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Osteoarthritis in cats (Proceedings)
Two basic types of joint disease afflict people and animals: degenerative joint disease (osteoarthritis) and inflammatory joint disease (e.g., rheumatoid arthritis).
Two basic types of joint disease afflict people and animals: degenerative joint disease (osteoarthritis) and inflammatory joint disease (e.g., rheumatoid arthritis). Inflammation may be present in osteoarthritis (OA) as well, but it is not the central feature, and may wax and wane. OA is a progressive disease where the articular cartilage is slowly destroyed and the underlying bone reacts with remodeling and production of osteophytes.
Knowledge about OA in cats – prevalence, impact on lifestyle, efficacy of therapy – is less well developed than for the dog. Since cats have a small body size, and are light and agile, they compensate for orthopedic diseases better than dogs. Cats are also notorious for hiding signs of illness, especially if onset is insidious, and it is more difficult to interpret signs of pain or discomfort (Taylor and Robertson 2004).
Signalment and Clinical Signs
Only recently has a study reporting the characteristics of a series of cats clinically affected with OA been published (Clarke and Bennett 2006). Cats were included in the study (n=28) if they had historical evidence and/or clinical signs of OA, along with radiographic evidence. The most commonly affected joints were the elbow (45%) and hip (38%). Most cats (22/28) had bilateral joint involvement. The median age of cats with OA was 11 years (range 3.2-16 years) and there was no gender predisposition. The average age of cats with OA was also older in other recent studies: 10.8 years (Godfrey 2005), 13.8 years (Godfrey 2002), and 15.2 years (Hardie, Roe et al. 2002).
Clinical signs associated with OA in cats include (Hardie 1997; Godfrey 2002; Beale 2005; Clarke and Bennett 2006):
2. Reduced activity
3. Anorexia, weight loss
4. Irritability, aggression
5. Restricted ability to do normal activities
6. Inappropriate elimination and constipation
7. Decreased grooming
8. Lameness or stiff gait
Physical exam findings associated with OA include (Beale 2005):
1. Pain on joint manipulation
2. Soft tissue swelling
3. Periarticular thickening
4. Joint effusion
5. Restricted range of movement
6. Muscle atrophy
The extent to which the general cat population suffers from OA is unknown. One retrospective study reviewed radiographs of 100 cats over 12 years of age that were presented for reasons unrelated to lameness (Hardie, Roe et al. 2002). Radiographic evidence of degenerative joint disease was found in 90% of the cats. The elbow was most frequently affected with severe lesions found in 17% of the joints examined. Four of the cats had neurologic disease associated with lumbosacral lesions. One limitation of this study was that relatively few hip joints were visible in the radiographs evaluated, possibly leading to underestimation of degenerative changes in this location. Only 4% of cats affected with OA had clinical signs noted in the medical record.
Evaluation of radiographs from a hospital population of 218 cats in the U.K. found a prevalence of radiographic signs of OA of 33.9% (Clarke, Mellor et al. 2005). The prevalence of signs of appendicular joint OA was 16.5% (36/218), and of these cats, only 6 had clinical signs of lameness noted in the medical record.
Another retrospective study of 292 adult cats in the U.K. radiographed for any reason found 22% with evidence of OA (Godfrey 2005). The elbow was also the most commonly affected joint in this study. Of the cats with radiographic OA, 33% had clinical signs. In many cases, there was no evidence of OA in the patient medical record. This suggests that correlation between radiographic and clinical OA is poor or that clinical signs of OA go unobserved by owners or unrecorded by veterinarians.
It is assumed that the etiopathogenesis of OA is the same for cats and dogs, although little evidence currently exists to support this assumption. Suspected causes include primary degeneration (wear and tear), joint dysplasia, joint injury, fractures, luxations and dislocations, congenital malformations, cranial cruciate ligament rupture, infection, and neoplasia. The clinical presentation of OA in cats is different from dogs, and the radiographic signs differ slightly. Joint injuries are less common in cats than dogs but hip dysplasia is probably underestimated in cats. In one study, 6.6% of 684 cats had radiographic signs of hip dysplasia and the incidence was breed dependant (Keller, Reed et al. 1999). Radiographic signs of hip dysplasia are different in cats than dogs. A shallow acetabulum with remodeling and proliferation along the craniodorsal margin were the most common signs.
The hallmark of OA is the progressive and permanent damage of articular cartilage (Neil, Caron et al. 2005). Injury of the chondrocytes leads to the production of inflammatory mediators such as cytokines (especially interleukin-1 [IL-1]) and tumor necrosis factor alpha. IL-1 stimulates production of degradative enzymes, inhibits production of proteoglycans, and stimulates fibroplasia of the joint capsule. The thickened joint capsule contributes to stiffness and decreased range of movement.
The degradative enzymes set in motion a process that damages collagen and causes it to swell. The abnormal cartilage cannot bear loads normally, causing increased load on certain areas of the joint, leading to further cartilage damage. The underlying subchondral bone is stressed and pain receptors are stimulated. Osteophytes are bony proliferations formed at the conjunction of the synovium, perichondrium, and periosteum. They are believed to be caused by mechanical instability of the joint and joint inflammation. They may contribute to joint pain.
Even though the clinical signs of OA may wax and wane, the changes to the joint are permanent, with limited ability to repair the articular surface or joint capsule. The vicious cycle of inflammation, degeneration, and mechanical dysfunction leads to progressive disease.
The diagnostic approach to joint disease in cats is similar to that in dogs. A medical history, physical examination, and radiographs are most commonly employed. Further diagnostic steps might include joint fluid analysis and culture, arthroscopy, myelography, or advanced imaging such as magnetic resonance imaging (MRI) or computed tomography (CT).
When taking a medical history, especially for senior cats, questions should be focused on changes in activity and behavior, rather than solely on lameness. Many signs of chronic pain are not obvious to owners, or may be misinterpreted as due to ageing (Taylor and Robertson 2004). The degree of impairment due to chronic pain may not be apparent to some owners until dramatic changes occur after treatment.
Unfortunately, gait analysis is rarely helpful in cats and orthopedic examinations are limited by lack of data on normal ranges of motion for feline joints and difficulty in detecting small changes associated with joint disease. Cats with lumbosacral joint disease may be reluctant to jump and may be painful when the lower back is petted or examined. Cats with hip dysplasia may have no clinical signs at all, although cats with more advanced disease may have lameness and pain.
Radiographic signs of OA in cats are variable (Allan 2000; Godfrey 2002; Clarke, Mellor et al. 2005). Radiographs are best at demonstrating bony changes and changes in the cartilage and synovium are not well demonstrated on plain radiographs. Joint effusions and joint capsule thickening are rarely evident. Typical bony changes include osteophyte development, subchondral sclerosis, perichondral bone erosion and change in congruity of articular surfaces. Soft tissue swelling around the joint may be present. Lumbosacral OA may be indicated by collapse of the L7-S1 disk space, sclerosis of the L7-S1 endplates and spondylosis deformans.
The goals of treatment for cats with OA include reduction of pain and inflammation, improvement in joint function, and slowing the disease process if possible. Treatments fall into four broad categories:
1. Weight loss
2. Drug therapy
Weight loss is indicated if the patient is overweight or obese and will reduce forces on the joint surfaces. Weight loss may also lead to decreased dose or frequency of drug administration. Drug therapy is indicated to control inflammation, provide pain relief, and improve function. The most commonly used drugs for OA in cats are the non-steroidal anti-inflammatories (NSAIDs). NSAIDs block the inflammatory effects of prostaglandins by inhibiting cyclo-oxygenase (COX). COX-1 is an endogenous form of the enzyme and is responsible for the production of prostaglandins that maintain the integrity of the gastric mucosa and vascular endothelium. COX-2 is an inducible form of the enzyme produced as part of the inflammatory response and is responsible for the production of the inflammatory prostaglandins. Many commonly used NSAIDs block COX-1 rather than COX-2, leading to adverse effects.
NSAIDs are considered potentially more toxic in cats than in dogs or humans due to deficient glucuronidation pathways in the cat. This prolongs the duration of effect and can lead to drug accumulation. Most NSAIDs have a relatively long half-life in cats so that dosing at the same level and frequency as in dogs is likely to result in toxicity. Although NSAIDs form the basis for the treatment of chronic pain in dogs and humans, they are not generally licensed for long-term use in the cat although licensing varies in different countries. The key to safe long-term NSAID use in cats is to use the smallest effective dose and to avoid, or used decreased doses, in cats with chronic renal failure.
Before starting NSAID therapy, a complete blood cell count, serum chemistries, and a urinalysis should be performed. Ideally, NSAIDs should only be prescribed to normotensive, normovolemic adult cats with no history of renal, hepatic, or gastrointestinal disease. However, for some cats, the benefits of NSAID therapy outweigh the risks, as the quality of life may be more important than the length of life. Blood work should be monitored periodically for cats on long term therapy and owners should be cautioned to monitor for vomiting, diarrhea, anorexia, or lethargy. One author suggests reevaluation every 8-12 weeks (Robertson and Taylor 2004).
Meloxicam (Metacam®, Boehringer Ingelheim) is known to be COX-2 selective in dogs and horses, although similar evidence for cats has not been published. It is supplied in a 1.5 mg/ml honey-flavored oral formulation that is well tolerated by cats, but not licensed for this species in all countries. Recommended doses for long term use vary, but a commonly used protocol is 0.2 mg/kg PO followed by 0.1 mg/kg PO q 24 hours for 2 days, then 0.025 mg/kg or 0.1 mg/cat 2-3 times/week (Wallace 2003; Carroll and Simonson 2005).
A few studies have evaluated the safety and efficacy of long term meloxicam for OA in cats. In one study, 28 cats with OA were given meloxicam for 4 weeks at 0.3 mg/kg the first day, 0.1 mg/kg once daily for 4 days, then 0.05 mg/cat once daily for 23 days (Clarke and Bennett 2006). Most of the cats (96%) accepted the medication well. During the study period, 18% of cats had intermittent signs of gastrointestinal disease (vomiting or diarrhea), although the signs were not persistent or severe enough to warrant withdrawal of the medication. Overall, 61% of the owners felt their cat made a marked improvement during the 4 weeks of treatment, 14% felt their cat had made a moderate improvement, and 25% reported a slight improvement. Statistically significant improvements were seen in willingness to jump, height of jumping, gait stiffness, lameness, and activity level.
A longer term study of meloxicam for OA in cats has recently been published (Gunew, Menrath et al. 2008). Forty cats with OA completed the trial with mean treatment duration of 5.8 months. Cats with pre-existing chronic renal insufficiency, diabetes mellitus or hyperthyroidism were not excluded if their disease was stable and appropriately managed. Meloxicam was administered at 0.1 mg/kg PO once daily for 4 days, then 0.1 mg/cat PO once daily. The only adverse effect noted was gastrointestinal upset in 4% of the cats. No adverse effects on renal function were detected. Owners assessed treatment efficacy as either good or excellent for 85% of the cats.
Glucocorticoids are controversial drugs for treatment of OA. These drugs can reduce inflammation through various mechanisms but chronic use has been found to delay healing and even damage cartilage (Beale 2005). As well, the potential adverse effects of glucocorticoids in cats are well known. Use of these drugs should be limited to cases where all other therapies have failed and for short periods only.
Chondroprotective agents are drugs intended to slow the progression of degenerative joint disease and are purported to have anti-inflammatory properties as well as to support repair processes within the joint (Beale 2005). Polysulfated glycosaminoglycan (Adequan®, Luitpold Animal Health) is said to have both chondroprotection and chondrostimulation properties. The results of clinical studies in other species are conflicting and no long term data exists for cats. Many protocols exist for administering Adequan® to cats, such as 5 mg/kg SQ twice weekly for 4 weeks, then once weekly for 4 weeks, then once monthly.
Nutraceuticals are popular as alternatives to NSAIDs. They are another class of products where little controlled research exists for safety and efficacy in cats. Nutraceuticals are poorly regulated since they are classed as dietary supplements by the FDA. This raises concerns about actual product contents and strength, as well as label claims of efficacy and safety. Commercially available products may vary widely in purity and quality. The best evaluated nutraceutical is glucosamine hydrochloride/chondroitin sulfate (Cosequin®; Nutramax Laboratories). Some studies have shown relief of clinical signs of OA in dogs, horses, and people. Results of trials suggest a cartilage-sparing or chondroprotective effect for glucosamine/chondroitin via a reduction in histologic severity of OA lesions (Neil, Caron et al. 2005). No published studies have evaluated safety or efficacy of glucosamine/chondroitin for long term therapy of OA in cats.
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