Orthopedics - Oleksa A.P. 2006

Joint Diseases
Degenerative-Dystrophic Joint Diseases
Primary Chronic Osteoarthritis

Primary chronic osteoarthritis ranks first in incidence among all degenerative-dystrophic processes and typically occurs in middle-aged and elderly individuals.

According to M. Astapenko and E. Pihlak (1966), statistical data vary somewhat across different countries. For instance, the prevalence of osteoarthritis in the former Czechoslovakia was about 3% of the population (Lenoch), in the Netherlands — 6.9% (Blecourt), and in Poland, According to the Warsaw Rheumatism Institute, — 10.3%. Such discrepancies in figures are very difficult to explain. This also applies to morbidity rates by gender, although, in principle, both women and men are affected with equal frequency.

The Hip and knee joints are most commonly affected, i.e., those subjected to the heaviest loads in daily life.

Disability resulting from coxarthrosis is three times higher than that from gonarthrosis, and seven times higher than from ankle joint involvement.

Etiology AND Pathogenesis. Primary osteoarthritis is a polyetiological disease whose cause cannot be established in the majority of cases; therefore, it is referred to as genuine arthrosis.

Medical literature is extremely rich in reports by authors from various countries who attempted to elucidate the causes and pathogenesis of primary chronic osteoarthritis.

There is no doubt that mechanical factors—namely, excessive joint stress and overloading—play an important role in The Development of the disease. However, the core of the etiopathogenesis of primary chronic osteoarthritis lies in a Background that triggers the onset and progressive chronic course of the process. First and foremost, this relates to the Aging of the articular Cartilage, which is supported by the high prevalence of the disease in the elderly. Yet it has been proven (Ye.P. Podrushniak, 1987) that destructive changes in articular cartilage can be detected in individuals as early as after 40 years of age. The Role of hereditary predisposition in the genesis of primary arthrosis is indicated in numerous publications based on both clinical observations (Stecher and Hersh) and experimental studies.

According to Sokoloff, hereditary predisposition is associated with multiple genes and has a recessive character. By cross-breeding separate genetic lines of mice (more and less resistant to arthrosis), he obtained offspring susceptible and resistant to the disease, indicating that genetic factors can determine the inherited predisposition to the condition.

Vascular (ischemia) and endocrine hypotheses (Climacteric period, imbalance between Parathyroid hormone and its antagonist coenzyme A, Lipid METABOLISM disorders, etc.) of the etiopathogenesis of osteoarthrosis have also been put forward. The onset of the disease has likewise been linked to the action of angiotrophic factors. Microcirculatory disturbances and venous stasis lead to Metabolic Disorders in the articular cartilage. Polarographic studies (A. Oleksa, 1972) have established not only reduced oxygen supply to the knee joint in gonarthrosis (during oxygen loading), but also its slowed utilization (using the tourniquet test).

Thus, articular cartilage degenerates As a result of various causes.

In the early stage of degenerative changes in cartilage, the chondroitin sulfate content decreases, the sulfated polysaccharide content in the synovial fluid decreases, and their amount in Blood serum increases. The cytological, protein, and enzymatic COMPOSITION OF THE synovial fluid changes.

Undoubtedly, the factor of cartilage wear plays a role in this situation, as proven by tribological studies by Gierzycska-Dolnam (1997) and reported at the 10th European Congress of Rheumatologists in 1983. Articular cartilage in overloaded areas becomes thinner, loose, and fibrillated, losing its normal luster, color, elasticity, and strength. Under The Influence of load, it can undergo secondary trauma, leading to the appearance of cracks. Lysosomal Enzymes of the synovial fluid, penetrating into the cracks, further destroy the degenerated cartilage.

Simultaneously with the development of arthrosis, the soft tissue elements of the joint are involved in the process. The synovial membrane hypertrophies, resulting in its hyperplasia with villous proliferation in areas adjacent to the articular cartilage. Clinically, this manifests as synovitis, which provides grounds for using the term "arthroarthritis." Initially, The amount of synovial fluid is not very pronounced; it is transparent, straw-colored, with a slightly reduced viscosity, which diminishes its lubricating properties. E. Maidyk, T. Wagner (1991), and P. Michalski, Gyrecki et al. (1994) point to elevated protein levels in the synovial fluid in arthrosis. Cell/15.html">Microscopy reveals no more than two thousand leukocytes, among which neutrophils and monocytes predominate. This simultaneously leads to the release of active oxygen metabolites and inflammatory cytokines — tumor necrosis factor-alpha (TNF) and interleukin (IL-1). These substances accelerate the destruction of articular cartilage by disrupting the balance between destruction and repair. The increase of TNF in the synovial fluid is explained by the excitation of Cells of the synovial membrane and those present in the joint cavity during inflammation. This disrupts joint Homeostasis and accelerates cartilage destruction.

Thus, the revealed biochemical and cytological Changes in the joint fluid can affect its tribological and rheological properties, altering the friction conditions within the joint (M. Furey, 1994; J.R. Dombrowski, 1994).

In late stages of arthrosis, microscopic examination of the synovial fluid reveals cartilage fibrils, indicating significant destructive changes.

Fibrillation and softening of the ground substance of the articular cartilage, destruction of chondrocytes, and mechanical friction cause The formation of defects within it. These defects can be so deep that the pink-colored subchondral Bone Structure, covered by a fibrous film, shines through. The articular cartilage is unevenly destroyed depending on its load-bearing area, which is why it often resembles a geographical map. Sometimes pieces of destroyed cartilage detach into the joint cavity and act as foreign bodies ("joint mice"), which can block joint movement.

The structure of the subchondral bone at the sites of erosions also changes. Bone trabeculae are replaced by chondroid, fibrous, or loose Connective Tissue, or combinations thereof. Radiographically, this manifests as single or multiple subchondral cysts.

Deforming osteoarthritis, which begins as a degenerative process, is simultaneously accompanied by reparative-regenerative manifestations during its development.

Cartilaginous outgrowths with The properties of fibrocartilage proliferate from the edges of the articular hyaline cartilage. Their ground substance is fibrillar with small spindle-shaped cells evenly distributed throughout. These outgrowths at the edges of the joint surfaces ossify and are clearly visualized as osteophytes on radiographs (Fig. 328). Such proliferations are explained by a compensatory increase in the load-bearing area of the joint surfaces, which reduces pressure per unit of support area. However, marginal exostoses, gradually increasing in size, significantly limit the range of motion in the joint and reduce the functional capabilities of the limb. A characteristic feature of osteoarthrosis is that, despite sharp restriction and painful movement, it never leads to ankylosis.

Summarizing the above, we present the main causative factors leading to joint tissue destruction according to B. Simenach (1998):

1. Environmental and ecological factors based on external impact on the joint regardless of the degree and type of destructive force, including increased joint wear.

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Fig. 328. Marginal osteophytes in idiopathic coxarthrosis radiographically.

2. Internal causative factors in the form of various joint pathologies, among which a special place is occupied by genetically determined abnormalities of joint structure (macromorphodysplasia), which cause its inadequacy.

3. Factors depending on the state of the body — various Diseases of the main human physiological systems that can cause joint inadequacy.

Simenach B. emphasizes The Importance of the prolonged action of both internal and external factors, regardless of their origin. Joint destruction is a direct consequence of external factors, whereas in cases of Dysplasia, metabolic disorders, or past inflammatory processes, the intra-articular factor is primary, while the external factor merely serves as an exposure condition. The Human Body reacts immediately to joint destruction without altering the destructive factor itself.

Under the influence of neurohumoral, vegetosomatic, biochemical, and immune factors, inflammation, hyperplasia, and sclerosis develop in the joint in a sequential manner. In cases of immunodeficiency, impaired cellular-tissue regulation, or endocrine dysfunction under continuous destructive impact, the body's defense mechanisms become depleted. This suppresses regenerative processes, predisposing the condition to a chronic course and sclerotic changes.

Breaking this complex pathological chain is possible only by eliminating the causative factor, which dictates the pathogenetic approach to Treatment. All forms of conservative management merely slow down joint destruction and fail to address the ROOT cause of the disease.

Clinically, deforming osteoarthritis manifests in various ways depending on the stage of the degenerative-dystrophic process. As previously noted, primary osteoarthritis typically localizes in one or both paired JOINTS OF THE lower extremities and develops progressively.

The disease begins subtly, and patients are often unable to pinpoint its exact onset. The earliest signs may include weakness and rapid fatigue of the limb during walking, occasionally accompanied by stiffness or crepitus, particularly in the knee joint.

Joint pain in most cases appears several years after the onset of the pathological process. Initially, patients experience vague joint pain following physical overexertion, which subsides with rest. In primary arthrosis, "start-up" pain may occur—upon standing up after rest, the pain is initially more intense and diminishes as the patient walks it off. Over time, the pain intensifies and troubles the patient not only during walking but also during movements without weight-bearing. This triggers a protective antalgic Muscle contracture, which increases pressure on the articular surfaces, negatively affecting the pathologically altered cartilage and further exacerbating the pain. In the early stages, accessory joint movements disappear, followed by the development of pronounced contracture. All of this leads to a limp caused by the functional shortening of the limb. Furthermore, the range of motion in the joint progressively decreases.

According to N. S. Kosynska, the clinical course of the disease comprises three stages:

♦ Stage I — "start-up" pain appears in the joint or arises after limb overexertion. The range of motion may remain within normal limits or be slightly restricted. Radiography reveals minor narrowing of the joint space and barely perceptible marginal bone proliferations (ossifications);

♦ Stage II is characterized by pronounced pain that diminishes after prolonged unloading, joint contracture with functional shortening of the limb, and limping. During movement, patients experience friction and crepitation in the joint. Radiographically, the joint space is sharply narrowed, marginal osteophytes are prominent, and the articular surfaces are deformed with signs of subchondral sclerosis and zones of cystic-dystrophic radiolucency;

♦ Stage III — marked by severe restriction of motion in the deformed joint, bordering on flail movement or complete rigidity. Persistent joint pain distresses the patient, yet medical help is typically sought only after significant impairment of limb function. Radiographically, the joint space is virtually absent, the joint is deformed, the epiphyses are flattened, and the articular surfaces are widened due to marginal osteophytic proliferations. Free osteocartilaginous intra-articular "mice" (joint bodies) may be present. Typically, subchondral sclerosis with cystic radiolucencies in the spongy bone structure is detected.

However, deviations from the features outlined in this Classification are possible during the course of the disease. For instance, N. S. Kosynska notes that subchondral sclerosis is detected In the second stage of the disease, although it is considered one of the earliest radiological signs of osteoarthritis (A. A. Lemberg, I. A. Klioner, et al.).

Nevertheless, this classification is widely accepted and remains utilized by practitioners, even though each anatomical localization of deforming arthrosis has its own specific features.