Extrasynovial Pain Sources

The most intriguing and important factor in pain mechanisms arising in deforming arthrosis is the formation of pain sources located outside the joint. They were discovered thanks to a specialized analysis of clinical manifestations of the disorder at various stages of development. Only by crossing outside the boundaries of a narrow and localized approach to the study of this pathology were we able to obtain a full understanding of both the structure of the pain syndrome and the mechanisms responsible for the formation of individual components of that syndrome, from which it becomes possible to create an individual pain profile for each specific patient.

Research has shown that the magnitude of the peripheral tissues drawn into the formation of extrasynovial pain is extensive, especially when the joints of the lower limbs are damaged. In consideration of this circumstance, we recommend a discussion of the patterns consistent in the formation of extrasynovial pain using as examples the two joints most characteristically afflicted by this illness – the knee and the hip. These joints are the clinical models that to the greatest degree reflect the sequence of inclusion of various factors involved in the formation of pain syndromes in deforming arthrosis (table 1). 

Table 1 provides data characterizing the patterns of appearance and growth of extrasynovial changes in deformative arthrosis of the hip joint. To compile these data, we used the results of clinical, radiological and anthropometric studies of 81 patients suffering from coxarthrosis. The studies were conducted for the purpose of clarifying the nature and severity of extrasynovial changes occurring at various stages in the development of the disorder.

Extrasynovial Changes

The most notable aspects (from the standpoint of biomechanical disruption) of damage to the aforementioned joints are the progressive limitation of their mobility (atrophy) and the associated functional contracture of the damaged limb. In turn, these lead to the appearance of previously-absent launch mechanisms responsible for various sources of extrasynovial pain. The resulting muscle group imbalance and osteoreflexive disruptions in the limb become pain triggers, appearing in conjunction with the irritation of osteoreceptors on articular surfaces of bones. Osteoreflexive disruptions occur typically in stages, during which the damaged joint loses the ability to protect itself from external overloads. 

The formation of extrasynovial pain factors in arthrosis of the knee or hip joint occurs gradually along with the increase in disruptions of the static-dynamic function of the damaged limb and the exhaustion of possibilities for compensation by auxiliary mechanisms. In conjunction with the appearance of structural disparities, disruptions are observed in all biomechanical elements of the locomotory system. The clear trend toward an increase in functional disruptions is evidence of the peak mobilization of compensatory mechanisms in such patients. Gradually these mechanisms are transformed from mere manifestations of compensatory functions (in conjunction with the increase in muscle imbalance and osteoreflexive disruptions) into pathological reactions. The completion of the process corresponds to the moment at which the compensatory mechanisms – in the form of a sag in the pelvic ring, an increase in pelvic tilt, an exacerbation of lumbar lordosis (anterior curvature of the spinal column), external or internal curvature of the limb’s axis – are no longer able to improve the disrupted function of the limb.

Extreme contracture of the limb, for which adaptive mechanisms may still compensate, equals three to four centimeters. Patients suffering from such contracture are at the limit of compensatory mechanisms, which allows us to place them in a separate group (risk group). Changes in the joints of these patients usually correspond to those common to the second and third stages in the development of the disorder, and are accompanied by moderate pain. Further progression of the pathology and an increase in the severity of extrasynovial changes lead to the failure of compensatory mechanisms and the appearance of intense pain. 

Widely varying structures may become extrasynovial sources of pain sensations in deforming arthrosis, such as the bone marrow (medulla), muscles, ligaments, fascia, and articular capsule. Local pain sectors (trigger points) are formed within these structures, serving as “generators” of pathological pain impulses and objectively intensifying pain in the damaged joint.

The extra-articular component of the pain syndrome often predominates over the arthrogenic component in the clinical manifestations of deforming arthrosis. Accordingly, the elimination of extra-articular pain provides a new quality of pain-relief therapy.  Miofascial, fasciocapsular, ligamentous, periosteal, and intraosseous (osteomedullary) components of the pain syndrome are distinguished. The diversity of the pain (algic) picture in arthrosis patients is explained in each specific case by the non-coincidence of the functional connections between particular sources of painful sensations.

Until now, the literature has lacked a clear notion of the mechanisms responsible for the formation of pain irritation centers caused by deformative arthrosis in conjunction with the progression of functional disruptions in the limb. The one-sided orientation of treatment measures on intrasynovial pain and the ignorance of pain factors of extrasynovial origin are the most frequent causes of failure of conservative treatment for deformative arthrosis. Without discovering the Law of Tissue Specificity and Mutation of Chronic Pain, medicine was unable for many years to ease the suffering of patients in pain.    

There is one more complication concerning the problem of pain in this category of patients. The difficulties encountered in achieving pain relief in deforming arthrosis in many ways is explained by the lack in wider practice of specially developed methods of analgesia for various components of pain syndrome.

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