Today, the role of the traumatic factor and inflammation in the development and progression of osteoarthrosis is generally recognized, but the available research results do not allow to establish the role of impaired biomechanics as a monofactor in the development of deforming ostearthrosis of the shoulder joint. Violation of the function of the bone and bone-cartilage elements of the joint, which is compensated by soft tissue formations, leads to overloads of the joints, upsets the normal balance of the load forces in the joint, creates abnormal biomechanics and the resulting pathological manifestations of deforming osteoarthrosis. The aim of the study is research of the dynamics of the disturbed biomechanics influence of the shoulder joint on the development of deformation osteoarthrosis and the features of the development of its structural changes. The experiments were conducted on guinea pigs weighing 380-420 grams at the age of 5 months. A model of surgical restriction of joint mobility was reproduced, which caused the formation of contracture. Using the methods of histology and scanning electron microscopy, we studied the relief of the articular surface, the topography of degenerative changes, and structural changes in the articular cartilage and subchondral bone. A statistical evaluation of the obtained data samples was carried out using Student t-test. The results were considered reliable at р<0.05. The results of an experimental study demonstrated a decrease in the thickness and structure of articular cartilage when modeling deforming osteoarthrosis and confirmed the hypothesis that pathological limitation of the mobility of the shoulder joint and violation of biomechanics is an independent factor in the formation of osteoarthrosis. After surgery on day 30, degenerative changes and their progression with the formation of contracture on day 90 of observation were found in the articular cartilage. The features of the development of articular surface degeneration, the dynamics of the pathological changes and topography, which can expand the understanding of the pathogenesis of the disease, were established. The loss of the superficial zone caused the progression of dystrophic changes in the articular cartilage and sclerosis of the subchondral bone at 60 and 90 days.
Biomechanical testing of the calcified metacarpal articular surface and its association with subchondral bone microstructure in Thoroughbred racehorses
