Differential Diagnoses of Arthropathies
Primary Osteoarthritis, degenerative joint disease
Secondary Osteoarthritis, degenerative joint disease
Systemic Lupus Erythematosus
Arthritis associated with chronic infection
Rocky Mountain Spotted Fever
Synovial cell sarcoma
Treatments for Osteoarthritis
Many inflammatory mediators may be involved in chronic OA, including interleukins, prostaglandins, leukotrienes, and metalloproteinases. The goals of treatment for OA are to reduce pain and discomfort, decrease clinical signs, maintain an acceptable quality of life, improve strength and fitness, slow the progression of the underlying disease if possible, and promote the repair of damaged tissue. Surgical treatment may focus on correcting the underlying condition, or performing a salvage procedure such as a total hip replacement.
Osteoarthritis (OA) is a common problem in veterinary medicine, affecting up to 60% of dogs. OA, often referred to as degenerative joint disease (DJD), 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 (ROM) and decreased quality of life. As animals reduce their activity level, a vicious cycle of decreased flexibility, joint stiffness, decreased cardiovascular fitness, and loss of strength occurs. Traditional management of dogs with OA has included anti-inflammatory and analgesic drugs, changes in lifestyle, and surgical management. Advances in the management of human OA have included 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 (ROM), 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 prostaglandins, leukotrienes, metalloproteinases and interleukins, with a progressive cascade of mechanical and biochemical events, resulting in cartilage destruction, subchondral bony sclerosis, synovial membrane inflammation, 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 symptoms, maintain an acceptable quality of life, control pain and discomfort, slow the progression of disease, and promote repair of damaged tissue when possible. Management of dogs with chronic OA is multifaceted and includes medication and physical modalities. Surgical treatment focuses on correcting joint disease to prevent further joint degeneration or joint replacement.
MANAGEMENT OF OSTEOARTHRITIS
The management of dogs with chronic pain due to OA includes anti-inflammatory and analgesic medications, disease-modifying osteoarthritis agents, weight reduction, low-impact exercise programs, physical modalities, alteration of the environment, and surgical procedures to reduce the clinical signs and reliance on medications to control pain and discomfort. The benefits of a complete program include decreasing inflammation, and improving muscle strength and endurance, joint ROM, performance, function, and quality of life. Veterinarians must impress on owners that the management of chronic OA is a lifelong commitment, and 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.
It is likely that nonsteroidal anti-inflammatory agents (NSAIDs) provide benefits to arthritic patients in several ways. One of the primary modes of action is the reduction of inflammatory mediators, especially prostaglandins, in the peripheral tissues and in the central nervous system. The inflammatory cascade is initiated when cell membranes are damaged as a result of inflammatory mediator activity, such as interleukins and tumor necrosis factor, releasing membrane phospholipids. The phospholipids are then acted on by phospholipase to produce arachidonic acid. Cyclooxygenase (COX) and lipoxygenase then act on arachidonic acid to produce eicosanoids, such as prostaglandins and leukotrienes. NSAIDs have been the foundation for the medical management of OA, particularly in advanced cases. NSAIDs inhibit the COX enzyme, thereby decreasing the production of inflammatory mediators and reducing pain associated with OA. Two forms of the COX enzyme have been identified, COX-1 and COX-2. COX-1 is a constitutive enzyme and is normally produced in relatively constant amounts and has “house-keeping” functions, such as protection of the gastric mucosa, maintaining renal perfusion, and production of platelet thromboxane A2. The COX-2 enzyme is inducible and its production increases in response to inflammation. In addition to the induction of COX-2 in peripheral tissues with inflammation, COX-2 is also induced in the central nervous system. The inhibition of the COX-1 enzyme by NSAIDs is believed to be responsible for adverse side effects, including gastric ulceration, platelet dysfunction, and decreased renal perfusion. Non-selective COX inhibitors inhibit both COX-1 and COX-2 enzymes. The identification of the two COX isoforms has resulted in the development of products that preferentially or selectively inhibit the inducible "bad" COX-2 enzyme while sparing the “good” COX-1 enzyme. Selective inhibition of COX-2 with preservation of COX-1 should reduce the adverse effects associated with the GI tract, kidneys, and platelets.
NSAIDs that are frequently used in veterinary medicine include deracoxib, carprofen, meloxicam, firocoxib, robenacoxib, and grapiprant (this drug is classified as an NSAID, but rather than block the COX enzyme system, it is a prostaglandin E2 receptor antagonist). Deracoxib, robenacoxib and firocoxib are COXIB class drugs, as defined by the World Health Organization, while carprofen and meloxicam have some preferential selectivity to inhibit COX-2.
While no NSAID is clearly more efficacious than others in the treatment of chronic OA, some dogs may have a better response to some drugs than others. Veterinarians should perform trials to evaluate various NSAIDs in a particular patient to determine which provides the best clinical improvement without side effects. Two-week trials of various NSAIDs should be performed to determine which provides the best response. Drugs with favorable safety profiles should be used as the initial medication, and if two or more medications are similarly effective on a patient, the medication having fewer side effects should be administered. Before prescribing any medication, the patient’s physiological state, especially liver and kidney function, should be assessed, and owners should be educated regarding potential side effects.
It is critical that only one NSAID is administered at a time to a patient, especially if a COX-2 selective drug is administered. When nonselective COX inhibitors, such as aspirin, are administered, Aspirin Triggered Lipoxins (ATL) are produced which help prevent margination of neutrophils in the gastric vasculature and damage to the gastric mucosa. ATLs are gastroprotective, and require the COX-2 enzyme for their formation. However, if aspirin is followed by a different NSAID, the second NSAID’s COX-2 component blocks the ATL pathway, and gives rise to a different pathway within the PMN that yields leukotriene B4, a very potent chemo-attractant. As a consequence, the ATL protective mechanism is blocked, ATLs are not formed, and neutrophils marginate in the vasculature, creating damage to the gastric mucosa and the potential for increased pathology is enhanced. Therefore, drugs such as deracoxib and carprofen should never be concurrently administered with drugs such as aspirin. Herein lies the foundation for suggesting a 10-14 day washout period from aspirin to any contemporary NSAID (because they all have COX-2 activity), and the emphasis on pet owner education to not supplement a veterinary NSAID drug with aspirin.
Efficacy of NonSteroidal Anti-Inflammatory Drugs for the Management of Osteoarthritis
There are relatively few studies comparing efficacy among the various NSAIDs in veterinary medicine, but one can gain some information regarding efficacy by reviewing results obtained from studies to gain approval of a drug.
Carprofen was evaluated in a double blinded multi-institutional study. Force plate analysis revealed no significant difference between the groups, with 19/34 placebo and 29/36 carprofen dogs improving. Owners assessed 13/34 placebo dogs as improved, and 26/36 carprofen-treated dogs as improved. In comparison, veterinarians assessed 9/34 placebo dogs as improved and 20/36 carprofen-treated dogs as improved. The odds ratios of treated dogs improving compared to dogs receiving placebo were 4.2, 3.5 and 3.3 as determined by owners, veterinarians, and force plate, respectively.
In two different clinical studies, lameness, weight-bearing, pain on palpation, and overall improvement were subjectively evaluated in dogs receiving meloxicam. In one study, significant improvement was noted on day 14 of the 14 day study. In the second study, a significant improvement was noted in the parameter of overall assessment, and then only on day 7 by veterinary assessors and day 14 by owners.
Deracoxib or placebo was administered for 42 days to dogs with elbow, hip or stifle osteoarthritis in a prospective, blinded multi-institutional study. Deracoxib treated dogs showed a significant 7.4% improvement in peak vertical force, and 4.9% improvement in vertical impulse. Owner-assessed quality of life and lameness were also significantly improved.
Relatively few studies have compared various NSAIDs to each other in dogs. In a laboratory model efficacy study, deracoxib was compared with carprofen and a placebo in an acute synovitis model. Results of this study indicated that deracoxib prevented lameness measured subjectively and by determining ground reaction forces with a force platform. It was significantly more effective at alleviating lameness than placebo at all time points, and more effective than carprofen at several time points.
Another study evaluated 71 dogs with elbow, stifle, or hip OA treated with placebo, carprofen, meloxicam, or a nutritional supplement containing chondroitin sulfate, glucosamine, manganese and ascorbate. Ground reaction forces were measured prior to, 30, and 60 days after medication. There was no overall response to placebo. Ground reaction forces were significantly improved in dogs receiving meloxicam and carprofen, while there was no improvement with the nutritional supplement. Only meloxicam resulted in a return to normal ground reaction forces for some situations.
An acute synovitis model was used in Beagle dogs to compare the analgesic and anti-inflammatory effect of single doses of carprofen, etodolac, meloxicam, and butorphanol to placebo. Compared with control dogs, treated dogs had significantly different vertical ground reaction forces and weight-bearing scores. Greatest improvement in lameness was observed in carprofen-treated dogs. Etodolac had the fastest onset of action. Carprofen and etodolac were also associated with significantly lower pain scores.
We have examined the effectiveness of carprofen, etodolac, aspirin, acetaminophen, deracoxib, meloxicam, firocoxib, and a placebo on ground reaction forces in dogs with mild to moderate OA of the stifle joint in our laboratory. A crossover study was performed so that all dogs received each drug for a 2 week period. A washout period was used between drugs to be certain the degree of lameness returned to pretreatment levels prior to initiating a new drug. Dogs were assessed by force plate analysis of gait prior to beginning the drug on day 0, and on days 7 and 14. Results from this study showed that each dog responded to at least one NSAID, but dogs that responded to one NSAID did not necessarily respond to other NSAIDs. As determined by peak vertical force, deracoxib gave the greatest improvement over the 2 week period. The next greatest response was for dogs receiving etodolac, firocoxib, and aspirin, which had similar effects. Dogs receiving carprofen and meloxicam had a mild response and mean responses were similar to each other. Acetaminophen was not effective in improving ground reaction forces.
Slow-Acting Disease-Modifying Osteoarthritic Agents
Slow-acting disease-modifying osteoarthritic agents are substances thought to alter the course of OA by improving the health of articular cartilage or synovial fluid. Nutraceuticals are nutritional supplements believed to have a positive influence on cartilage health by providing precursors necessary for repair and maintenance or by stimulating the body to produce substances beneficial to articular cartilage. Unlike the pharmaceutical industry, there is no requirement that manufacturers of nutraceuticals use good manufacturing practices (GMP), and end products vary greatly in purity and content. There is no requirement that a particular product be efficacious, and many products boast unrealistic claims. It is important to select products of companies that produce quality products. Studies have demonstrated significant variability in product content of chondroitin sulfate and glucosamine, with some formulations containing essentially no active ingredient. The Arthritis Foundation suggests, “when a supplement has been studied with good results, find out which brand was used in the study, and buy that product.”
Glucosamine and chondroitin sulfate (CS) are routinely combined as disease-modifying agents. Glucosamine is a precursor to the disaccharide units of glycosaminoglycans (GAGs), part of the proteoglycan (PG) ground substance of articular cartilage. Studies have shown that glucosamine helps to improve cartilage metabolism and upregulate proteoglycan synthesis. In addition, it may have cyclooxygenase-independent anti-inflammatory properties. One study of humans found glucosamine to be as effective as ibuprofen in controlling signs of OA. CS is the predominant GAG found in articular cartilage. Extracellular and intracellular mechanisms are also stimulated by CS to produce GAG and PG. CS also competitively inhibits degradative enzymes in cartilage and synovium.
Cell culture studies show that glucosamine and chondroitin sulfate have different mechanisms of action and are not interchangeable therapeutic agents. CS has been noted to decrease interleukin-1 production, block complement activation, inhibit metalloproteinases, inhibit histamine-mediated inflammation, and stimulate GAG and collagen synthesis. There may be a synergistic effect with the combination of glucosamine and CS on production of cartilage matrix by chondrocytes, with greater effect in retarding the progression of degenerative cartilage lesions than either individual ingredient alone.
When articular cartilage explants were cultured in a nutraceutical combination of glucosamine HCl, CS, ascorbate and manganese, it was observed that compared to controls, there was greater production of aggrecan, less chondrocyte degradation, and increased expression of genes coding for both aggrecan and collagen II. These results suggest that this combination product may actually contain signaling molecules for up-regulation of the genes for aggrecan and collagen II, not just act as substrates for cartilage production. Another study showed that and experimental study of cranial cruciate deficient dogs treated with glucosamine HCl, CS, ascorbate and manganese for 5 months had fewer clinical signs of OA and less periarticular fibrosis than controls. Furthermore, treated dogs had fewer histologic OA changes.
Polyunsaturated Fatty Acids
Certain forms of polyunsaturated fatty acids (PUFA), especially omega-3 fatty acids, may reduce the production of certain eicosanoids, especially the more potent inflammatory leukotrienes and help reduce the degree of inflammation. Controlled clinical trials in the treatment of pain associated with OA in dogs have shown increased weight bearing as measured by force plate analysis of gait. Commercial diets have omega-3 fatty acids in the diet. These have been effective clinically in patients with osteoarthritis, and may reduce the amount of anti-inflammatory drugs needed to manage patients with OA.
Avocado-Soybean Unsaponifiables (ASU)
Avocado-soybean unsaponifiables are commonly used treatments for symptoms of OA in Europe in people. Most ASU preparations are composed of one third avocado and two thirds soybean unsaponifiables (ASUs).
In vitro, ASUs have anabolic, anticatabolic, and anti-inflammatory effects on chondrocytes. In one study, ASUs increased collagen synthesis and inhibited interleukin (IL)-1β-induced collagenase activity. They also increased aggrecan synthesis and reversed the IL1β- induced reduction in aggrecan synthesis. ASUs also reduced IL1β-induced production of matrix metalloproteinases (enzymes involved in cartilage destruction), IL-6, IL-8, and prostaglandin E2 (PGE2) while weakly reversing the IL1β- induced decrease in TIMP (tissue inhibitors of metalloproteinase, endogenous molecules that counteract destructive enzymes) production. Another study showed that ASUs decreased the production of nitric oxide (NO) 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 MMP activation. ASU 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 ASU could have structure-modifying effects in OA by inhibiting cartilage degradation and promoting cartilage repair. NF-kB activation is mandatory for the expression of many genes involved in chondrocyte activation such as interleukin-6, interleukin-8, nitric oxide and PGE2 that are proinflammatory mediators. ASU prevented mechanical stress-induced NF-kB activations in chondrocytes. The inhibitory effect of ASU seems to be due, in part, to the inhibition of the NF-kB pathway.
A multicenter, double blind, study compared 300mg or 600mg of ASU daily with placebo for 3 months in aged human patients with knee osteoarthritis. At day 90, intake of NSAIDs and analgesics decreased by more than 50% in 71% of the patients receiving ASU 300mg or 600mg, compared to 36% of the patients receiving placebo. ASUs may also slow down narrowing of joint space width in people with severe hip OA. Based on the present evidence, ASUs provide symptom-modifying effects in people with knee and hip OA, and there is also some evidence of structure-modifying effects.
Methylsulfonylmethane occurs naturally in small amounts in some green plants, fruits and vegetables, and most people have some MSM present in the 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 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 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. These doses are considered five to seven times the maximum dose used in humans. There have been reports of mild adverse effects 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.
One randomized controlled trial of people with knee OA evaluated MSM during a 12-week trial. Patients received either 1.5 g MSM, 1.5 g glucosamine sulfate, 1.5 g MSM plus glucosamine sulfate, or placebo. Significant decreases in a standardized arthritis index were reported with MSM, glucosamine sulfate, and their combination. 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. MSM 3 g or placebo twice a day for 12 weeks (6 g/day total) was evaluated. Compared to placebo, MSM produced significant decreases in standardized pain scores, physical function impairment, and improved performance of activities of daily living. 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 (celecoxib decreased WOMAC pain, stiffness and physical function by 28.6 mm, 27.9 mm, and 24.9 mm, respectively, and etoricoxib decreased by 22.29 mm, 19.01 mm, and 22.87 mm, compared to the MSM trial, which decreased by 14.6 mm, 10.1 mm, and 15.7 mm, respectively). 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 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 humans indicate that it has analgesic and anti-inflammatory properties, possibly by inhibiting COX activity. Efficacy in animals has not been established. 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 regarding the use of SAMe for OA in people has been consistently positive. A review and meta-analysis, as well as several randomized clinical trials, have shown that SAMe is more effective than placebo in reducing osteoarthritis pain. In a recent trial, SAMe (1,200 mg per day) was compared with celecoxib (200 mg per day). 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 symptoms substantially improve. SAMe may also increase chondrocytes and cartilage thickness and may also decrease cytokine-induced chondrocyte damage.
The polysulfated glycosaminoglycan (PSGAG) is a drug that is anti-inflammatory, inhibits enzymes that degrade GAGs and hyaluronic acid (HA) within the joint and has a positive effect on HA and GAG synthesis in diseased joints. It is therefore said to be a disease modifying osteoarthritis drug (DMOAD). Polysulfated glycosaminoglycans have been reported to stimulate existing chondrocytes, increase concentrations of synovial fluid HA, inhibit metalloproteinases, inhibit production of complement activation, inhibit enzyme release from leukocytes, and to inhibit PGE2 and toxic oxygen radical synthesis.
Support for the efficacy of polysulfated glycosaminoglycans as a treatment for canine osteoarthritis was evaluated in a Pond-Nuki dog model, in which treated dogs received 4 mg/kg PSGAG twice weekly for 4 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 to the operated control joints. In addition, PSGAGs improved stifle range of motion, clinical use of the limb, and the health of the synovium in dogs recovering from experimental cranial cruciate ligament transection and stifle stabilization surgery. The greatest uptake occurs in the superficial layers of cartilage and PSGAG has a predilection for inflamed or diseased cartilage.
Hyaluronic acid (HA) is a major component of synovial fluid and cartilage. HA is available as an intra-articular injection and helps to restore synovial viscosity, reduce inflammation and prostaglandin production, and scavenge free-radicals. Some patients may benefit from periodic administration of HA.
Other Analgesic Agents
Because of the changes that occur in the processing of pain signals, the pain that is experienced is often increased in amplitude and duration. Chronic pain may become “resistant” to treatment with NSAIDs, necessitating a multimodal approach to therapy.
Amantadine is the most commonly used oral NMDA receptor antagonist. NMDA receptor antagonists are used as an adjunct 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, CNS hyperresponsiveness may be reduced, allowing other analgesics to function more effectively.
The standard dose used to block receptors in dogs and cats is 3-5 mg/kg SID. Oral antagonists often have a slower onset of action, taking up to a week to produce noticeable results. It may be given on a continual basis if needed, though in most cases it can be given daily for 7-14 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.
The mechanism of action of gabapentin is unclear, although it may involve inhibition of post-synaptic neuron firing, possibly acting as an inhibitor of voltage-dependent calcium channels. 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 BID, though doses as low as 1.25 mg/kg SID have been reported effective. It is metabolized by the liver and excreted by the kidneys. Possible side effects may include sedation and weight gain.
Amitriptyline is a tricyclic antidepressant that has been used in humans and animals as adjuncts to other analgesics for chronic pain. It inhibits serotonin and norepinephrine reuptake, although it may have other analgesic effects as well (including possible actions at opioid receptors and on nerve transmission). Dogs are usually dosed at 1-2 mg/kg SID-BID. Side effects can include sedation and anticholinergic effects.
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 an analgesic effect. 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, and is generally dosed in dogs at 1-2 mg/kg of the codeine portion TID-QID. It should NOT be used in cats in combination with acetaminophen due to 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 0.5-2.0 mg/kg QID (some dogs experience unacceptable constipation at doses exceeding 1 mg/kg).
Tramadol has been used to treat chronic osteoarthritic pain, but it has been found to not be effective in dogs. Despite its wide use, there is little-to-no safety or data on the use of tramadol in veterinary patients. Tramadol has adverse events in people, including vomiting, diarrhea, and sedation. Because of tramadol’s monoamine reuptake inhibition, it should not be given with TCAs, SSRIs, or MAO inihibitors due to the risk of serotonin syndrome. Metabolism is principally via hepatic biotransformation, with a small amount excreted unchanged by the kidneys.
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 loss of 5 kg decreases the odds of developing OA by over 50%. Additionally, weight loss results in less joint pain and a decreased need for medication to treat OA. In a study of 48 Labrador Retrievers, a control–fed group was allowed food ad libitum, while a limit-fed group was fed 25% less. Hip, shoulder, elbow and stifle joints were monitored over a lifetime. OA was significantly less common in the limit-fed group, with OA of the hip occurring in 15 of 22 in the control group and in only 3 of 21 of the dogs in the restricted fed group. Similar trends were apparent in the shoulder joint.
Additionally, weight loss results in less joint pain and a decreased need for medication to treat OA. Weight reduction of 11-18% of the initial body weight of obese dogs resulted in significantly improved hind limb lameness associated with hip OA in one study. Another study investigated 16 moderately overweight to obese dogs with hip dysplasia. After undergoing a weight loss program with 20 to 60 min of daily leash walking, body condition scores improved to 4 to 5 out of 9. In addition, there was a significant increase in peak vertical force and vertical impulse as assessed by force plate analysis of gait.
In addition to restricting intake of the normal diet and eliminating treats, prescription diets are available that can dramatically assist in achieving and maintaining ideal body weight. In general, a goal is to reduce fat composition to 20-25% 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.
Exercise is a vital component of weight loss for OA treatment. Caloric restriction alone in obese patients results in decreased resting metabolic rate. Acute exercise increases the resting metabolic rate for 2 to 48 hours. Frequent exercise over an extended period may prevent the reduced resting metabolic rate associated with a diet and caloric restriction. One of the goals of therapeutic exercise is to increase muscle mass. As lean mass increases, the resting metabolic rate increases, making it easier to burn calories. Providing 20-60 minutes of daily activity is a goal that will benefit overweight patients with OA.
Physical Rehabilitation Modalities
Physical modalities for treating dogs with painful OA have been increasingly recognized. Cryotherapy, heat, therapeutic and aquatic exercises, transcutaneous electrical nerve stimulation, extracorporeal shock wave therapy, massage, and therapeutic laser have the potential to reduce the pain of OA.
Cold decreases blood flow, inflammation, hemorrhage, and metabolic rate. Commercially available cold packs or ice wrapped in a towel may be applied to an area for 15 to 20 minutes, 3 to 6 times daily. An entire limb may be immersed in a cold water or 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 ROM, although some discomfort is initially associated with application of cold.
Superficial heat modalities
Superficial heating agents typically heat the skin and subcutaneous tissues to a depth of 1-2 cm. The tissue is usually heated to 40 to 45C 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, may decrease pain, muscle spasm and joint stiffness, and causes general relaxation. Heat is contraindicated if swelling or edema are present, and there is the potential to increase inflammation with heat.
Therapeutic and Aquatic Exercise
Most studies of mild to moderate exercise and training in normal humans and dogs have indicated that 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 which predispose to the development of OA, and exercise may hasten OA if joint instability is present.
The benefits of controlled exercise for patients with OA are valuable but underutilized. Humans with OA participating 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 and strengthening of 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 to each 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 owner will likely decrease compliance, and the physical condition of the owner must be considered. Joint instability should be corrected before initiating an exercise program. 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. Tissue warming promotes blood flow to the area, promotes tissue and collagen extensibility, and decreases pain, muscle spasms and joint stiffness. Stretching and massage may be 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 titrated so there is no increased pain after activity. Also, it is better in the early phases of training to provide three 20 minute sessions than one 60 minute session, for example. 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 bouyancy of water is significant and limits the impact on the joint while promoting muscle strength and tone, and joint motion. Training in an underwater treadmill may increase peak weight bearing forces by 5-15%, which is comparable to achievements obtained using medication.
Controlled exercise must be titrated 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 decreased by half. When stepping up the amount of activity, the increase should be approximately 5-15% and should not be stepped more than once each week. The exercise periods should be evenly spaced throughout each day and over the entire week. Training helps maintain an ideal body weight, improves ROM, and increases muscle strength and tone.
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 ROM 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 15-20 minutes to control post-exercise inflammation. Application of cold decreases blood flow, inflammation, hemorrhage and metabolic rate.
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 inside environment. A soft, well-padded bed or waterbed should be provided. A circulating warm-water blanket under the blankets provides heat which may reduce morning stiffness. Provide good footing to avoid slipping and falling. Minimize stair climbing through the use of handicapped ramps and keeping pets on ground floors. Steps are negotiated easier if they are wider and spaced farther apart. Portable ramps are available to assist patients getting in and out of vehicles. 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 painful. 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 approached frequently to treat arthritic patients. Management of the arthritic patient involves a number of modalities and must be tailored to each patient and their owner. Weight control, physical rehabilitation, and medication are the main components for OA management. A variety of pharmaceutical agents are available for the treatment of canine osteoarthritis. When selecting medications for treatment, veterinarians should consider the efficacy, safety profile, mechanism of action, and patient response. It should be remembered that not all dogs respond equally to all medications. Avoid concurrent administration of nonsteroidal and steroidal anti-inflammatory drugs. Cooperation among the veterinarian, veterinary nurse and owner are vital to carry out an appropriate management program. Regular monitoring of achievements is essential to help with decision-making for further treatment and maintaining enthusiasm for the program.