using nutrition to ease the pain of osteoarthritis - HillsVet

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nutrition myths and truths, facts and fallacies Physical Stress DOD Weight Trauma Structural & Functional Failure Cartilage Damage X Inflammation EPA X Matrix Damage Degradation caused by aggrecanases processes. Normally, arachidonic acid is the precursor for the synthesis of these inflammatory cytokines. EPA, an omega-3 fatty acid, competes with arachidonic acid for the same enzyme systems; and the eicosanoids derived from EPA promote minimal to no inflammatory activity. Thus, a diet containing n-3 fatty acids results in a decrease in membrane arachidonic acid levels and an associated decrease in the pro-inflammatory cytokines that perpetuate OA. Studies have documented that inflammatory eicosanoids produced from arachidonic acid are depressed when dogs consume foods with high levels of n-3 fatty acids, and specifically foods containing EPA. Though the exact molecular mechanisms for reducing inflammation (likely via resolvins and protectins) have not been fully explained, it is conceivable that omega-3 fatty acids modulate this process at the level of the genome or proteome. Four randomized, double-masked, controlled studies have been conducted in which arthritic dogs were fed a control food or a test food containing various levels of EPA (omega-3 fatty acid). These studies reported that the dogs fed the EPA-supplemented food improved in range of motion and ability to bear weight, had a decrease in pain and lameness, had significantly improved ability to rise form a resting position, and improved ability to run and play at 6 weeks. In one of these studies, biomechanical force plate analysis was also performed and found that dogs fed a diet containing EPA had an increase in weight bearing on the affected limb. Only 31% of the “control” dogs had improved weight bearing after the 90-day feeding trial, whereas 82% of dogs in the “EPA” group showed increased weight bearing. These clinical studies indicate that nutritional management using a therapeutic food supplemented with n-3 fatty acids helped improve the clinical signs of osteoarthritis in dogs as noted by pet owners, clinical orthopedic examination, and gait analysis of ground reaction forces. Disease-modifying osteoarthritis agents: These agents reportedly enhance cartilage health by providing the necessary precursors to maintain and repair cartilage. Many have been shown to positively affect cartilage matrix, enhance hyaluronate production, and inhibit catabolic enzymes. Oral disease-modifying OA agents typically contain glucosamine and chondroitin sulfate in various forms. Glucosamine is a precursor to the disaccharide unit of glycosaminoglycans, which comprise the proteoglycan matrix of articular cartilage. Studies using radiolabeled compounds have shown that 87% of orally administered glucosamine is absorbed and is eventually incorporated into the cartilage matrix. Glucosamine reportedly acts by providing the regulatory stimulus and raw materials for synthesis of glycosaminoglycans. Since chondrocytes obtain preformed glucosamine from the circulation (or synthesizes it from glucose and amino acids), adequate glucosamine levels in the body are essential for synthesis of glycosaminoglycans in cartilage. Glucosamine is also used directly for the production of hyaluronic acid by synoviocytes. In vitro biochemical and pharmacological studies indicate that the administration of glucosamine may normalize cartilage metabolism and stimulates the synthesis of proteoglycans. Clinical trials in man and animals indicate that glucosamine may have a positive effect on cartilage health and helps control symptoms associated with OA. X Figure 4: Pathophysiology of OA — In the dog, high levels of EPA help control pathways of inflammation and degradation.
nutrition myths and truths, facts and fallacies Chondroitin Sulfate (CS) is the predominant glycosaminoglycan found in articular cartilage. Bioavailability studies have shown 70% absorption of CS following oral administration. The effect of CS on cartilage has been investigated in several in vivo and in vitro studies. The findings suggest that CS reduces collagenolytic activity, inhibits degradative enzymes, increases hyaluronate concentrations, and reduces symptoms of OA. Most research indicates that glucosamine and chondroitin sulfate work synergistically. Numerous studies performed on one such combination (Cosequin ® Nutrimax Laboratories, Inc.) have demonstrated improved synthesis of glycosaminoglycans and reduced proteolytic activity. Clinical trials have repeatedly shown a positive clinical effect in OA patients. Injectable disease-modifying OA agents are also available, the most common one used in dogs being Adequan ® * (used under license, Novartis Animal Health). Adequan is a polysulfated glycosaminoglycan (PSGAG), and studies have shown it has a positive anabolic effect on cartilage and decreases cartilage catabolism. Anti-inflammatory and analgesic medications (NSAIDs): NSAIDs are used because of their ability to reduce joint pain and decrease synovitis. A variety of NSAIDs are available for use in animals and are effective, in part, by decreasing prostaglandin synthesis through the inhibition of cyclooxygenase (COX). Newer NSAIDs have been shown to have no detrimental affect on the synthesis of cartilage proteoglycans in vitro at the recommended dosing. Drugs commonly used to control pain in dogs with OA include acetaminophen (15 mg/ kg q 8h), carprofen (4.4 mg/kg q 24h), etodolac (10-15 mg/kg q 24h), meloxicam (0.1 mg/kc q 8h), deracoxib (1-2 mg/kg q 24h), and tepoxalin (10mg/kg q 24h) among others. It is important to recognize that individual patients respond to specific NSAIDs quite differently. Corticosteroid treatment for OA remains controversial. Corticosteroids decrease the production of arachidonic acid, are potent anti-inflammatory agents, and decrease catabolic activity within the joint. However, corticosteroids may also damage cartilage (with long-term usage) by decreasing synthesis of collagen and matrix proteoglycans. Summary Although prevention of osteoarthritis is ideal, it is not always possible. Because osteoarthritis is a heterogeneous disease with diverse origins, it can present with a range of clinical manifestations. As a result, therapeutic recommendations should be customized for each patient. When appropriate, surgical correction of underlying conditions should be considered. After osteoarthritis is diagnosed, clients should be educated to foster realistic expectations. Osteoarthritis is usually irreversible but good management can minimize pain and slow progression of the disease. The goals of management include: ✔ mitigation of risk factors ✔ controlling clinical signs ✔ slowing progression of the disease. Thus, effective treatment requires a multimodal approach, of which therapeutic nutrition is an important component. The goals of nutritional management include reducing inflammation and pain, enhancing cartilage repair, slowing cartilage degradation and providing tangible improvement in clinical signs of osteoarthritis. Foods designed for patients with osteoarthritis should supply age-appropriate nutrition and specific nutrients that may help reduce inflammation and pain, slow the degradative process, complement prescribed medications and provide tangible improvement in clinical signs. * As with all drugs in this class, side effects involving the digestive system, kidneys or liver may occur. These are normally mild, but may be serious. Pet owners should discontinue therapy and contact their veterinarian immediately if side effects occur. Evaluation for pre-existing conditions and regular monitoring are recommended for pets on any medication, including Adequan. ® Use with other NSAIDs or corticosteroids should be avoided.
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