The Principle of Hormone-induced Avascular Necrosis of the Femoral Head
There are two theories about the pathogenesis of hormone-induced avascular necrosis of the femoral head:
1. The osteoporosis theory. Hormones can slow down the synthesis of bone collagen in existing osteoblasts and hinder the transformation of pre-osteoblasts into osteoblasts. Meanwhile, hormones directly stimulate the activity of osteoclasts and indirectly increase the secretion of parathyroid hormone, thereby reducing the absorption of calcium from the intestine and affecting the transport of calcium in the intestine. This leads to increased bone resorption, resulting in osteoporosis, finer and disappearing trabeculae. On this basis, minor stress can easily cause micro-fractures in the trabeculae. Due to the accumulation of minor injuries, mechanical resistance decreases, leading to stress concentration, collapse, and compression. In the compressed area, compressed marrow cells and capillary necrosis can be observed, ultimately leading to bone ischemic necrosis.
2. The vascular and hemodynamics changes theory. Some people believe that hormones cause inflammation in peripheral arterioles, making the inner walls of the vessels prone to increased blood viscosity. After kidney transplantation, patients may experience systemic fat embolism and bilateral femoral head ischemic necrosis. Therefore, it is speculated that intraosseous lipids originate from fatty liver, where lipid emboli block the microvessels beneath the articular cartilage, causing bone ischemia and death. Hormone therapy can lead to increased blood coagulability, causing venous thrombosis. These tiny venous thrombi can create intraosseous hypertension within the bone cortex, leading to impaired bone microcirculation and bone ischemic necrosis.
Hormones can cause inflammation in small vessels within the femoral head, affecting the blood supply to bone cells and leading to bone cell damage.