Orthopedics - Oleksa A.P. 2006

Osteochondropathies

Osteochondropathy is described in literature under the eponyms of the authors who first reported its various localizations, as well as under such terms as aseptic bone necrosis, epiphysionecreosis, and osteochondritis dissecans. Typically occurring in childhood and adolescence, this condition has a slow clinical course and is characterized by subchondral aseptic necrosis of certain weight-bearing bones.

The disease was first described by König in 1888 as osteochondritis dissecans, a term still in use today. G. Axhausen classified osteochondropathy as an independent nosological entity in 1923.

Table 7 presents the localizations of osteochondropathies along with the names of the authors who first described them. Figure 344 provides a schematic diagram of the Skeleton showing these localizations.

According to M. V. Volkov (1974), among orthopedic pathologies, osteochondropathy

accounts for 2.7 %, most frequently affecting the hip joint (34 %), the Carpal Bones and the wrist region (42.6 %), and less commonly the elbow (14.9 %) and knee joints (8.5 %). Overall, Osteochondropathy of the upper extremity bones occurs in 57.5 % of cases, and of the lower extremity in 42.5 % (N. S. Kosinskaya, 1961).

The Etiology of osteochondropathies remains incompletely understood. A significant number of orthopedists believe that recurrent trauma plays a role in the onset of the disease. However, the majority consider the condition to be polyetiologic, with potential causative factors including local ischemia, abnormal ossification of ossification centers (Petrie P.W., 1977; Pappas A.M., 1981; Mubarak S.J., Carrol N.C., 1981), as well as inflammatory processes, endocrinopathies, and congenital factors. M. V. Volkov (1974) suggests that osteochondropathy is a consequence of osteodystrophy of angioneurotic origin.

Class="center">Table 7. Localization of osteochondropathies and the authors who first described them

Gruntovsky G. H., Kolesnichenko V. A., Volkov E. B. et al. (1995) investigated Metabolic Disorders in lumbar spinal osteochondropathy. They established that spinal osteochondropathy is accompanied by a significantly elevated alkaline phosphatase activity (up to 13.4 Bodyansky units), specifically due to the bone isoenzyme. Serum levels of carbohydrate-Structure/178.html">Protein Complexes (sialic acids, Glycoproteins, chondroitin sulfates) remained within normal limits.

Since alkaline phosphatase is a marker enzyme of Cytoplasmic membranes, this increase in activity likely indicates structural alterations in the membranes.

It may also signify the onset of a cytolytic process within the Bone tissue. The presence of such a process—whose morphological substrate typically involves destructive Changes in the bone—is confirmed by the hyperexcretion of hydroxyproline (90.83 mg/day) and glycosaminoglycans (11.98 mg/day).

These patients also exhibited hormonal imbalances, manifested by an increased urinary excretion of 17-oxysteroids (22.0 µmol/day). It can be inferred that elevated glucocorticoid levels may be associated with the structural remodeling of cytoplasmic membranes accompanied by an upregulation of alkaline phosphatase.

M. Aufdermaur (1981) demonstrated that spinal osteochondropathy involves impaired Collagen synthesis in the matrix of the vertebral endplates. D. S. Bradford et al. (1976) note that these alterations manifest as a decreased collagen-to-proteoglycan ratio, which is accompanied by hydroxyproline hyperexcretion and increased alkaline phosphatase activity.

Thus, patients with osteochondropathy develop pronounced destructive changes in the bone tissue.

The morphological substrate of spinal osteochondropathy is now considered to be alterations in the vertebral endplates, specifically their thinning and irregularity.

Pathomorphological changes across all localizations of osteochondropathy are generally identical. Circulatory Disorders with foci of varying size and shape are identified in the epiphyses and subchondral bone regions. Microscopic examination reveals a chaotic arrangement of necrotic bony trabeculae and fragments devoid of osteocytes. This indicates the occurrence of a primary subchondral infarct within the epiphysis.

Fig. 344. Schematic diagram of the skeleton showing localizations of osteochondropathies: 1 - hip joint; 2 - carpus and wrist joint; 3 - scaphoid bone; 4 - second and third Metatarsal Bones.

Depending on the localization, osteonecrosis areas of various sizes develop in the zones of maximum mechanical load on the bone and typically feature a demarcation line formed by highly vascularized skeletogenic or fibrous tissue. Subsequently, necrotic masses are resorbed by osteoclasts, and reparative processes are initiated. The articular hyaline Cartilage overlying the osteonecrotic area becomes homogenized, calcifies, and, under METABOLISM/18.html">The Influence of loading, cracks; occasionally, it may sequester and detach into the joint cavity as an intra-articular "joint mouse," which is most classically observed in König's disease (osteochondropathy of the femoral condyle).

Aseptic osteonecrosis is characteristic of all osteochondropathies, with the exception of Osgood-Schlatter disease (osteochondropathy of the tibial tuberosity), in which it does not present in a classic manner. It is also worth noting certain morphological differences in osteochondropathy of the vertebral apophyses (Scheuermann-Mau disease), which, In addition to alterations in the trabecular Bone Structure, involves Ossification of the epiphyseal plates, degeneration of the intervertebral discs with The formation of Schmorl's nodes, and other changes.

Depending on the localization of the pathological process within the epiphysis, apophysis, certain spongy bones, or the subchondral layers of the articular ends, osteochondropathies are divided into four groups (according to S. A. Reinberg, 1964).

Group I. Osteochondropathies of the epiphyseal ends of long bones: femoral head (Legg-Calvé-Perthes disease), heads of the second and third metatarsal bones (Köhler II disease), humeral head (Hass disease), phalanges of the hand (Thiemann disease), and sternal end of the clavicle.

Group II. Osteochondropathies of short spongy bones: carpal scaphoid (Preiser disease), tarsal navicular (Köhler I disease), lunate bone (Kienböck disease), vertebral body (Calvé disease), and the sesamoid bone of the first metatarsophalangeal joint.

Group III. Osteochondropathy of apophyses: tibial tuberosity (Osgood-Schlatter disease), calcaneal tuberosity (Haglund-Schinz disease), apophyseal rings of the vertebral bodies (Scheuermann-Mau disease), patella (Sinding-Larsen-Johansson disease), and apophysitis of the fifth metatarsal bone (Iselin disease).

Group IV. Partial wedge-shaped osteochondropathies of articular surfaces — osteochondritis dissecans (König's disease) of the femoral head or distal femoral epiphysis (more commonly the medial condyle), the head or distal epiphysis of the humerus, the body of the talus, etc.

Given the prolonged course (2–3 years) of osteochondropathy, clinical practice relies on staging classifications based on the radiological manifestations of pathomorphological bone changes. Several classifications reflect the sequential changes that develop throughout the disease process. For instance, D.G. Rokhlin (1952) identified three Phases of the clinical course of aseptic necrosis: the necrosis phase, the degenerative-productive phase (or fragmentation phase), and the terminal outcome phase.

M.P. Novachenko distinguishes five stages: aseptic necrosis, impression fracture, fragmentation, repair, and restoration of bone structure and shape.

Axhausen likewise distinguishes five stages: necrosis, impression fracture, fragmentation, repair, and restoration.

What is meant by the term "stage of impression fracture"? Our clinical observations indicate that even with early detection and proper Treatment, a compression fracture of the bone cannot be prevented in all cases, not even during the fragmentation stage. A fracture is considered a complication during the fragmentation stage, whereas bone tissue Condensation ("trabecular accumulation", "pseudosclerosis") detected radiologically indicates osteonecrosis and compression.

Therefore, we agree with the Classification by James T. Guille and J. Richard Bowen (1997), which comprises four stages: 1) stage of necrosis; 2) stage of resorption (fragmentation); 3) stage of repair (reossification); 4) stage of remodeling.

This classification most accurately characterizes the sequential bone changes occurring in osteochondropathy. This is most clearly evident in osteochondropathy of the femoral head—Legg-Calvé-Perthes disease—which is the most common form encountered in clinical practice. According to Studenikin and Yakovleva (1987), it accounts for 25.3% of all joint disorders in children, and according to Volkov, 34%.