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PRP Preparation


Pentosan Molecule


Until recently, osteoarthritis (OA) has been managed with drugs designed to treat the symptoms rather than the underlying cause of the disease.  Symptomatic relief has been accomplished by the use of analgesics for pain relief as well as steroids and nonsteroidal antiinflammatory drugs (NSAIDS) to reduce inflammation.

Recently, researchers of osteoarthritis have directed their efforts towards developing structure-modifying osteoarthritis drugs (SMOADs), which are designed to treat the cause of the disease.Pentosan polysulfate, which has recently undergone clinical trial by the Orthopaedic Research Center at Colorado State University, has shown promise as a SMOAD.

Pentosan effects on Proteoglycans

Proteoglycans are an important component of the extracellular matrix within cartilage, which is the supporting material surrounding the cells.  Proteolgycans enable cartilage to withstand compression, as occurs during limb weightbearing. Osteoarthritis results in proteoglycan loss from cartilage, thereby deleteriously affecting its compressability.

Both sodium pentosan polysulfate (NaPPS) and glycosaminoglycan polysulfate ester (PSGAG or Adequan®), another antiarthritic drug, have been shown to stimulate synthesis of proteoglycans.  Only NaPPS increased the amount of proteoglycan incorporated into the extracellular matrix, however; PSGAG did not.  In addition, PPS can increase proteoglycan production without the help of the cytokine interleukin 1. PPS also preserves the normal ratio of the components of cartilage.

Pentosan effects on Hyaluronan

A major component of synovial fluid is hyaluronan (or hyaluronic acid).  Hyaluronan is produced by synoviocytes or synovial fibroblasts residing in the joint capsule, and is important for the lubrication of articular cartilage. Osteoarthritis causes a decrease in the amount of hyaluronan produced as well as a decrease in its molecular weight, both of which reduces the lubricating properties of synovial fluid. Studies have shown that pentosan polysulfate increases both the synthesis and molecular weight of hyaluronan produced in osteoarthritic joints. In contrast, glycosaminoglycan polysulfate ester (PSGAG) was not effective in accomplishing either within an inflammatory environment.

Pentosan effects on Vascularity

Normal articular cartilage is avascular (without blood supply) and depends on the underlying (subchondral) bone for nutrition.  Osteoarthritis results in a reduction in subchondral bone vascularity via deposition of the clotting factor fibrin and lipids in associated blood vessels, thereby occluding them.  PPS discourages clot formation through its antithrombotic-antilipidemic activity and also encourages the regrowth of endothelial cells lining these vessels. This improved blood supply increases the nutrition of the bone and cartilage cells, which in turn improves their metabolic activity and overall function.

Pentosan effects on Leukocytes

Osteoarthritis causes components of the articular cartilage to be degraded and released into the synovial fluid, which results in an immunological response in the form of synovial inflammation (known ar "synovitis).  These degraded cartilage components are attacked by antibodies and complement, which starts an inflammatory cascade resulting in accelerated cartilage degradation.  Pentosan polysulfate provides an antiinflammatory effect by binding to and inhibiting the action of leukocytes.

Pentosan effects on Degradative Enzymes and Chemical Mediators

Stromelysin (MMP-3) is a matrix metalloproteinase that degrades components of the cartilage matrix, including aggrecan, type II collagen, and link protein. Pentosan polysulfate inhibits the activity and decreases the levels of MMP-3.

Cytokines such as interleukin 1 (IL-1) and tumor necrosis factor (TNF) promote articular cartilage degradation by reducing the synthesis of proteoglycan and collagen type II and by increasing the release of matrix metalloproteinases.  These two cytokines are counteracted by a third cytokine, interleukin-6 (IL-6), which inhibits IL-1 and TNF and supports cartilage repair.  Although PPS does not affect IL-1, it has been shown to decrease the production of TNF and increase IL-6 synthesis.

Learn more about Pentosan and other JOINT THERAPIES in our CLIENT EDUCATION LIBRARY.



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THE ATLANTA EQUINE CLINIC: 1665 Ward Road, Hoschton, Georgia 30548 - ph. 678-867-2577

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