastrointestinal symptoms but also as extraintestinal bone complications, including osteopenia and osteoporosis. However, the association between IBD and osteoporosis is complex, and the presence of multifactorial participants in the development of osteoporosis is increasingly recognized. Unlike in adults, delayed puberty and growth hormone/insulin-like growth factor-1 axis abnormalities are essential risk factors for osteoporosis in pediatric patients with IBD.
Areas covered
This article reviews the potential pathophysiological mechanisms contributing to osteoporosis in adult and pediatric patients with IBD and provides evidence for effective prevention and treatment, focusing on pediatric patients with IBD. A search was performed from PubMed and Web of Science inception to February 2023 to identify articles on IBD, osteoporosis, pediatric, and fracture risk.
Expert opinion
A comprehensive treatment pattern based on individualized principles can be used to manage pediatric IBD-related osteoporosis.
Article highlights
Among pathophysiological mechanisms, chronic inflammation, corticosteroid exposure, and vitamin D deficiency are vital contributors to IBD-related osteoporosis.
The mechanism of pediatric IBD-related osteoporosis is partially different from that in adults, mainly due to delayed puberty and abnormalities in the GH-IGF-1 axis.
The treatment strategy for pediatric patients with IBD must be considered in the context of the underlying multifactorial mechanisms, and a comprehensive treatment pattern based on individualized principles should be applied to pediatric patients with IBD.
Declaration of interest
Author Lisha Xiang has received research support from the Sichuan Science and Technology Program and the Chengdu Science and Technology Program. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
Acknowledgments
We would like to thank Editage (www.editage.cn) for English language editing. We would like to thank Bai Feng and Li Ying for plotting the figures (Created with BioRender.com).