8/18/2023 0 Comments Subchondral sclerosis![]() In end-stage OA, synovitis displaying high infiltration of CD68 + macrophages is present in up to 90% of the patients. Synovial tissue thickness and the extent of inflammatory cell infiltration are clearly correlated. In knee OA, synovitis is predominantly located posterior to the crucial ligament and in the suprapatellar region. The histologic hallmark of OA-induced synovitis is proliferation and hyperplasia of the lining cells along with moderate inflammatory cell infiltration and neoangiogenesis ( Fig. The subintimal layer has a complex vascular network of lymphatic and blood vessels. Villi increase the synovial surface further and allow adaption of the shape of the capsule during movement. Areolar synovial tissue is a loose and highly viscoelastic connective tissue that permits stretching or folding. Depending on the joint-specific biomechanics, the subintima can be composed of different types of connective tissue: fibrous, fatty or areolar. Synoviocytes do not possess a basal layer and lack cell–cell junctions, which facilitate the exchange between SF with blood or lymphatic vessels. Type A cells resemble macrophages and phagocytes whilst type B cells are fibroblasts secreting hyaluronan and other proteins. The inner layer of synovial tissue is called the intima and consists of a lining of cells, the type A and type B synoviocytes. Hyaluronan is also responsible for ensuring constant SF volume during exercise. By the production of hyaluronan and plasminogen activator, the synovium preserves articular mobility. Apart from cartilage nutrition and lubrication, the main function of synovial tissue is to prevent adherence of the capsule with cartilage. Synovial tissue separates the joint capsule from the joint cavity. The focus of this translational review therefore is on histopathological changes of the synovium and subchondral bone along with the consequences, notably in cartilage damage. Despite both synovial and subchondral bone pathology seeming to play a pivotal role in OA progression, it is still unclear if and how they are associated with each other and how they trigger cartilage damage. Owing to this, osteoclast inhibition by bisphosphonates or strontrium ranelate has been shown to be an effective treatment for OA in controlled clinical trials. However, newer imaging modalities such as CT osteoabsorptiometry (CT-OAM) and hybrid SPECT-CT demonstrate that a constant and potentially reversible bone remodelling already takes place in early OA. Osteosclerosis and osteophyte formation in conventional radiography are considered as features of advanced OA. BMLs are increasingly recognized as a reliable marker for OA as they develop and reverse earlier than cartilage damage. Bone marrow lesions (BMLs) are regularly encountered, for example, in early knee OA, as a sign of mechanical overload. A nested case–control longitudinal MRI study identified the presence of effusion and Hoffa synovitis at baseline as major risk factors for development of radiographic OA. A substantial volume of synovitis in suprapatellar, infrapatellar and intercondylar regions considerably increases the risk for incident radiographic knee OA. The advent of MRI has underlined the pathogenic role of both synovitis and the subchondral bone tissue in OA. Inflammatory symptoms such as joint effusion or articular stiffness are common in OA and synovial inflammation detected by sonography occurs in more than half of the patients with early OA. These include muscle, ligaments, entheses, synovial tissue and the subchondral bone. Instead of being a pure cartilage disorder, OA is now considered as a whole-joint disease that affects various anatomical structures in and around the joint capsule. While mechanical overload, malalignment or joint instability frequently underlie OA in the lower extremity, metabolic factors such as hypercholesterolaemia and genetic predisposition seem to play a larger role in hand or facet joint OA. Due to substantial anatomical and biomechanical differences, OA is a highly joint-specific disorder. One reason for this is the heterogeneity of OA and its complex pathogenesis. Arthroplasty has been a major breakthrough in the treatment of advanced OA, yet a non-invasive disease-modifying treatment notably for early or intermediate OA stages is lacking. OA is a major socioeconomic health burden leading to chronic pain and disability. In OA, synovitis triggers osteoclastogenesis, pannus formation and increases adherence of synovial tissue to cartilage.Ĭhronic mechanical impairment in combination with metabolic dysregulation is a common trigger of subchondral bone changes and osteophytosis. Both synovitis and subchondral bone remodelling are actively involved in OA and often precede cartilage damage. ![]()
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