Page 536 - WSAVA2018
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 25-28 September, 2018 | Singapore
R. Koh1
1Veterinary Teaching Hospital, Louisiana State University School of Veterinary Medicine, Baton Rouge, USA
2Veterinary Medical Center, University of Florida College of Veterinary Medicine, Gainesville, USA
Degenerative joint disease (DJD) also known as osteoarthritis (OA), is a chronic, debilitating disorder affecting a wide range of animal species and humans. It has been reported that OA may affect up to 20%
of the canine population over one year of age, and
likely a similar percentage of cats (and has increased
in incidence 38% in dogs and 67% in cats since 2007 according to data from Banfield Pet Hospitals). It is estimated that more than 11 million dogs, or 1 of out 5 dogs, in the US alone, was affected by OA. It is regarded as the number 1 cause of chronic pain in dogs. Unlike in humans where the DJD is primarily as a result of aging and “wear and tear”, DJD in dogs and cats is typically secondary, initiated by a previous insult to the joint
or joint instability. It is a common cause of joint failure with stiffness, loss of mobility, and varying degrees of inflammation and pain. It is a slowly progressive condition for which no specific treatment can restore the articular cartilage to normal. Therefore, early identification of
DJD is critical to provide patients with the most effective treatment strategies and relief of clinical signs.
What is cartilage?
Cartilage is made up of three main components:
1) Chondrocytes, which by weight comprise the smallest proportion of the cartilage;
2) Extracellular matrix (ECM), made up of type II collagen fibers and proteoglycans (PG), which serve to trap water within the matrix;
3) Water, which makes up 70% of the cartilage by weight and gives cartilage it’s unique biomechanical properties.
Chondrocytes function to synthesize the components
of the ECM and also produce the enzymes that
degrade the ECM, thus regulating cartilage anabolism and catabolism. Various cytokines and growth factors balance these anabolic and catabolic activities in healthy cartilage. In a joint affected by DJD, catabolic processes outweigh the anabolic processes. This imbalance is driven by cytokine cascades and inflammatory mediators, such as interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α). It results in reduced proteoglycan concentration,
altered aggregation of the PGs and ultimately, reduced ability of the ECM to retain water. Collagen fibers also become disrupted. These cytokines and other cytokines (IL-8, IL-6, etc.) also upregulate the expression of proinflammatory enzymes cyclo-oxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) that lead to increased production of prostaglandin E2 (PGE2) and nitric oxide (NO).
Although we tend to focus on the articular cartilage when discussing OA, it is important to remember that OA is
a global process within the joint, affecting not only the hyaline cartilage, but the synovial membrane, synovial fluid, and subchondral bone as well. Clinical effects in patients suffering from OA include joint instability, joint mal-alignment, joint pain and diminished range of motion, joint effusion, and varying degrees of lameness and immobility. The patient as whole begins to lose muscle strength and cardiovascular fitness while gaining weight. This catabolic process takes on a “snowball effect” that affects the family interactions with the pet and becomes difficult to reverse. It is important to remember that once patients begin showing these signs, the disease process is typically quite advanced.
Recent years have seen a dramatic shift toward multimodal management strategies for OA management, including anti-inflammatory medications, analgesics, therapeutic modalities, therapeutic exercise, and nutraceuticals or so called “disease modifying osteoarthritis agents” (DMOAs). The potential benefits
of the majority of these recommendations are readily recognized.
Where’s The Evidence For Nutraceuticals? A. Adequan (Novartis)
Adequan is probably the most well-known and frequently used DMOA and is chemically referred to as
a polysulfated glycosaminoglycan (PSGAG). It is typically given intramuscularly (IM) and studies have shown that
it does reach therapeutic levels in serum, synovial fluid, cartilage and tendons. It modifies the progression of OA by maintaining a more normal cartilage histology through stimulation of increased glycosaminoglycan (GAG) synthesis by chondrocytes and inhibition of destructive enzymes such as MMPs. Though experimental evidence of Adequan’s positive anabolic effect on cartilage is conflicting, its ability to decrease cartilage catabolism has been shown in numerous studies on both horses and dogs. Adequan also has a poorly understood anti- inflammatory effect. Ultimately, the PSGAG allows the cartilage to hold more water and makes it more resistant to degradation. For optimal results, Adequan should probably be used earlier in the disease process than
it has typically been employed in the past. In dogs, a dosage of 5 mg/kg intramuscularly (IM) twice weekly is commonly recommended.

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