Current concepts in the management of osteoarthritis (Sponsored by Iams)
Medical treatment of osteoarthritis is multifaceted and includes physical modalities, controlled exercise, weight reduction, slow-acting disease-modifying osteoarthritic agents, alteration of the environment, and anti-inflammatory medications.
Joint disease is a common problem, affecting up to 20% of dogs.1 Osteoarthritis (OA) is a progressive degenerative condition that affects synovial joints and has an insidious onset. Patients with OA have restricted activity, limited ability to perform, muscle atrophy, pain and discomfort, decreased range of motion, and decreased quality of life. As animals reduce their activity level, a vicious cycle of decreased flexibility, joint stiffness, and loss of strength occurs.
Traditional management of dogs with OA has incorporated anti-inflammatory and analgesic drugs, changes in lifestyle, and surgical management. Advances in the management of human OA include weight loss, exercise programs, and physical modalities to reduce the severity of symptoms and to control pain and discomfort. Some of the benefits of a complete program include increasing muscle strength and endurance, increasing joint range of motion, decreasing edema, decreasing muscle spasm and pain, and improving performance, speed, quality of movement, and function. OA is cytologically categorized as a noninflammatory condition, but many inflammatory mediators are involved, including metalloproteinases and interleukins, with a progressive cascade of mechanical and biochemical events, resulting in cartilage destruction, subchondral bony sclerosis, synovial membrane inflammation (synovitis), and the development of periarticular osteophytes. Much of the pain associated with OA has been attributed to synovitis. The goals of treatment are to reduce the severity of clinical signs, maintain an acceptable quality of life, control pain and discomfort, slow the progression of the disease, and promote repair of damaged tissue when possible.
Management of OA
Medical treatment of OA is multifaceted and includes physical modalities, controlled exercise, weight reduction, slow-acting disease-modifying osteoarthritic agents, alteration of the environment, and anti-inflammatory medications. Veterinarians must impress on owners that the management of chronic OA is a lifelong commitment, and it is hard work. It is critical to evaluate patients on a regular basis and provide feedback and encouragement to owners. Management of the arthritic patient should be approached in a logical, stepwise progression.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most popular analgesic drugs used in small-animal veterinary practice to manage pain from OA. NSAIDs function, in part, by inhibiting cyclooxygenase (COX) isozymes to different degrees. COX isozymes play an important role in converting arachidonic acid to prostaglandins, associated with normal functions and with inflammation. Typically, traditional NSAIDs (tNSAIDs) — such as aspirin, carprofen, etodolac and meloxicam — inhibit both COX-1 and COX-2 to varying degrees when administered at labeled doses, although there are exceptions. It is believed, based on in vitro and ex vivo studies, that when coxib-class NSAIDs are given at labeled doses, these drugs inhibit COX-2 activity with relative sparing of COX-1 activity (COX-2 selective NSAIDs). It is also believed that coxib-class NSAIDs (deracoxib and firocoxib) offer analgesic and anti-inflammatory effects that are at least comparable to those of tNSAIDs without interfering with the homeostatic functions of prostaglandins in the gastrointestinal tract and platelets. The clinical relevance of the laboratory data on which these beliefs are based is not known, although coxib-class NSAIDs appear to result in fewer gastrointestinal side effects.
Comparative efficacy of NSAIDs
So which NSAID is the best? Many different parameters might influence the answer, including patient history, patient medical condition, the veterinarian's experiences, owner preference, product efficacy and safety, concurrent medications, patient response, and cost. Ground reaction force has also been used as an objective differentiator between an NSAID and a nutraceutical. Moreau et al measured ground reaction force response in 71 arthritic dogs (elbow, stifle, or hips) after 30 and 60 days of administration of either placebo, carprofen, meloxicam, or a combination nutraceutical (chondroitin sulfate, glucosamine, and manganese ascorbate).2 Although ground reaction force significantly improved in both the meloxicam and carprofen groups, only meloxicam-treated dogs returned to normal ground reaction force values for some situations. Performance of the meloxicam group was superior to the carprofen group, and no improvement was seen in the combination nutraceutical group. One case of hepatotoxicosis was reported in the carprofen group.
In another study,3 experimentally induced acute synovitis in beagles was used to compare the analgesic and anti-inflammatory effect of single doses of carprofen, etodolac, meloxicam, and butorphanol to a placebo. Compared with control dogs, treated dogs had significantly different vertical ground reaction forces and weight-bearing scores. Etodolac had the fastest onset of action, but the greatest improvement in lameness was observed in carprofen-treated dogs. Both carprofen and etodolac were associated with significantly lower pain scores.
One study4 investigated the effectiveness of several NSAIDs further, examining aspirin, acetaminophen, carprofen, deracoxib, etodolac, meloxicam, tepoxalin, and firocoxib in comparison to a placebo. The study was a 3x3 crossover study of nine mixed-breed hounds, weighing 40 to 60 lb. The dogs had mild to moderate OA resulting from cranial cruciate ligament transection with immediate stifle stabilization, and each had measureable differences in peak vertical force in the rear limbs. Results from this study showed that each dog responded to at least one NSAID, but not every dog responded to each. As determined by peak vertical force, deracoxib gave the greatest response; dogs responded equally to etodolac, firocoxib, and aspirin; and acetaminophen was not effective. Dogs receiving meloxicam, carprofen, and tepoxalin had results intermediate between the placebo and the other NSAIDs.
Other analgesic agents
Because of the changes that occur in the processing of pain signals, the pain that is experienced with OA is often increased in amplitude and duration. Chronic pain may become "resistant" to treatment with NSAIDs, necessitating a multimodal approach to therapy.
Amantadine. Amantadine is the most commonly used oral NMDA receptor antagonist. NMDA receptor antagonists are used as an adjunctive therapy to improve pain control. Central sensitization may occur with chronic pain and is mediated in part by activation of NMDA receptors. By blocking these receptors, central nervous system hyperresponsiveness may be reduced, making other analgesics more effective.
The standard oral amantadine dose used to block receptors in dogs is 3 to 5 mg/kg once daily. Oral antagonists often have a slower onset of action, taking up to a week to produce noticeable results. Amantadine may be given on a continual basis if needed, but in most cases it can be given daily for seven to 14 days and then discontinued until pain worsens again. Elimination is almost exclusively via the kidneys, so dose reductions should be considered in cases of renal disease. Side effects are rare, but can include agitation or diarrhea.
Gabapentin. The mechanism of action for gabapentin is unclear, although it may involve inhibition of post-synaptic neuron firing. Gabapentin has been used for many forms of chronic pain, though its best application may be for neuropathic pain. A suggested dose is 10 mg/kg twice daily, though doses as low as 1.25 mg/kg once a day have been reported to be effective. Gabapentin is metabolized by the liver and excreted by the kidneys. Possible side effects may include sedation and weight gain.
Amitriptyline. Amitriptyline is a tricyclic antidepressant that has been used in people and animals as an adjunct to other analgesics for chronic pain. It acts to inhibit serotonin and norepinephrine reuptake, though it may have other analgesic effects as well (including possible actions at opioid receptors and on nerve transmission). Dogs are usually dosed at 1 to 2 mg/kg, once or twice daily. Side effects can include sedation and anticholinergic effects.
Opioids. Opioids are the most powerful analgesics available, with actions at peripheral, spinal, and supraspinal levels. Their use is best limited to short-term "rescue" analgesia. With chronic use, tolerance often develops, necessitating progressively higher doses to achieve analgesia.
Codeine has been used as an oral mu agonist, though it is usually less efficacious than morphine. It is most commonly available in combination with acetaminophen as a Class III preparation. The usual dose for dogs is 1 to 2 mg/kg of the codeine portion, three to four times daily. (It should NOT be used in cats in combination with acetaminophen because of the risk of fatal methemoglobinemia.)
Morphine sulfate (Class II) is available in oral tablet, capsule, and liquid preparations. A suggested dose range in dogs is 0.5 to 2 mg/kg, four times daily. (Some dogs experience unacceptable constipation at doses exceeding 1 mg/kg.)
Tramadol may be useful for treating chronic osteoarthritic pain. It has a dual mode of action. It is a synthetic mu agonist and a monoamine reuptake inhibitor (principally serotonin and norepinephrine), which enhances the endogenous spinal inhibitory mechanisms and produces mild anti-anxiety effects. The degree of mu agonism is relatively weak. (The parent compound has very little affinity for the mu receptors; most of the mu effects come from the M1 metabolite.) However, in conjunction with the monoamine reuptake inhibition, a synergistic action occurs, leading to analgesia comparable to codeine. Combining tramadol with other analgesics (NSAIDs, mu agonists) may further enhance its efficacy, but it may also increase the incidence of adverse events. Despite its wide use, there is little to no safety or efficacy data on the use of tramadol in veterinary patients. Tramadol has its own set of adverse events in people, including vomiting, diarrhea, and sedation. Because of tramadol's monamine reuptake inhibition, it should not be given with tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), or monamine oxidase inhibitors (MAOIs) due to the risk of serotonin syndrome. In dogs, a starting dose of 1 to 2 mg/kg twice daily (up to 5 mg/kg b.i.d.) works well, though more frequent administration (t.i.d. to q.i.d.) can be used if needed. Metabolism is principally via hepatic biotransformation, with a small amount excreted unchanged by the kidneys.
Slow-acting disease-modifying osteoarthritic agents
Slow-acting disease-modifying osteoarthritic agents (SADMOAs), sometimes called chondroprotective agents, are thought to have a positive effect on cartilage matrix synthesis, and thereby benefit OA patients. This is believed to be attributable to their influence on hyaluronan synthesis and their inhibitory effect on catabolic enzymes in the osteoarthritic joint. SADMOAs include chondroitin, glucosamine, hyaluronic acid, polysulfated glycosaminoglycans, doxycycline, and others.
It appears that the mechanism of action for glucosamine is to stimulate chondrocytes to secrete glycosaminoglycans. In human studies, glucosamine alone was found to be as effective as ibuprofen in controlling signs of OA.5,6 Cell culture studies show that glucosamine and chondroitin sulfate have different mechanisms of action and are not interchangeable therapeutic agents. Chondroitin sulfate has been noted to decrease interleukin-1 production, block complement activation, inhibit metalloproteinases, inhibit histamine-mediated inflammation, and stimulate glycosaminoglycan and collagen synthesis. Lippiello et al showed a significant synergistic effect with the combination of glucosamine and chondroitin sulfate on production of cartilage matrix by chondrocytes, with greater effect in retarding the progression of degenerative cartilage lesions than either individual ingredient alone.7
In Europe, avocado-soybean unsaponifiables (ASUs) are commonly used to treat OA symptoms in people. Most ASU preparations are composed of one-third avocado and two-thirds soybean ASUs, the oily fractions that do not produce soap.
In vitro, ASUs have anabolic, anticatabolic, and anti-inflammatory effects on chondrocytes. In one study,8 ASUs increased collagen synthesis and inhibited interleukin (IL)-1β-induced collagenase activity. They also increased aggrecan synthesis and reversed the IL-1β-induced reduction in aggrecan synthesis. ASUs also reduced IL-1β-induced production of matrix metalloproteinases (enzymes involved in cartilage destruction)-3, IL-6, IL-8, and prostaglandin E2 (PGE2), while weakly reversing the IL-1β-induced decrease in tissue inhibitors of metalloproteinase (TIMP) production. TIMPs are endogenous molecules that counteract destructive enzymes. Another study9 showed that ASUs decreased the production of nitric oxide and macrophage inflammatory protein-1β, while stimulating the expression of transforming growth factor-β and plasminogen activator inhibitor-1. The production of plasminogen activator inhibitor-1 could be one mechanism for decreased matrix metalloproteinase (MMP) activation. ASUs also prevent the inhibition of matrix production caused by osteoarthritic osteoblasts, suggesting that this compound may promote OA cartilage repair by acting on subchondral bone osteoblasts. These results suggest ASUs could have structure-modifying effects in OA by inhibiting cartilage degradation and promoting cartilage repair. NFkB activation is mandatory for the expression of many genes involved in chondrocyte activation, such as IL-6, IL-8, nitric oxide, and PGE2 that are proinflammatory mediators. ASUs prevented stress-induced NFkB activation in chondrocytes.10 The inhibitory effect of ASUs seems to be due, in part, to the inhibition of the NF-kB pathway.
In a multicenter, double-blind study of aged human patients with knee OA, researchers compared 300 mg or 600 mg of ASU daily with a placebo for three months.11 At Day 90, intake of NSAIDs and analgesics could be decreased by more than 50% in 71% of the patients receiving either 300 or 600 mg of ASU, compared with 36% of the patients receiving placebo. ASUs may also slow down narrowing of joint space width in patients with severe hip OA. Based on the present evidence, ASUs provide for symptom-modifying effects in knee and hip OA, and there is also some evidence of structure-modifying effects.
Methylsulfonylmethane (MSM) occurs naturally in small amounts in some green plants, fruits, and vegetables, and most people have some MSM present in their body. It is a naturally occurring organic molecule and a methyl donor, which may give MSM antioxidant capabilities. Because of MSM's sulfur content, it may be used by the body to maintain normal connective tissues. MSM may also have anti-inflammatory activities, prostacyclin (PGI2) synthesis inhibition, beneficial effects on eicosanoid metabolism, and free radical scavenging activity.
Acute and subchronic animal toxicity studies using a single dose of 2 g/kg and daily doses of 1.5 g/kg MSM for 90 days showed no adverse events, organ pathology, or mortality.12 These doses are considered five to seven times the maximum dose used in people. There have been reports of mild adverse effects in people, including gastrointestinal symptoms, headaches, amplified effects of blood thinning drugs resulting in easy bruising and blood in stool, increased blood pressure, increased hepatic enzymes, and insomnia. However, there are no clinical studies on adverse effects, changes in blood chemistry, safety monitoring data, or possible subclinical neurotoxicity signs involving MSM in animals.
One randomized, controlled trial of people with knee OA, evaluated MSM during a 12-week period.13 Patients received either 1.5 g MSM, 1.5 g glucosamine sulfate, 1.5 g MSM plus glucosamine sulfate, or a placebo. Significant decreases in a standardized arthritis index were reported with MSM, glucosamine sulfate, and their combination (p <0.05). The authors reported a 33% decrease in pain in the MSM group. Joint mobility, swelling, global evaluation, and walking time also improved. Another randomized, double-blind, placebo-controlled trial of 50 people with knee OA pain was performed.14 Patients received either 3 g of MSM or placebo twice a day for 12 weeks (6 g/day total). Compared with the placebo, MSM produced significant decreases in standardized pain scores and physical function impairment and improved performance of activities of daily living (p<0.05). No notable changes were found in stiffness or aggregated total symptoms scores. While improvements in pain and physical function were statistically significant, the effect was modest and changes in similar studies of COX-2 drug trials were greater.15
The Western Ontario MacMaster [WOMAC] is a validated instrument designed specifically for the assessment of lower extremity pain and function in OA of the knee or hip in people. It has been used to compare the efficacy of MSM and various NSAIDs. Celecoxib improved WOMAC pain, stiffness, and physical function scores by 28.6 mm, 27.9 mm, and 24.9 mm, respectively, and etoricoxib improved these scores by 22.29 mm, 19.01 mm, and 22.87 mm, compared with the MSM trial, which improved these scores by 14.6 mm, 10.1 mm, and 15.7 mm, respectively. However, patients in these COX-2 studies typically had more severe arthritis compared with the patients enrolled in the MSM study. While MSM appears to be less effective than COX-2 drugs, its use as an adjuvant with other treatments for OA could be considered.
S-adenosyl-l-methionine (SAMe) is a molecule involved in numerous anabolic and catabolic reactions, such as cell proliferation and protein synthesis. It is also a free radical scavenger and has anti-inflammatory and analgesic properties. SAMe enhances proteoglycan synthesis and secretion in vitro. Clinical trials in people indicate that it has analgesic and anti-inflammatory properties, possibly by inhibiting COX activity. Although efficacy in animals has not been established, it is available commercially for animals. It is most commonly used for liver problems. Side effects sometimes associated with SAMe include anxiety, headache, insomnia, and nervousness. It also has the potential to interact with other serotoninergic drugs, such as antidepressants, tramadol, and meperidine, possibly resulting in serotonin syndrome.
Research results on the use of SAMe for OA in people have been consistently positive. A review and meta-analysis, as well as several randomized clinical trials, have shown that SAMe is more effective than placebos and comparable to NSAIDs in reducing OA pain.16,17 In a recent trial, SAMe (1,200 mg per day) was compared with celecoxib (200 mg per day).18 Celecoxib was much more effective than SAMe in reducing pain during the first month of treatment, but after two months of use, no difference in pain relief was noted. Although SAMe does provide pain relief, it can take several weeks of treatment before clinical signs substantially improve. SAMe may also increase chondrocytes and cartilage thickness and may also decrease cytokine-induced chondrocyte damage.
The polysulfated glycosaminoglycan (PSGAG) Adequan is polysulfated chondroitin sulfate; i.e. it has a higher sulfur content than chondroitin sulfate. This drug is anti-inflammatory, inhibits enzymes that degrade glycosaminoglycans and hyaluronic acid within the joint, and has a positive effect on hyaluronic acid and glycosaminoglycan synthesis in diseased joints. It is therefore said to be a disease-modifying osteoarthritis drug. PSGAGs have been reported to stimulate existing chondrocytes, increase concentrations of hyaluronic acid in synovial fluid, inhibit metalloproteinases, inhibit complement activation, inhibit enzyme release from leukocytes, and inhibit PGE2 and toxic oxygen radical synthesis.
Support for the efficacy of PSGAGs as a treatment for canine OA was published by Altman et al.19 In this Pond-Nuki dog model (an experimental model of OA induced by sectioning the anterior cruciate ligament), treatment dogs received 4 mg/kg PSGAG twice weekly for four weeks. The mean histological scores of the operated control joints were significantly worse than in the operated PSGAG-treated joints. More cartilage swelling was measured in the operated control joints than in the operated PSGAG-treated joints. The total metalloproteinase activity in the operated PSGAG-treated joints was significantly lower compared with the operated control joints.
Polyunsaturated fatty acids
Certain forms of polyunsaturated fatty acids (PUFAs), especially omega-3 fatty acids, may reduce the production of certain eicosanoids, especially the more potent inflammatory leukotrienes, and help reduce inflammation. Some people with rheumatoid arthritis respond to treatment with PUFAs. Controlled clinical trials have been performed in dogs, and it appears that these products have efficacy in the treatment of OA.
Cold decreases blood flow, inflammation, hemorrhage, and metabolic rate. Commercial cold packs or ice wrapped in a towel may be applied to an area for 15 to 20 minutes, three to six times daily. An entire limb may be immersed in cold water or a water-and-ice bath to decrease inflammation. Most studies of cryotherapy treatment for OA indicate that patients experience positive benefits, including less stiffness and pain and improved joint range of motion, although there is some initial discomfort with application of cold.
Superficial heat modalities
Superficial heating agents typically heat the skin and subcutaneous tissues to a depth of 1 to 2 cm. The tissue is usually heated to 40 to 45 C for 15 to 20 minutes. Superficial heating agents include hot packs (moist and dry), circulating warm water heating blankets, and warm baths. Heat increases blood flow to the area; promotes tissue extensibility; decreases pain, muscle spasm, and joint stiffness; and causes general relaxation. Heat is contraindicated if swelling or edema is present.
Extracorporeal shock wave therapy
Shock waves are a focused pulse of high-pressure acoustic waves of various frequencies that travel through soft tissue to reach their target area. When the shock wave reaches a density interface (e.g. a ligament or bone), energy is released. The larger the change in impedance, the greater the energy released. It is this energy release that is thought to stimulate healing. When a shock wave travels through the target area, very high pressures build up for a very short period, energy is released, and the pressure returns to normal.
Orthopedic applications for which shock wave therapy is useful include non-union fractures, plantar fasciitis, lateral epicondylitis, Achilles and patella tendonitis, and, with limited experience, OA. For people, focal extracorporeal shock wave treatment is currently FDA-approved in the United States for use in chronic heel pain (plantar fasciitis) and tennis elbow (lateral epicondylitis).
The clinical effects of shock wave treatment include reduced inflammation and swelling, short-term analgesia, improved vascularity and neovascularization, increased bone formation, realignment of tendon fibers, and enhanced wound healing. The mechanisms of action that underlie the clinical effects are not clearly understood, but studies have indicated that there is induction of cytokines, such as TGF-β1, substance P, and osteocalcin.20-22 In addition, there is induction of nitric oxide synthase and thus bone healing, with increased osteoblastic activity. There may also be stimulation of nociceptors, which in turn inhibit afferent pain signals.
My colleagues and I have recently completed a study evaluating the use of extracorporeal shock wave therapy for the treatment of canine OA.23 In this study, we treated dogs with moderate to severe OA of the elbow that had relatively obvious clinical signs of lameness and pain. The clinical signs were relatively stable and the dogs were receiving other treatments for their arthritis. Patients receiving shock wave treatment demonstrated significant increases in weight bearing and comfortable joint range of motion, similar to what is typically expected with the use of NSAIDs. Although the dogs were already on medication and the signs of their arthritis were stable, patients had a measurable reduction in their clinical signs, indicating that this form of treatment has additive or synergistic effects with medication. Further study of shock wave treatment is warranted to determine more optimal treatment protocols, including the frequency of treatment, energy level, and the number of shocks per treatment.
Neuromuscular electrical stimulation
A wide variety of neuromuscular electrical stimulators (NMES) are available. NMES provides several benefits, including increasing muscle strength and joint range of motion, decreasing edema and pain, and improving function. Pulsed AC (alternating current) units are the most useful for increasing muscle strength and joint range of motion and decreasing edema and pain. The commonly used transcutaneous electrical nerve stimulation (TENS) refers only to a particular type of electrical stimulator that is applied for pain control, but it is not used for muscle strengthening or other applications. In general, NMES appears to relieve pain in human patients with OA as long as the treatment is continued. Its role in pain relief of OA in animals is unknown, but it appears to attenuate muscle atrophy after some surgical procedures. In addition, my colleagues and I have performed a small study of the effects of a single application of TENS on dogs with mild to moderate stifle arthritis.24
Although all dogs started with mild decreases in weight bearing as assessed by force plate analysis of gait, dogs receiving a 30-minute TENS application had a significant increase in weight bearing, which persisted for nearly 24 hours. The magnitude of increase was similar to that which is typically expected of NSAIDs. There are some disadvantages of TENS application, including the expertise necessary to use the equipment and the need for daily application, but it may give added benefit to medications and may be used in patients that cannot tolerate certain medications.
Physical rehabilitation modalities
In normal people and dogs, it is generally believed that mild to moderate exercise and training do not, by themselves, cause OA. However, they do cause biochemical, histologic, and biomechanical changes in articular cartilage. Most studies of moderate running exercise in people have indicated that this activity produces no injury to articular cartilage, assuming that there are no abnormal biomechanical stresses acting on the joints. Heavy training programs, however, may result in changes that predispose individuals to OA development.
Controlled exercise for patients with OA has valuable benefits. People with OA who participate in controlled, low-impact exercises have improved function and reduced pain and need for medication. The goals of therapeutic exercise should be to reduce body weight, increase joint mobility, and reduce joint pain through the use of low-impact weight-bearing exercises designed to strengthen supporting muscles. Muscle disuse results in atrophy and weakness. Muscles also act as shock absorbers, so strengthening periarticular muscles may help protect joints. Mild weight-bearing exercise also helps stimulate cartilage metabolism and increases nutrient diffusion. Exercise may also increase endogenous opiate production and relieve OA pain.
An exercise program must be tailored for the condition of each patient and its owner. An improper program could hasten the progression of OA. Overloading joints should be minimized by performing activities such as walking and swimming until weight loss occurs. Unrealistic demands placed on the pet owner will reduce compliance, and the physical condition of the owner must be considered. Additionally, joint instability should be corrected before initiating an exercise program, and exercise programs must be tailored to account for the typical course of exacerbations and remissions of OA. The animal should not be forced to exercise during times of aggravation because inflammation may increase.
In preparation for exercising, warming and stretching affected muscle groups and joints during a warm-up period is recommended. As mentioned earlier, tissue warming promotes blood flow to the area, improves tissue and collagen extensibility, and decreases pain, muscle spasms, and joint stiffness. Heat is contraindicated if swelling or edema is present in the limb or joint. Any stretching should be done during the latter part of warming or immediately after. Furthermore, massage has been used to increase blood flow to muscles to warm up the area before activity and to decrease stiffness after activity.
Controlled leash walking, walking on a treadmill, jogging, swimming, and going up and down stairs or ramp inclines are excellent low-impact exercises. The length of the exercise should be gradually adjusted so there is no increased pain after activity. Also, it is better in the early phases of training to provide three 20-minute sessions rather than one 60-minute session. Walks should be brisk and purposeful, minimizing stopping. Avoiding sudden bursts of activity will help avoid acute inflammation of arthritic joints.
Swimming and walking in water are some of the best activities for dogs. The buoyancy of water is significant and limits the impact on the joint, while promoting muscle strength and tone and joint motion. Training on an underwater treadmill may increase peak weight-bearing forces by 5 to 15%, which is comparable to what many patients achieve using medication.
Controlled exercise must be gradually adjusted based on patient response so that there is no increase in pain after the activity. If joint pain is perceived to be greater after exercising, the length of the activity should be cut in half. When stepping up the amount of activity, the increase should be about 20% and should not be stepped up more than once each week. Ideally, anti-inflammatory drugs should not be administered immediately before stepping up activity because it is important to determine if the level of exercise is too great and causes pain. The exercise periods should be evenly spaced throughout each day and over the entire week. Training helps maintain an ideal body weight, improves range of motion, and increases muscle strength and tone, which helps to stabilize joints.
Following exercise, a 10-minute warm-down period allows muscles to cool down. A slower paced walk may be initiated for 5 minutes, followed by range of motion and stretching exercises. A cool-down massage may help decrease pain, swelling, and muscle spasms. Finally, cryotherapy (cold packs or ice wrapped in a towel) may be applied to painful areas for 15 to 20 minutes to control postexercise inflammation. Application of cold decreases blood flow, inflammation, hemorrhage, and metabolic rate.
Obesity is strongly associated with the development of OA in people and likely contributes to the progression of OA in dogs. For example, heavy people are 3.5 times more likely to develop OA than light people, and weight loss of 5 kg decreases the odds of developing OA by more than 50%. Additionally, weight loss results in less joint pain and reduces the need for medication to treat OA. In one study, when obese dogs lost 11 to 18% of their initial body weight, it significantly improved the hind limb lameness associated with hip OA.25 In addition to restricting intake of the normal food and eliminating treats, therapeutic diets can dramatically assist in achieving and maintaining ideal body weight. In general, the goal is to reduce fat composition to 20 to 25% of an animal's total body weight. Clinically, the ribs should be easily palpable and there should be a "waist" when the animal is viewed from above.
Altering the environment may be helpful for dogs with moderate to severe arthritis. The principles for dogs are similar to those for arthritic humans. Whenever possible, animals should be moved from a cold, damp outdoor environment to a warm, dry indoor environment. A soft, well-padded bed or waterbed should be provided. A circulating warm water blanket provides heat, which may reduce morning stiffness. Good footing will help avoid slipping and falling. Using handicapped ramps and keeping pets on ground floors can minimize stair climbing. Steps are easier to negotiate if they are wider and spaced farther apart. Portable ramps are available to help patients get in and out of vehicles. Owners should avoid overdoing activities on the weekends, and prevent excessive play with other pets because arthritic animals may attempt to keep up, and in the process, become more lame and feel more pain. In some instances, however, play with other animals stimulates activity and provides a welcome break in the exercise routine.
Osteoarthritis is a common problem in dogs. Veterinarians are frequently asked to treat arthritic patients. Managing arthritic patients involves a number of modalities that must be tailored to each patient and its owner. Weight control, physical rehabilitation, and medication are the main components for OA management.
A variety of pharmaceutical agents are available to treat canine OA. When selecting medications, veterinarians should consider the efficacy, safety profile, mechanism of action, and patient response. Not all dogs respond equally to all medications. Avoid concurrent administration of nonsteroidal and steroidal anti-inflammatory drugs. Cooperation among the veterinarian, therapist, veterinary technician, and owner are vital to carry out an appropriate management program. Regular monitoring is essential for making decisions about further treatment and for maintaining enthusiasm for the program.
Darryl L. Millis, MS, DVM, DACVS, DACVSMR, CCRP, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996.
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