The pathogenetic influence of inflammatory mediators on the development of secondary osteoarthritis depending on the stage of articular cartilage degeneration

Background. Osteoarthritis (OA) is one of the most common diseases of the musculoskeletal system. According to statistical data, this disease most often affects large joints, especially knee joints. To date, there are many views on the mechanisms of the development of OA, which has been the subject of debate for a long time. It is believed that the development of OA is based on chronic productive inflammation with degradation of articular cartilage structures, proteoglycans, fragments that enter the joint cavity, which is accompanied by their phagocytosis by leukocytes with the release of inflammatory mediators and lysosomal enzymes. As a result, a cascade of pro-inflammatory cytokines is triggered, intensifying degenerative processes in articular cartilage. The study of these factors is relevant for the diagnosis of the stages of degeneration and the development of pathogenetic therapy for OA. Purpose – is to study the pathogenetic influence of inflammatory mediators in patients on the development of secondary osteoarthritis depending on the stage of articular cartilage degeneration. Materials and Methods. A study was conducted in 117 patients aged 19 to 45 years who were undergoing inpatient treatment at Artz Klinic in Kharkiv for secondary OA of the knee joint. The diagnosis was established according to the International Classification of Diseases of the 10th revision – M18.1. The control group consisted of 25 healthy volunteers. To determine the stage of degenerative changes, the classification of the International Society for the Study of OA (OARSI) was used, which distinguishes 4 stages of articular cartilage damage from the volume (%) of degenerative changes: 1 – < 10%; 2 – 10–25%; 3 – 25–50%; 4 – > 50%. To identify the stage of the inflammatory process, the level of the histamine mediator in whole blood was determined (according to accepted methods). The level of autoantibodies to histamine, hemolysate, hyaluronidase, phytohemagglutinin, hyaluronic acid, chondroitin sulfate, and heparin was determined by using the Ouanier nephelometric reaction with quantitative determination of antibodies as modified by N.M. Klemparska. The obtained results were statistically processed with the determination of the average statistical value and its error. The reliability of the obtained results was determined according to the Studentʼs criterion. Results. It was established that in patients with 1st and 2nd degree of articular cartilage degradation, an increase in histamine in whole blood and autoantibodies was determined, which characterized the exudative-alterative phase of inflammation, and in patients with 3rd and 4th degree of articular cartilage degradation, we diagnosed a decrease in histamine, which indicated on the switch to the proliferative phase of inflammation in such patients. It is shown that an increase in the level of autoantibodies to hemolysate, hyaluronidase, hyaluronic acid, chondroitin sulfate, and heparin characterizes the increase of the autoimmune component. The increased level of autoantibodies to phytohemagglutinin indicates a predominant reaction of slow-type hypersensitivity, production of proinflammatory cytokines by effector cells in patients with stage 3 and 4 (25–50%) of articular cartilage degradation. These dataprovide an opportunity to expand immunodiagnostics and develop pathogenetic approaches to the treatment of this contingent of patients. Conclusions. For the immunodiagnosis of secondary OA in patients, an immunodiagnostic complex has been developed based on the level of histamine and autoantibodies to him, which allows diagnosing the alternative-exudative stage, and based on the level of autoantibodies to hemolysate, PHA, hyaluronic acid, chondroitin sulfate, heparin, it is possible to outline the pathogenetic features of the development of the productive stage chronic inflammation and degeneration of articular cartilage and develop pathogenetic approaches to therapy for secondary OA.