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There is growing evidence that vascular pathology plays a role in the onset and / or progression of an underlying joint disease: osteoarthritis deformans (DOA). Possible mechanisms: an episodic decrease in blood flow in small vessels in the subchondral bone at the ends of long bones and a related decrease in the flow of interstitial fluid in the subchondral bone. Blood flow can be reduced due to venous occlusion and stasis or due to the development of microembolism in the subchondral vessels. There are several probable factors of subchondral ischemia: the first of them is a violation of the metabolism of nutrients in the articular cartilage, which is a potential initiator of degradation changes in the cartilage. The second is apoptosis of osteocytes in the regions of the subchondral bone, which initiates the resorption of osteoclasts of this bone and, at least temporarily, reduces the bone support for the overlying cartilage. It may be important to recognize these potential etiological factors in order to develop more effective therapies that prevent progression of OA.