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Progress in understanding Legg-Calvé-Perthes disease etiology from a molecular and cellular biology perspective
Xinda Zheng1, Zhuqing Dong2, Xiaofei Ding1
1Department of Trauma Orthopedic and Hand Surgery, The First Afliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.
Insights
Legg-Calvé-Perthes disease (LCPD) involves femoral epiphysis ischemia in children. Research explores molecular and cellular factors, including COL2A1 mutations and microvascular endothelial cell abnormalities, to understand LCPD etiology.
Area of Science:
- Pediatric Orthopedics
- Molecular Biology
- Cell Biology
Background:
- Legg-Calvé-Perthes disease (LCPD) is a childhood hip disorder characterized by femoral epiphysis ischemia.
- Etiology remains unclear despite over a century of study, affecting children aged 4-8 years, predominantly males.
Purpose of the Study:
- To review recent basic research on Legg-Calvé-Perthes disease.
- To provide an overview of LCPD from molecular and cell biology perspectives.
Main Methods:
- Literature review of previous basic studies on LCPD.
- Analysis of molecular and cellular alterations implicated in LCPD pathogenesis.
Main Results:
- Potential roles of COL2A1 mutations in epiphyseal cartilage matrix collapse.
- Evidence suggests abnormalities in microvascular endothelial cells, osteoclast activation, and immune system involvement.
- Investigated factors include Factor V Leiden mutation and IGF-1 abnormalities, requiring further confirmation.
Conclusions:
- LCPD pathogenesis involves complex molecular and cellular events.
- Understanding these biological alterations is crucial for elucidating LCPD etiology.
- Further research is needed to confirm proposed etiological factors and mechanisms.
Abstract:
Legg-Calvé-Perthes disease (LCPD) is a hip disease caused by ischemia of the femoral epiphysis in children, which occurs in children aged 4-8 years (mean 6.5 years), with a male-to-female ratio of about 4:1. The disease has been reported for more than 100 years, but its etiology has not been elucidated. In recent years, a considerable amount of research has been carried out on the etiology of the disease, and the development of the disease is believed to involve a variety of molecular biological alterations, such as the COL2A1 mutation, which may be one of the causes of necrotic collapses of the epiphyseal cartilage matrix in LCPD. Tissue factor V Leiden mutation and insulin-like growth factor (IGF-1) abnormalities have also been reported in LCPD, but most theories need further confirmation. The in-depth study of LCPD cell biology has facilitated the suggestion regarding structural and/or functional abnormalities of microvascular endothelial cells in LCPD. This conjecture is supported by epidemiological and clinical evidence. Abnormal activation of osteoclasts, ischemic damage to epiphyseal cartilage, and activation of the bone marrow immune system all play important roles in the onset and progression of the disease. In this paper, we review the previous basic studies on LCPD and give an overview from the molecular biology and cell biology perspectives.
