Aseptic Necrosis. Pathogenesis

An original view on the pathogenesis of aseptic (avascular) necrosis of the femoral head.

According to our view, the pathogenesis of aseptic (avascular) necrosis of the femoral head is based on mechanical damage to the ligamentum capitis femoris (LCF) or its dysfunction. Due to excessive stress on the LCF, it can rupture completely or partially, or tear off with or without a bone fragment. The most common mechanism of injury is forced adduction or rotation of the hip in the horizontal plane (pronation-supination). Damage can occur immediately or gradually, with prolonged existence of bioeffective stresses in the LCF. Partial damage to the LCF with elongation and dysfunction is not excluded at the initial stage. We consider the commonly held opinion about the vascular genesis of the disease to be incorrect.

Due to the violation of the integrity of the LCF, the hip joint in the single-support period of the step is not converted into a lever of the second kind. Accordingly, in all phases of walking, as well as in any vertical position, only the upper sector of the femoral head and acetabulum are loaded. The actual average daily stresses in them naturally increases. They, being higher than the level of optimal daily average stresses, cause the appearance of bioeffective stresses. The latter, in turn, induce biological adaptive processes (for more details, see the Law of Bioinduction).

One of the first manifestations is the formation of compact bone tissue in the subchondral zone of the femoral head (radiological symptom of "eggshell"). If, due to traumatic impact, along with damage to the LCF, an impression fracture of the upper pole of the femoral head does not occur, it develops gradually. The high intensity of internal forces in the upper sector of the femoral head leads to fractures of individual trabeculae in areas of stress concentration, which further weakens bone tissue and reduces the level of optimal average daily stresses.

Mechanical processes form a kind of bone-cartilaginous sequestrum at the upper pole of the femoral head. Along its periphery, bioeffective stresses induce adaptive processes, and granulation tissue appears, which is gradually transformed into fibrous tissue. Bone cysts develop in the femoral head, and the separated part of the bone undergoes lysis. Osteophytes appear at the edges of the femoral head and acetabulum due to metaplasia of fibrous tissue induced by bio-effective stresses. Thanks to osteophytes, the area of the contacting elements of the hip joint increases, which partly reduces the level of actual average daily stresses in them.

Restructuring of the acetabulum is also observed: the semilunar surface expands, the acetabular canal is eliminated, and the cartilaginous cover is worn out. Due to the death of part of the head of the femur and slow adaptive changes, it cannot fully adapt to the situation that has arisen. The inability to neutralize bio-effective stresses in the hip joint area leads to its further deterioration not only mechanically but also through biological processes.

The disruption of congruence and functioning of the hip joint leads to a change in the level of actual average daily stresses in all adjacent elements of the musculoskeletal system. Bioeffective stresses appear in them, leading to pathological changes. The energy intensity of locomotion increases, including due to an increase in the activity of the abductor group of muscles of the hip joint, which keep the pelvis in the single-support step period and in single-support vertical poses.

Keywords: ligamentum capitis femoris, ligamentum teres, ligament of head of femur, hip joint, biomechanics, aseptic necrosis, avascular necrosis, pathogenesis

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The first version of the text in:

Архипов-Балтийский СВ. Рассуждение о морфомеханике. Норма. В 2 т. Т. 2. Гл. 5-6. испр. и доп. изд. Калининград, 2004. (Archipov-Baltic SV. Reasoning about Morphomechanics. The norm – Kaliningrad, 2004. [Rus]) [aleph.rsl.ru]

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