The laboratory assessment of synovial fluid includes an evaluation of physical characteristics, chemical tests, cell counts, and differential count. The following list summarizes the causes of inflammatory and noninflammatory joint diseases in dogs and cats : The type and number of leukocytes that infiltrate the synovium and migrate into synovial fluid define the cellular components of the joint effusion and the clinical features of the arthritis. The newly arrived leukocytes promote further inflammatory changes and cause the release of degradative enzymes from multiple cell types. In response to an insult, chondrocytes and synoviocytes release cytokines, which causes vasodilation of the subsynovial capillaries, leading to increased vascular permeability and extravasation of fluid, protein, and inflammatory cells into the joint space. The formation of abnormal synovial effusions is similar whether it is mediated by cartilage injury that occurs in degenerative joint disease or by the synovitis of immune-mediated arthritis and differs mostly in the character and severity of the cellular infiltrate and articular damage. Together, these cells prevent large molecules, such as plasma proteins, from entering the joint fluid and participate in the maintenance of articular cartilage. The inner synovial lining consists of two cell types: type A synoviocytes, macrophage-like cells with phagocytic function, and type B synoviocytes, fibroblast-like cells that produce hyaluronic acid. These vessels are the source of the plasma ultrafiltrate that becomes synovial fluid ( Fig. Next, the subsynovium contains a vascular and neural network enmeshed in a loose fibrous connective tissue. The outermost fibrous layer provides stability and flexibility to the joint. The joint capsule is made up of three layers. Assays for these enzymes are not readily available for diagnostic purposes. As a result of normal cartilage maintenance, degradative enzymes, such as stromelysin (MMP-3), and proteoglycan fragments can be detected in synovial fluid. The rigid collagen framework restricts the expansion of hydrophilic proteoglycans, providing articular cartilage with its unique ability to withstand compressive forces. Type II collagen predominates in articular cartilage, with smaller amounts of types VI, IX, X, and V/XI. The major proteoglycan of articular cartilage is aggrecan, a large polymer consisting of numerous proteoglycan moieties noncovalently bound to a nonsulfated GAG, hyaluronan. The GAGs of articular cartilage include keratin sulfate (KS), chondroitin sulfate (CS), and heparan sulfate. Proteoglycan consists of a polypeptide core with one or more negatively charged glycosaminoglycan (GAG) side chains. The proteoglycan matrix and collagen of articular cartilage are synthesized and maintained by chondrocytes located in lacunar spaces embedded within the cartilage. Joints are made up of two opposing cartilage surfaces surrounded and supported by a multilayer capsule and bathed in synovial fluid. To understand the formation of joint effusions, knowledge of the anatomy and physiology of healthy joints is important. Arthrocentesis and examination of the synovial fluid can confirm the presence of arthritis, characterize the response as inflammatory or noninflammatory, and, in some circumstances, reveal the etiologic agent. All cases of lingering lameness and those unresponsive to nonsteroidal anti-inflammatory drugs should have synovial fluid analyzed to rule out a chronic infectious process. In general, joints that contain excessive fluid should be sampled however, if none exist, at least two to three joints should be sampled, especially the carpal and tarsal joints. Synovial fluid analysis is also recommended in disorders characterized by persistent or fluctuating fever of unknown origin, shifting leg lameness, or generalized malaise in which arthralgia is suspected. The technique of arthrocentesis to acquire synovial fluid for analysis is no more difficult or imbued with risk than pleurocentesis or abdominocentesis. Arthrocentesis and joint fluid analysis are integral to the clinical evaluation of not only primary joint disorders but systemic diseases in which joint effusion is part of the clinical picture.
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