College of Veterinary Medicine North Carolina State University, Raleigh, NC Osteoarthritis (OA) is a complex, ubiquitous disease affecting dogs, particularly older, large-breed dogs. OA was once thought to be an inevitable consequence of mechanical wear and tear. It is now defined not simply as a wear and tear disease, but rather the result of a multifactorial set of predisposing factors superimposed on an individualâ€™s quality and quantity of attempted repair processes leading to varying levels of pain, joint dysfunction, and structural damage.1 While the prevalence of OA in dogs is not known, it has been estimated to be affect approximately 25% of dogs.2 In a lifelong study of 43 Labrador retrievers from seven litters, all dogs had OA at the end of their life.3 Half of the dogs were overweight and three quarter of these overweight dogs had OA in at least two joints by the time they were 8 years of age. Being overweight greatly increased the prevalence of OA for the dogs in that study. THE SOURCES OF ARTHRITIC PAIN OA has a significant impact on dogsâ€™ lives because of the pain resulting from joint subluxation, damage to the subchondral bone, changes in joint capsule, loss of joint motion, loss of strength, loss of muscle and cardiovascular fitness. The relative importance of these changes for various forms of osteoarthritis is not known based on epidemiological studies, but clear trends exist. While we treat arthritis as a whole, it is nevertheless fundamental to assess the presence of various components of the disease because specific treatment strategies that address these problems may be implemented. Joint Subluxation Joint subluxation is a common feature of arthritic joints in dogs, particularly for the hip joint. Hip subluxation secondary to hip laxity is the trigger to the development of hip OA in dogs (and cats).4 The subluxation means that loads during weight bearing are concentration over a small region of the femoral head and dorsal acetabular rim rather than distributed over the entire surface of acetabulum. The stress concentration in the femoral head and rim increases with increases in joint subluxation. Increased stress leads to fractures and wear and to cartilage wear in the femoral head. In many dogs, full thickness cartilage wear is present in the head and rim at the time of hip surgery. Some dogs with severe hip laxity develop (complete) luxations of the femoral head out of the acetabulum. If that occurs before 4 or 5 months of age, the acetabulum may fail to develop. The clinical signs caused by hip subluxation are variable and appear more intense in larger and heavier dogs compared with smaller and lighter dogs. Some dogs modify their gait to avoid subluxation, for example by walking, pacing, or trotting with a wide base stance their (pelvic limbs adducted) or by reducing their hip joints with small, jerky movements of their pelvis during the swing phase of their gait. Most dogs with hip subluxation are painful when the hip joint is extended. Surprisingly, we have the clinical impression that dogs with complete luxation do not exhibit clinical signs as severe as dogs with subluxation because dogs with luxation do not have intense load concentrations and rapid wear of the femoral head and dorsal acetabular rim. With time, the pain resulting from hip subluxation decreases, even though the subluxation remains. The damage to the head and dorsal rim appears to stabilize after several months and the clinical signs of hip OA become more discreet. There are no conservative therapeutic measure that positively impact hip subluxation. An external orthosis has been proposed (bilateral hip orthosis, K-9 Orthotics and Prosthetics, Beaver Bank, NS, Canada), but little is known regarding its effectiveness. Several surgeries have been proposed to indirectly decrease the hip subluxation, including juvenile public symphysiodesis at 16 weeks of age and triple pelvic osteotomy at 6 to 9 months of age. Joint subluxation is a key factor in ACL injuries. In fact, the main goal of the surgical management of the ACL injuries, beyond the removal of torn ligament fibers and meniscal fibrocartilage, is to eliminate subluxation. Stifle joint subluxation cannot be predictably controlled with conservative measures. Several stifle joint braces have been proposed, but they do not appear to limit craniocaudal subluxation. In humans, while knee braces limit side to side instability, they seem ineffective and decreasing up and down knee joint instability. Joint subluxation is also a factor in patients with knee cap luxations. Again, while knee braces could potentially be beneficial, there is no evidence documenting their benefits. Joint subluxation is also a factor in elbow dysplasia but, unlike other joints, by applying external forces on the bones that are subluxated cannot eliminate the subluxation because it occurs between the radius and the ulna and these two bones are tightly connected to each other. There are no conservative strategies that effectively eliminate elbow joint subluxations. Cartilage Damage Damage to the articular surface is a source of pain in part because of the inflammation resulting from the exposure of subchondral bone to joint fluid. The pain present in joints with osteochondritis dissecans (OCD) best illustrates the importance of controlling subchondral bone inflammation. Young dogs with OCD have severe clinical signs that include toe-touching lameness, severe loss of muscle mass and severe pain response to joint palpation. Yet these dogs have normal articular cartilage, with the exception of the osteochondral flap, and minimal capsular changes. Once the osteochondral flap is eliminated, the clinical signs subside. Loss of articular cartilage is most likely present in the elbow joint and hip joints than in other joints. Damage to the articular cartilage is less common in ACL deficient stifle joints and in stifle joints with knee cap luxation. In patients with severe loss of cartilage, there are no proven nonsurgical strategies that positively impact cartilage thickness. Capsular and Periarticular Changes Joints with OA tend to have thickened joint capsules and possible adhesions to periarticular fascias and muscles. These changes may lead to loss of joint motion. Also, pain is perceived when these abnormal joint capsules are stretched when joints are near maximal flexion or extension. While a loss of joint motion seems to be somewhat irrelevant, the combination of loss of motion and pain perceived at the end of joint motion greatly increases the clinical impact of capsular fibrosis. For example, in dogs with hip dysplasia, loss of hip extension may be the key factor leading to severe clinical signs. Normal hip extension in Labrador retrievers is 162 degrees. Labrador retriever move their hip joints from 111 to 147 degrees when they walk. In an ongoing clinical trial assessing the motion of joints with OA performed by the author, many Labrador retrievers with hip dysplasia lose 20 degrees and some lose as much as 35 degrees of hip extension when they are affected by hip dysplasia (managed without surgery). This means that many Labrador retrievers with OA are at maximal extension or near it when they walk. The clinical signs present in these dogs tend to be severe and include an abnormal posture, abnormal gait, and reluctance to jump, gallop, or trot. No strategy has been proven to be effective to protect OA joints against losses of motion but it seems intuitive to recommend an active lifestyle for dogs with OA, following a â€œuse it or lose itâ€ approach. In patients who already have lost joint motion, home-based stretching programs may effectively increase the motion of joints with OA. Loss of Limb and Core Strength Patients with chronic OA lose muscle mass, because of limb disuse and because of the reflex inhibition of contraction of muscles crossing painful joints. Muscle atrophy indirectly contributes to OA pain because weak muscles cannot protect joints from the excessive stresses occurring during locomotion. Also, weak patients are more likely to fall and to be exercise intolerant. Their lack of ability or willingness to exercise leads to a further loss of muscle mass and fitness. Little is known about the impact of low-impact repetitive activity on the maintenance.7 Based on what is known about the impact of therapeutic exercises in people with OA, it is logical to consider that leash walks are very beneficial to dogs with OA. OVERALL PAIN MANAGEMENT STRATEGIES IN OA PATIENTS Principles Pain management is the most important aspect of the management of OA in dogs because pain is the fundamental factor that leads to the long-term consequences of OA, including loss of muscle mass, loss of willingness to exercise, loss of cardiovascular fitness, loss of mobility. OA pain is optimally managed using pharmacological and non-pharmacological methods. Pharmacological methods primarily rely on nonsteroidal anti-inflammatory drugs (NSAIDs). Nonpharmacological methods include rest, nutritional management (weight loss and nutritional supplementation), ice, heat, and therapeutic exercises. The options used should be as brief and simple as possible provided that they are effective. Pain management should be aimed at immediate relief and at long-term modifications that are likely to decrease the reoccurrence of clinical signs. Practical Applications OA pain is most effectively managed with NSAIDs.8 It is most logical to give NSAIDs in dogs showing early clinical signs of OA (to eliminate their clinical signs), in dogs with OA flares (to control their flares), in dogs with exercise intolerance (to facilitate the implementation of exercise programs), in dogs with loss of joint motion (to facilitate the implementation of stretching programs), and in dogs with limited mobility (to enhance the likelihood of success of fitness programs). Adjunctive drugs, including tramadol, amantadine, and gabapentin, have been used off-label to possibly enhance OA pain management but the evidence supporting their efficacy is very weak. In a recent report, dogs receiving an NSAID and amantadine were more active than dogs receiving that NSAID alone after 42 days of treatment.9 There is some evidence supporting the use of glucosamine- and chondroitin-rich supplements and food rich in eicosapentaenoic acid (EPA), an omega-3 fatty acid. In people, joints with OA are sometimes protected during exercise. Joint protection may be achieved using braces made of elastic tape or neoprene and may have metal hinges. Protective braces for dogs are available but hard to fit, cumbersome to use, and have no proven efficacy. It is very important to provide ambulation assistance to the most severely impaired patients because older dogs may be euthanatized when OA flares limit their locomotion. Slings or carts may be used to provide ambulation assistance to these severely affected OA patients. Aquatic exercises may greatly increase their comfort during exercise and may be used for a few weeks while the patients conditioning and limb strength increase and while their weight is managed, if deemed necessary. It may be acceptable to hospitalize a large, nonambulatory patient for a couple of weeks to allow him to have brief exercise sessions several times daily in a controlled environment and under specialized supervision. Adapting the home environment of patients with severe OA is recommended. Dogs with limited mobility should have easy access to water and food, possibly by using elevated bowls. A ramp may be used to facilitate ingress and egress from the house. Allowing dogs to sleep in a temperature-controlled environment may limit OA flare, based on information available from people with OA. ****The acetabulum is a concave surface of the pelvis. The head of the femur meets with the pelvis at the acetabulum, forming the hip joint.