Pathogenesis and molecular mechanisms of steroid-induced femoral head necrosis in children: a narrative review

In recent years, significant progress has been made in the study of the pathological mechanisms and pathology of steroid-induced osteonecrosis of the femoral head (SONFH) in adults. However, research on the molecular mechanisms and clinical translation of SONFH in children remains relatively limited. This narrative review synthesizes recent studies and reviews the latest advances in etiology, pathogenesis, genetic susceptibility, and molecular mechanisms, with a particular focus on pediatric-specific features. Unlike adults, children's skeletons are still in the developmental stage, and their vascular architecture, metabolic characteristics, and injury repair mechanisms differ significantly from those of adults. Specifically, the open growth plate in children creates a unique vascular architecture with distinct epiphyseal and metaphyseal blood supplies, while the growth plate's elasticity provides a biomechanical buffering effect against increased intraosseous pressure. Children's bones also exhibit superior remodeling and regenerative capacity compared to adults. However, these advantages gradually diminish with age, particularly as the growth plate approaches closure during puberty. Furthermore, pediatric SONFH is a complex disease involving the combined effects of multiple genes and pathways, and the impact of genetic variations may vary depending on treatment regimens and ethnic backgrounds, further increasing the disease's complexity. In summary, pediatric SONFH has a unique molecular biological basis that is distinct from adult SONFH. Future efforts should incorporate assessment methods based on genetic susceptibility loci and biomarkers to establish a treatment model ranging from early warning to personalized intervention, thereby achieving precise prevention and treatment of steroid-induced pediatric femoral head necrosis.