[Clinical and laboratory features of different forms of osteoarthrosis]

Inflammation is currently believed not only to influence clinical manifestations ofosteoarthrosis (OA) but also to be a key pathogenetic link in the chain reaction underlying progress of the disease. Patients with OA and signs of local inflammation undergo a change of algofunctional index and markers of inflammation, such as C-reactive protein (C-RP) and interleukin-6 (IL-6). Inflammation markers in patients with isolated disease of large joints are more affected than in women with OA and concomitant pathologies. Increased levels of C-RP and IL-6 in women with gonarthrosis/coxarthrosis confirm the key role of inflammation in the progress of this OA variant. Imbalance of IL-6 and its soluble receptors is an indicator of substantial impairment of the adaptive capacity in these patients. Elevated C-RP and IL-6 levels in patients with OA suggest chronic inflammation in patients with degenerative-dystrophic joint affection. Derangement of compensatory and adaptive processes in OA is associated with chronic immuno-inflammatory changes accompanied by hypersecretion of cytokines and proteolitic enzymes. Aggressive action of inflammation mediators in isolated affection of large joints accounts for the predominance of catabolic processes over anabolic ones which leads to further progress of OA due to low efficiency of the recovery of cartilage tissue and activation of its destruction. OA with concomitant pathologies leads to the disturbance of coordinated inflammatory response and cytokine cascade associated with inadequate IL-6 production. It is concluded that local and systemic immunopathologic processes in patients with OA form a vicious circle and contribute to the progress of degenerative-dystrophic processes in the joints.