Research progress on the effect of bone microenvironment on hormonal femoral head necrosis.
10.12200/j.issn.1003-0034.20240634
- Author:
Xu-Sheng ZHANG
1
;
Hao-Fei YANG
1
;
Jin-Sheng LI
1
;
Ming-Wang ZHOU
1
;
Hai-Ping LIU
2
;
Xiao-Ping WANG
3
Author Information
1. Clinical College of Traditional Chinese Medicine, Gansu University of Traditional Chinese Medicine, Lanzhou 730000, Gansu, China.
2. Clinical College of Traditional Chinese Medicine, Gansu University of Traditional Chinese Medicine, Lanzhou 730000, Gansu, China; Department of Joint and Orthopedics, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou 730050, Gansu, China.
3. Department of Joint and Orthopedics, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou 730050, Gansu, China.
- Publication Type:English Abstract
- Keywords:
Bone microenvironment;
Homeostasis;
Review;
Steroid-induced osteonecrosis of the femoral head
- MeSH:
Humans;
Femur Head Necrosis/physiopathology*;
Animals;
Signal Transduction;
Bone and Bones/metabolism*;
Glucocorticoids/adverse effects*;
Cellular Microenvironment
- From:
China Journal of Orthopaedics and Traumatology
2025;38(8):867-872
- CountryChina
- Language:Chinese
-
Abstract:
Steroid-induced osteonecrosis of the femoral head (SONFH) is avascular necrosis of the femoral head caused by long-erm use of corticosteroids, and its pathogenesis is complex and affected by changes in the dynamic balance of the bone microenvironment. With the deepening of research, the role of bone microenvironment in the pathogenesis of SONFH has been gradually revealed. In the case of excessive use of glucocorticoids (GCs), the bone microenvironment changes significantly, causing imbalance in bone lipid metabolism, microcirculation disorders and disorders of immune regulation, which promotes the increase of the number and activity of osteoclasts, and interferes with the differentiation of osteoblasts and adipoblasts. Through the regulation of PI3K/AKT, OPG/RANKL/RANK, MAPK, JAK/STAT, Hedgehog and other signaling pathways, it eventually leads to osteocyte apoptosis, bone microvascular rupture and destruction of trabecular bone structure, which in turn leads to osteonecrosis, bone density reduction and bone microstructure destruction due to bone microcirculation ischemia, and finally leads to necrosis of the femoral head. This article reviews the role of bone microenvironment homeostasis in GCs-induced ONFH and the regulatory mechanism of bone microenvironment, which is helpful to reveal the pathogenesis of SONFH and provide a theoretical basis for exploring effective intervention strategies.
