New Information about
Proc 17th Annual Veterinary Medical Forum, 1999 Randolph H. Stewart, DVM, PhD, and Glen A. Laine, PhD, College Station, TX
Pathophysiology of synovial effusions Speaking at the 1999 Medical Forum, Dr. Randolph H. Stewart described the latest understanding of synovial joint effusion and the role it plays in joint disease. He emphasized that our knowledge of the determinants of normal synovial fluid balance and the causes and effects of synovial effusion is incomplete and continues to evolve. He pointed out that the synovial cavity does not possess a basement membrane as in the peritoneal cavity. The synovial membrane itself is a layer of vascular interstitium covered by an incomplete layer of synoviocytes. He made the distinction that synovial fluid is interstitial fluid rather than a true cavity fluid, meaning that the rules that govern its formation and removal differ. Synovial fluid traverses only the capillary membrane and surrounding interstitial matrix to enter the joint space and must return across the same interstitial matrix before it can enter the lymphatic system, while pleural and peritoneal fluids must be filtered across the capillary membrane and the cavity basement membranes during formation. The normal resting intraarticular pressure (lAP) reported in most joints is 1 to 2 mmHg subatmospheric. When the limb is flexed or when isometric tension is applied by contraction of the limb muscles, the IAP increases by as much as 3 mmHg. lAP has been shown to increase as a function of both synovial fluid volume and limb movement or muscle activity. "In joints with effusion, the IAP is slightly over atmospheric pressure at rest and increases dramatically, often over 60 mmHg, when the limb is exercised," Dr. Stewart said. "This increase in IAP appears to be more characteristic of inflammatory effusions than of effusions associated with acute joint trauma. The importance of this increase in IAP has been brought into focus by studies demonstrating an inverse relationship between IAP and synovial blood flow." In one study there was an 84% decrease in synovial membrane blood flow in horses when the IAP of the midcarpal joint was increased from control values (-2.86 + 1.45 mmHg) to over 30 mmHg. He pointed out that several studies have provided evidence supporting the adverse effect of increased synovial fluid volume and pressure on synovial blood flow. He suggested that part of the pathophysiology of persistent synovitis/arthritis is a cycle of hypoxic-reperfusion injury. This was described as follows: "The intraarticular hypoxia occurs when the limb is flexed or exercised due to increased IAP and decreased synovial blood flow. When the limb is subsequently rested, normal blood flow is restored and this reperfusion results in liberation of reactive oxygen species. These radicals then create further tissue damage perpetuating the inflammation and effusion. This hypothesis is supported by the finding that exercise of joints suffering inflammatory synovitis caused an increase in the synovial fluid concentration of lipid peroxidation end-products characteristic of the action of reactive oxygen species." The reactive oxygen radicals in the joint lead to degradation of hyaluronan (HA), resulting in decreased molecular weight. Dr. Stewart pointed out that HA is known to play important roles in wound healing, cell proliferation, cell locomotion and regulation of immune function in inflammation. He explained that these activities are mediated JOURNAL OF EQUINE VETERINARY SCIENCE
through a family of HA-binding proteins called hyaladherins that allow HA to interact with and exert an effect on the behavior of leukocytes and endothelial cells. The HA produced by the synoviocytes within the joint must pass through the synovial interstitial tissue to be removed by the lymphatic system. He believes it is possible that the behavior of the cells in and around the arthritic joint is altered by the damaged HA aggravating the inflamed state, and points out that this provides another mechanism by which the cycle of hypoxia and reperfusion could perpetuate the inflammation within synovial tissues. "Synovial fluid is not static, but is undergoing constant turnover," he explained. "It is an ultrafiltrate of plasma arising from the microvasculature of the synovial lining and it is eventually drained by the lymphatic system. Hyaluronan produced within the joint is removed along with the synovial fluid and much of it is degraded within the lymph nodes. An important barrier to fluid movement into and out of the joint cavity is the complex fibrous matrix (hyaluronan, collagen, chondroitin and heparan proteoglycans, fibronectin, etc.) that composes the synovial interstitium. Currently, little is known concerning the properties of this matrix as a barrier and the factors that affect this barrier function. Recent studies have demonstrated that the behavior of interstitial matrices and the interaction with interstitial fluid is much more complex than previously thought and that this behavior can change in response to (or as part of) the process of inflammation. A series of studies showed that fluid accumulation within inflamed interstitial tissue is accompanied by a decrease, rather than an increase, in interstitial fluid pressure. The explanation is that the inflammatory stimulus caused a primary change in the structure of the interstitial matrix that changed the pressure-volume relationship within the interstitium and caused a fall in the interstitial fluid pressure. This pressure decrease then resulted in accumulation of more interstitial fluid." The most recent view of synovial effusion is that it is not only a result of synovitis/arthritis, but also is a contributor to and perpetuator of the inflammatory process. More information is needed concerning the effect of inflammation on the synovial interstitium or the normal or pathologic behavior of the synovial lymphatic system, according to Dr. Stewart. He said we currently have no clear idea of why synovial effusions occur in the first place.
Arthroscopic surgery study A retrospective study of 176 Standardbred horses that had arthroscopic surgery for carpal chip fractures over a seven-year period was done in order to determine fracture location and post operative performance. Chip fractures of the proximal third carpal bone and the distal radiocarpal bone occurred with equal frequency (49.2 and 49.6%, respectively), and chip fractures involving the antebrachiocarpal joint were rare. Trotters had significantly more third carpal bone lesions than radiocarpal bone lesions when compared to pacers (P = 0.0304). Seventy-four percent of horses made at least one start following surgery. It is concluded that the majority of Standardbreds will be useful racehorses following carpal arthroscopy; however, most earn less money per start and many race at a lower class. Volume 19, Number 8, 1999
Lucas JM, et al.: Post operative performance of racing Standardbreds treated arthroscopically for carpal chip fractures: 176 cases (1986-1993) Eq Vet J 1999;31 (1).