A growing body of evidence suggests that we should re-assess our management of osteoarthritis (OA) in dogs. Pain is not only a consequence of OA, but may also play a part in driving the disease process. This new understanding has profound implications for the way we manage dogs. Intermittent NSAID treatment, to treat flareups, may not provide the best long-term outcome. Continuous NSAID therapy (daily for 28 days or longer) may be more beneficial.
A growing body of evidence suggests that we should re-assess our management of osteoarthritis (OA) in dogs. Pain is not only a consequence of OA, but may also play a part in driving the disease process. This new understanding has profound implications for the way we manage dogs. Intermittent NSAID treatment, to treat flareups, may not provide the best long-term outcome. Continuous NSAID therapy (daily for 28 days or longer) may be more beneficial.
A growing body of evidence suggests that we should re-assess our management of osteoarthritis (OA) in dogs. Pain is not only a consequence of OA, but may also play a part in driving the disease process. This new understanding has profound implications for the way we manage dogs. Intermittent NSAID treatment, to treat flareups, may not provide the best long-term outcome. Continuous NSAID therapy (daily for 28 days or longer) may be more beneficial.
A growing body of evidence heightens the intensity of pain experienced Reassessing pain management following noxious stimuli. This is very important suggests that we should re-assess because the changes are anatomical and – Clinical evidence supporting our management of osteoar- long lasting. Once established, central this theory thritis (OA) if we are to provide sensitization is difficult to control, even with A soon-to-be-published systematic review potent analgesics – so prevention can be the of all the published studies on long-term pets with the best possible key to management. continuous NSAID therapy (daily for 28 days long-term prognosis. or longer) in dogs with OA indicated a benefit Osteoarthritic pain is harmful in several ways: of long-term continuous treatment with In recent years our understanding of joint A vicious cycle develops whereby repeated NSAIDs over short-term treatment and no pain, and in particular the mechanisms that exposure to pain leads to central sensitization evidence of any increase in side-effects.10 drive it, has changed. It is now apparent that which in turn makes the pain more severe and pain is not only a consequence of osteoarthritis, difficult to control and further perpetuates Will owners play their part? but may also play a part in driving the disease central sensitization. process.1 Dogs with painful OA are reluctant to With continuous NSAID therapy owners can exercise. Reduced activity leads to muscle be reassured that their pet is relieved of the This new understanding has profound implica- wasting, which is one of the factors that may pain and inflammation of OA, allowing tions for the way we manage dogs with contribute to OA disease progression.4 improved joint function and mobility, and osteoarthritis. It increases the importance of Central sensitization can increase the level perhaps slower disease progression. minimising or preventing pain. Providing of inflammation in joints.5 Inflammatory However this approach requires an increased intermittent NSAID treatment, to treat flare- mediators such as PGE2 have been shown to commitment from the owner. Daily dosing is ups, may not provide the best long-term contribute to cartilage degradation.6 undoubtedly inconvenient and at times may outcome. Instead, continuous NSAID therapy reduce compliance. One answer lies in the may be more beneficial. use of a new long-acting NSAID. The role of NSAID therapy COX-2 enzymes have been shown to play Sensitization a role in the development of central Trocoxil™ – the first and Research has shown that the components of the sensitization7, and their inhibition by NSAIDs only once-monthly NSAID pain pathway can change in response to a can prevent its development.8 Treatment of Trocoxil (mavacoxib) is a new, innovative pain stimulus. Pain receptors `up-regulate´ in central sensitization has been shown to preferential COX-2 inhibitor with a profile response to painful stimuli and become more reduce joint inflammation in models of which is ideally suited to continuous sensitive to subsequent pain. As a result, arthritis.9 treatment of pain and inflammation previously non-painful events (such as touch) associated with canine OA. After the can be interpreted as painful stimuli. Pain second dose, Trocoxil is administered If administration of daily NSAIDs is not once a month in the form of flavoured sensitization (`wind-up´) can also result in continuous, there is a risk that dogs will suffer chewable tablets. hyperalgesia where the pain threshold to pain which will stimulate pain pathways noxious stimuli is lessened, so that mild to A multicentre study involving client owned resulting in central sensitization. dogs with OA has shown that successive moderate pain is experienced as a more monthly dosing with Trocoxil leads to contin- intense pain. These changes occur in both The message is clear: potentially if pain ued improvement. 11
peripheral and central pain pathways.2,3 can be prevented by continuous
In the central pain pathways, exposure to In clinical field studies, the side-effects pain management, then the pain seen with Trocoxil have been similar in repeated painful stimuli changes the way pain is pathways will not be sensitized and type, frequency and duration to those seen processed. This so-called `central sensitization´ central sensitization will not occur. with daily carprofen. 11
References 1. Fiorentino PM et al. Spinal Interleukin-1β in a mouse model of arthritis
and joint pain. Arthritis Rheum 2008. 58(10): 3100-9 2. Hellyer P et al. AAHA/AAFP PAIN Load Pain Management Guidelines for Dogs & Cats. J Am Anim Hosp Assoc 2007; 43(5): 235-48 3. Schaible HG et al. Pathophysiology and treatment of pain in joint disease. Adv Drug Deliv Rev 2006; 58(2): 323-42 4. Herzog W et al. The role of muscles in joint degeneration and osteoarthritis. J Biomech 2007; 40(suppl 1): S54-63 5. Sluka KA et al. Joint inflammation is reduced by dorsal rhizotomy and not Obesity by sympathectomy or spinal cord transection. Ann Rheum Dis 1994; 53(5): 309-14 6. Hardy MM et al. Cyclooxygenase 2-dependent Prostaglandin E2 modulates cartilage proteoglycan degradation in human osteoarthritis explants. Arthritis Rheum INFLAMMATION 2002; 46(7): 1789-803 7. Samad TA et al. Interleukin-1β–mediated induction of COX-2 in the CNS contributes to inflammatory pain hypersensitivity. Nature 2001; Central 410(6827): 471-5 8. Veiga AP et al. Prevention by celecoxib of secondary Sensitization Inactivity hyperalgesia induced by formalin in rats. Life Sci 2004; 75(23): 2807-17 9. Sluka KA et al. Reduction in joint swelling and hyperalgesia following post-treatment with a `WIND-UP´ non-NMDA glutamate receptor antagonist. Pain 1994; 59(1): 95-100 10. Innes et al. Systematic review of the safety and efficacy of long term NSAID use in the treatment in canine osteoarthritis. Vet Record. (In press) 11. Payne-Johnson et al. Determination of the efficacy and safety of mavacoxib tablets administered monthly at 2mg/kg bw in the treatment of pain and inflammation associated with Rate osteoarthritis in dogs. BSAVA abstract 2009. of cartilage DISUSE degradation muscle wasting Joint instability The pain sensitization `wind-up´ cycle For further information please contact Pfizer Animal Health, Walton Oaks, Tadworth, Surrey KT20 7NS POM-V Trocoxil contains Mavacoxib. AH314/09