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Chapter 21. Osteochondropathies (osteonecroses)

The group of osteochondropathies includes bones and cartilage diseases in children and adolescents, characterized by a specific change in the apophyses, spongy substance of short bones and epiphyses of long tubular bones, occurring on a hypovascular (avascular) basis.

Anatomical and physiological features

It may be assumed that the bone tissue dies due to insufficient blood supply with the local development of osteoporosis. Typical changes occur during the period of accelerated growth, when the processes of tissue formation and metabolism in them are the most intense. During the period of final musculoskeletal system formation (on average until 25 years), an increase or decrease in functional load becomes permanent, which leads to an imbalance between osteogenesis and osteoresorption. Changes in the structural organization of the entire bone (osteoporosis or work hypertrophy) continue until a new level of the average daily functional load stereotype is established when the intensity of osteogenesis and osteoresorption is balanced. During the period of body growth, these changes should be assessed as compensatory. In case of anatomical and functional discrepancy in the bones, areas of overstrain may occur with the development of pathological changes (first of all, a reaction is noted in the growth zones), known in the literature under numerous names. This may include a group of osteochondropathies (avascular necrosis).

Regardless of the localization, osteochondropathies have a chronic benign course and a relatively favorable outcome. The essence of the disease consists in a local disruption of the bone blood circulation under the influence of various causes, the occurrence of avascular necrosis areas in the spongy bone (subjected to the greatest mechanical stress), subsequent pathological bone restructuring, as well as possible occurrence of pathological fractures. Most often, the process is localized in the lower limb bones. Osteochondropathies of the femoral head, spine, tuberosity of the tibial and calcaneal bones are most common in children and adolescents.

Application of such diagnostic methods as CT, MRI, scintigraphy, densitometry, allow to establish the correct diagnosis at an early stage of the disease, which results in more favorable treatment prognosis.

Classification

Depending on the localization of the pathological process in the bone, four subgroups of osteochondropathies (avascular necrosis) are distinguished.

  1. Osteochondropathies of tubular bone epiphyses:
    • of the femoral head (Legg-Calve-Perthes disease);
    • of the II-III metatarsal bone heads (Kohler disease II);
    • of the sternal clavicle end (a rare form of osteochondropathy);
    • of finger phalanges (Thiemann disease).
  2. Osteochondropathies of short cancellous bones:
    • of the navicular bone (Kohler disease I);
    • of the lunate bone (Kienbock disease);
    • of the vertebral body (Calvé disease, flat vertebra);
    • of the patella [Sinding-Larsen-Johansson (SLJ) syndrome];
    • of tarsal bones (Iselin disease);
    • of the talus (Sever-Haglund disease);
    • of the sesamoid bone of the first finger (Renander-Muller's disease).
  3. Osteochondropathy of apophyses:
    • of the tibial tuberosity (Osgood-Schlatter disease);
    • of the calcaneal tuberosity (Haglund-Schinz disease);
    • of vertebral apophyseal rings (Scheuermann-Mau disease, or juvenile kyphosis);
    • of the humeral head (Hass disease);
    • of the pubic bone (Burmann's disease).
  4. Partial osteoarthropathies of articular surfaces (Koenig disease).

Clinical course and diagnosis

A gradual onset and a prolonged course without acute attacks with uncharacteristic pain and laboratory findings are typical.

There are five stages of the disease development.

  1. Pre-radiological stage (avascular necrosis).

The spongy substance of the bone is affected while the cartilage is intact (subchondral avascular necrosis, stage of osteoporosis). Osseous pathology is not detected on X-ray, which requires application of diagnostic methods with higher resolution (CT, MRI, densitometry, scintigraphy) if bone damage is suspected (based on clinical data). The duration of this stage is up to 6 months.

  1. Sclerosis stage (pathological fracture).

There are distinct radiological signs of osseous pathology (for example, femoral head deformity, wedge-shaped deformity of vertebral bodies with the most frequent localization in the thoracic spine). Duration - from 3 to 6-8 months.

  1. Fragmentation stage (resorption).

Revascularization of the affected area occurs, connective tissue grows into the necrotic area of the bone along with the vessels. Simultaneously, with the resorption of the old bone, the process of a new bone formation is underway. Duration - 1-1.5 years.

  1. Reparation stage.

Sequestered shadows on X-rays disappear, there is a complete replacement of the necrotized bone with a newly formed radiolucent one.

  1. Final stage (secondary changes).

Bone reconstruction of the affected area is completed, which is close to its normal anatomical characteristics in case of favorable outcomes. However, in case of the most ideal outcomes, recovery occurs for 85% at the most. In less favorable cases, pronounced deformities persist: the femoral head acquires a mushroom shape, the height of vertebral bodies decreases, which provokes subsequent progression of degenerative processes (deforming arthrosis, osteochondrosis).

If osteochondropathy proceeds for several years, minor functional disorders may be noted, accompanied by pain and restriction of movement in the affected segment. Self-healing is possible, although deforming arthrosis may develop in the future.

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