Hip Osteoarthritis. Pathogenesis

An original view on the pathogenesis of osteoarthritis of the hip joint.

Coxarthrosis is a disease that can develop either independently or against the background of other pathological conditions: congenital hip dislocation, Perthes' disease, aseptic necrosis of the femoral head, and some others. From our point of view, the basis of its pathogenesis, as a rule, is the pathology of ligamentum capitis femoris (LCF). This may involve its complete or partial damage, changes in size, mechanical properties, and the localization of attachment areas.

The pathogenesis of coxarthrosis is a clear illustration of the Law of Bioinduction that we have established. LCF dysfunction results in disruption of normal hip mechanics. In the single-support period of the step and the single-support orthostatic position, it begins to function not as a lever of the second kind, but as a lever of the first kind. Accordingly, only the upper sectors of the femoral head and acetabulum are constantly loaded; the values of the actual average daily stresses in them significantly increase. The bioeffective stresses that arise in this case induce a complex of biological processes.

In the upper sector of the hip joint, the cartilage wears out and becomes thinner. Decentration of the femoral head and its cranial subluxation gradually develop. Microfractures of trabeculae are observed in the bone tissue. The majority of ongoing biological processes aim to neutralize bio-effective stresses. Osteophytes form on the periphery of the articular surfaces, which increases the area of their contact, and at the same time deformation of the articular ends of the bones occurs. The first and second reduce the intensity of internal forces in the bone elements. As the acetabular canal has lost its functional role, the acetabular fossa is eliminated, and the facies lunata expands.

In the subchondral layer of the femoral head, a layer of compact bone tissue appears and gradually thickens, reducing local stresses in the underlying spongy substance. There is a reorientation of the trabecular systems of the proximal end of the femur. The first system of bone trabeculae is strengthened, the second system is eliminated. Bone cysts appear and enlarge as one of the ways to eliminate stresses concentrations inside the bone at the ends of microcracks. The presence of bioeffective stresses is also reflected in soft tissues: fibrosis is observed in tendons, joint capsules and muscles, and in the areas of their attachment there are foci of heterotopic ossification.

There is a shortening of the femoral neck and an increase in the femoral neck-diaphyseal angle. The size and shape of the entire proximal femur changes, and the depth of the acetabulum increases. To a large extent, the listed phenomena are compensatory processes. In some cases, they change the actual average daily stresses, and in others, the optimal average daily stresses; the meaning of both is to level out the existing bioeffective stresses.

The mechanics of a hip joint affected by arthrosis is the mechanics of a hip joint that is devoid of LCF. In this case, the kinematics of locomotion changes significantly and their energy intensity increases. Bioeffective stresses appear not only in the hip joint area, but also in all adjacent elements of the musculoskeletal system, which leads to their pathological changes. With a reduced adaptive potential of tissues and significant violations of the mechanics of the lower limb girdle, bioeffective stresses remain uncompensated. This gradually leads to complete destruction of the hip joint, as well as gross changes in the anatomical elements of adjacent kinematic chains.

Keywords: ligamentum capitis femoris, ligamentum teres, ligament of head of femur, abductor muscle group, hip joint, biomechanics, osteoarthritis, 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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ETIOLOGY AND PATHOGENESIS

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