Skip to main content

REVIEW article

Front. Physiol.
Sec. Skeletal Physiology
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1514302

Progress in Understanding Legg-Calvé-Perthes disease Etiology from a Molecular and Cellular Biology Perspective

Provisionally accepted
Xinda Zheng Xinda Zheng 1Zhuqin Dong Zhuqin Dong 2*Ding Xiaofei Ding Xiaofei 1Qian Huang Qian Huang 2*Shengping Tang Shengping Tang 1*Yuchen Zhang Yuchen Zhang 1*Shijie Liao Shijie Liao 1*Boxiang Li Boxiang Li 3*
  • 1 First Affiliated Hospital, Guangxi Medical University, Nanning, China
  • 2 Guangxi Key Laboratory of Regenerative Medicine, Orthopaedic Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China., nanning, China
  • 3 Department of Orthopedic, Affiliated Ethnic Hospital of Guangxi Medical University, Nanning, Guangxi, 530001,China., nanning, China

The final, formatted version of the article will be published soon.

    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.

    Keywords: Perthes disease, etiology, Pathogenesis, Molecular Biology, cellular biology Etiology

    Received: 21 Oct 2024; Accepted: 27 Jan 2025.

    Copyright: © 2025 Zheng, Dong, Xiaofei, Huang, Tang, Zhang, Liao and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Zhuqin Dong, Guangxi Key Laboratory of Regenerative Medicine, Orthopaedic Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China., nanning, China
    Qian Huang, Guangxi Key Laboratory of Regenerative Medicine, Orthopaedic Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, China., nanning, China
    Shengping Tang, First Affiliated Hospital, Guangxi Medical University, Nanning, China
    Yuchen Zhang, First Affiliated Hospital, Guangxi Medical University, Nanning, China
    Shijie Liao, First Affiliated Hospital, Guangxi Medical University, Nanning, China
    Boxiang Li, Department of Orthopedic, Affiliated Ethnic Hospital of Guangxi Medical University, Nanning, Guangxi, 530001,China., nanning, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.