ABNORMALITIES IN THE OSTEOARTHRITIS SYNOVIUM

(Wikipedia def)

Synovitis is the medical term forinflammation of the synovial membrane. This membrane lines joints which possess cavities, known as synovial joints. The condition is usually painful, particularly when the joint is moved. The joint usually swells due to synovial fluid collection.

Synovitis may occur in association witharthritis as well as lupus, gout, and other conditions. Synovitis is more commonly found in rheumatoid arthritis than in other forms of arthritis, and can thus serve as a distinguishing factor, although it can be present to a lesser degree in osteoarthritis. Long term occurrence of synovitis can result in degeneration of the joint.

(Medscape select portions)

The Role of Synovitis in Osteoarthritis

Claire Y. J. Wenham, BM BS, MRCP, Philip G. Conaghan, MBBS, PhD, FRACP, FRCP

Disclosures

Ther Adv Musculoskel Dis. 2010;2(6):349-359. 

Synovitis is very common in the OA joint and has been associated both with symptoms and with structural progression. Many of the current effective treatments used for OA have an antisynovial effect but further large-scale clinical trials are needed to confirm the role of antisynovial agents in symptom and structure modification.

The gold standard for the diagnosis of synovitis is histology. The normal synovium is composed of 1–4 layers of cells which merge on their deep surface with a zone of loosely arranged fibrocollagenous tissue containing adipocytes, fibroblasts, mast cells and macrophages. The synovial membrane has an abundant blood and nerve supply running throughout the loose fibrocollagenous tissue. Biopsies from the synovium of OA knees (taken at arthroscopy for knee pain or at joint replacement) have demonstrated several key changes in the synovium, which although more pronounced in advanced OA, are present from the earliest stages of the OA process [Loeuille et al. 2005; Smith et al. 1997; Myers et al. 1990]. These synovial abnormalities include: thickening of the lining layer; increased vascularity; inflammatory cell infiltration.

Synovial membrane histology in classical inflammatory arthritides such as rheumatoid arthritis (RA) is characterized by a wide heterogeneity. OA synovium also displays this spectrum of changes, although there is a lesser degree of inflammation than in RA. The OA spectrum ranges from marked hyperplasia of the lining layer, with a dense cellular infiltrate composed largely of lymphocytes and monocytes, through to a synovial membrane which is thickened by fibrotic tissue [Haraoui et al. 1991]. Surface fibrin deposition and fibrosis within the synovium is common in OA, particularly in the later stages [Loeuille et al. 2005]. Direct comparison of the synovium between 12 OA subjects and 18 RA subjects at time of total knee replacement has shown more hyperplasia of the lining cell layer and cellular infiltrate in severe RA (treated with steroids and methotrexate) than in OA. However, in milder RA (subjects treated with nonsteroidal anti-inflammatory drugs [NSAIDs] only) the histological changes are similar to those seen in OA [Haraoui et al. 1991]. The synovitis seen in OA knees tends to be diffuse and is generally not localized to areas of chondral defects, although an association has been reported between chondral defects and associated synovitis in the medial tibiofemoral compartment of the knee [Ayral et al. 2005; Loeuille et al. 2005]. Interestingly, work by Blom and colleagues demonstrated that in an OA mice model, using an MMP3-knockout model, macrophage activation in the synovium is essential for cartilage damage via the production of matrix metalloproteinases (MMPs), suggesting that inflammation within the synovium may be pivotal for cartilage damage [Blom et al. 2007].