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:
ETIOLOGY AND PATHOGENESIS
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