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Published on: September 27, 2024
Research progress in the pathogenesis of hormone-induced femoral head necrosis based on microvessels: a systematic
Tiancheng Ma1,2,3, Yan Wang1,2,3, Jianxiong Ma4,5,6
1Tianjin Hospital of Tianjin University, Tianjin, 300211, China.
Insights
Glucocorticoids impair femoral head blood flow by disrupting microvessel formation, leading to hormonal necrosis. This review explores the role of impaired angiogenesis in this common non-traumatic necrosis.
Area of Science:
- Orthopedics
- Vascular Biology
- Endocrinology
Background:
- Hormonal necrosis of the femoral head is a common non-traumatic condition linked to glucocorticoid use, abnormal bone and lipid metabolism, and impaired microcirculation.
- Impaired blood circulation is a critical factor in femoral head necrosis pathogenesis, particularly affecting the femoral head's microvasculature.
- H-type vessels are crucial for the "angiogenesis and osteogenesis coupling," significantly influencing the development of femoral head necrosis.
Purpose of the Study:
- To review the current understanding of the mechanisms behind hormone-induced femoral head necrosis, focusing on microvascular blood flow.
- To explore how glucocorticoids impact femoral head microcirculation and bone metabolism.
- To provide insights for future research and clinical strategies for treating femoral head necrosis.
Main Methods:
- Literature review of domestic and international studies on hormone-induced femoral head necrosis.
- Analysis of the role of microvascular dysfunction, including H-type vessels, in necrosis development.
- Examination of glucocorticoid-induced changes in coagulation, endothelial function, and angiogenesis.
Main Results:
- Glucocorticoids contribute to femoral head blood flow injury through coagulation and endothelial dysfunction, and impaired angiogenesis.
- Glucocorticoids may inhibit H-type vessel formation by downregulating key factors like HIF-1α, PDGF-BB, and VEGF.
- This disruption damages the "angiogenesis-osteogenesis coupling," hindering the femoral head's natural repair and reconstruction capabilities.
Conclusions:
- Impaired microvascular blood flow, especially the dysfunction of H-type vessels, is central to glucocorticoid-induced femoral head necrosis.
- Understanding the molecular mechanisms, such as the reduced expression of angiogenesis factors, is key to addressing this condition.
- This review offers a foundation for developing novel therapeutic approaches for hormonal femoral head necrosis.
Abstract:
Hormonal necrosis of the femoral head is caused by long-term use of glucocorticoids and other causes of abnormal bone metabolism, lipid metabolism imbalance and blood microcirculation disorders in the femoral head, resulting in bone trabecular fracture, bone tissue necrosis collapse, and hip dysfunction. It is the most common type of non-traumatic necrosis of the femoral head, and its pathogenesis is complex, while impaired blood circulation is considered to be the key to its occurrence. There are a large number of microvessels in the femoral head, among which H-type vessels play a decisive role in the "angiogenesis and osteogenesis coupling", and thus have an important impact on the occurrence and development of femoral head necrosis. Glucocorticoids can cause blood flow injury of the femoral head mainly through coagulation dysfunction, endothelial dysfunction and impaired angiogenesis. Glucocorticoids may inhibit the formation of H-type vessels by reducing the expression of HIF-1α, PDGF-BB, VGEF and other factors, thus causing damage to the "angiogenesis-osteogenesis coupling" and reducing the ability of necrosis reconstruction and repair of the femoral head. Leads to the occurrence of hormonal femoral head necrosis. Therefore, this paper reviewed the progress in the study of the mechanism of hormone-induced femoral head necrosis based on microvascular blood flow at home and abroad, hoping to provide new ideas for the study of the mechanism of femoral head necrosis and provide references for clinical treatment of femoral head necrosis.
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