Treating Canine Osteoarthritis – Part 2
To recap from Part One of this article (Fall 2013), osteoarthritis (OA) is the most common joint disease in dogs. Our focus on managing it must evolve from simply the palliative treatment of well-established disease using a few modalities, to early intervention and a comprehensive multimodal approach. In the last issue, we covered diet, supplementation, weight management and assistive devices. We will now look at:
• Acupuncture and physical manipulation (chiropractic)
• Regenerative medicine therapy
• Rehabilitation therapy
• NSAIDs and adjunct medications
• Disease modifying agents and corticosteriods
Acupuncture and physical manipulation (chiropractic)
Dogs have approximately 360 acupuncture points located throughout their bodies. The exact mechanism of action is not completely understood, but research suggests acupuncture needles stimulate nerves and offer benefits as described by the gate theory. Response varies in dogs, with some showing significant improvement in discomfort and mobility. Some dogs experience no obvious benefits and a few do not tolerate needling.
Because the entire “chi” of the dog is being treated, a referral to veterinarians trained in TCVM provides the best chance of successful treatment in cases of OA. TCVM can help with weight management, improve vitality and energy, and assist with concomitant diseases as well as joint issues.
Spinal manipulative therapy (chiropractic) can improve comfort and mobility in dogs with OA. These dogs often develop improper spinal biomechanics secondary to gait changes. Adjustments can restore proper bony relationships and reset receptors responsible for maintaining correct posture, balance and mobility.
Regenerative medicine therapy
1 – Stem cell therapy
Published literature supports the use of stem cell therapy (SCT) to treat OA in dogs. However, there are still many unanswered questions. Most veterinary research has focused on adult stem cells, specifically mesenchymal stem cells, derived from bone marrow (BM-MSC) or adipose tissue (AD-MSC). To date, there is no definitive evidence in dogs that supports one tissue source over the other for regenerative treatments.
Adipose tissue may be a preferred source in dogs due to ease of access, low morbidity and pain associated with collection, and high-yielding mesenchymal stem cell counts (especially falciform). The cells isolated from the adipose tissue not only include mesenchymal stem cells but endothelial progenitor cells, pericytes, immune cells, fibroblasts and other growth factor-secreting bioactive cells. This is known as stromal vascular fraction therapy. The stem cells along with this mix of other regenerative cells can be injected directly into the injured tissue or joint and/or given intravenously.
Alternatively, the stem cells can be isolated from adipose tissue, cultured and expanded. This yields a more homogenous population with a larger quantity of cells for injection. This is known as adipose derived progenitor cell therapy. Because cells are obtained from the intended recipient, the risk of rejection and disease transmission is eliminated regardless of culture or direct injection, adipose or bone marrow source.
There are multiple mechanisms by which these regenerative cells initiate change. MSCs decrease pro-inflammatory and increase anti-inflammatory mediators. MSCs are activated to become immunosuppressive by soluble factors, and in turn secrete soluble factors that inhibit T-lymphocyte activation and proliferation. MSCs secrete bioactive levels of cytokines and growth factors that support angiogenesis, tissue remodeling, differentiation, and antiapoptotic events. The cytokines and growth factors secreted by MSCs can also assist in neovascularization. MSCs demonstrate a diverse plasticity and are able to migrate to sites where needed.
2 – Platelet-rich plasma (PRP)
PRP is autologous blood plasma with concentrated platelets. The concentrated platelets found in PRP contain bioactive proteins and growth factors, including platelet-derived growth factor (PDGF), transforming growth factor-1 (TGF-1), transforming growth factor-2 (TGF-2), vascular endothelial growth factor (VEGF), basic fibroblastic growth factor (bFGF), epidermal growth factor (EGF) and stromal-derived factor (SDF-1). These growth factors work by binding to cell surface receptors and activating intra-cellular signaling cascades. They promote cell proliferation, cell migration and differentiation, and work as anti-inflammatory factors counteracting the inflammatory cytokines at work in OA.
3 – Combination therapy
By combining SCT with PRP, it is possible to achieve the positive effects of both regenerative therapies. Combination therapy provides cells for regeneration, growth factors, and a scaffold to provide a template for cell attachment.
Rehabilitation therapy may be used in conjunction with other therapies. In some cases of mild to moderate OA, it may actually eliminate the need for additional medical therapies. The goals of rehabilitation therapy for the OA patient include pain relief, maintaining or building muscle strength, flexibility, and joint range of motion, core strengthening and overall conditioning.
• Cold therapy causes vasoconstriction to reduce inflammation, muscle spasms, pain and deceleration of nerve conduction velocity. It benefits dogs with acute exacerbation of chronic OA.
• Heat therapy causes vasodialation, increasing enzymatic activity and collagen extensibility. It also reduces muscle tension and spasm, improves flexibility of the joint capsules and surrounding tendons and ligaments, and provides pain relief.
• Transcutaneous electrical nerve stimulation (TENS) has been shown to reduce pain. It works by stimulating large cutaneous nerve fibers that transmit sensory impulses faster than pain fibers as explained by the gate theory. In addition, TENS also increases the release of endogenous endorphins, which interact with pain receptors and block pain perception.
• Neuromuscular electrical stimulation (NMES) involves the stimulation of muscle fibers for strengthening. Dogs with OA typically lose muscle mass due to weakness and disuse. NMES may help minimize the extent of atrophy, and provide proprioceptive, kinesthetic and sensory input directly to the muscle as well as give pain relief.
• Therapeutic Ultrasound (TUS) uses sound energy to affect biological tissues. It provides deep heating of tissues (3cm to 5cm). TUS can increase blood flow, collagen extensibility, metabolic rate and pain thresholds. It can also decrease muscle spasm.
• Low Level Laser Therapy (LLLT) influences cellular processes through photobiomodulation. It may have positive effects on injured cartilage. In addition, LLLT may reduce pain through the increased metabolism of endogenous opiates, a change in the conduction latencies of nerves, or through stimulation of acupuncture or muscle trigger points.
• Extracorporeal Shock Wave Therapy (ESWT) uses sound waves characterized by a rapid and steep rise in pressure followed by a period of negative pressure. Mechanisms of action are not yet fully understood, but it is postulated that mechanical and chemical effects on a cellular level stimulate healing and modulate pain signals.
• Manual Modalities – PROM/Stretching – Most dogs with OA have some degree of inflexibility due to shortened muscles and intrinsic joint restriction. Performing gentle passive range of motion therapy and stretching has been shown to increase overall range of motion. Heat therapy applied prior to these therapies enables collagen fibers to be maximally stretched.
– Joint Mobilization – May help improve joint range of motion and decrease pain in dogs with mild to moderate OA. Joint mobilization involves low-velocity movements within or at the limit of the dog’s range of motion. Gentle distraction following joint mobilization may improve results. Care must be given when performing this modaility for dogs with more severe OA, as it may increase discomfort.
– Massage – Decreases myofascial pain, adhesion formation and muscle tension, and increases vascular and lumphatic circulation. It can help reduce edema, improve blood flow, decrease muscle stiffness and improve muscle flexibility and joint mobility. Clients can be trained to do this at home.
• Therapeutic Exercises can be of significant benefit to dogs with OA. Most of these dogs have moderate to severe muscle atrophy and loss of motion within affected joints. Therapeutic exercises are used to maintain and rebuild muscle mass, strengthen muscle force, maintain and improve joint range of motion and overall function and conditioning.
• Hydrotherapy includes underwater treadmill and swim therapy. Extensive studies in human physical therapy have demonstrated that hydrotherapy encourages range of motion, and improves muscle tone and mass with reduced stress to joints and tissues. In addition, the buoyancy of the water may allow the therapist to perform standing therapeutic exercises.
The benefits of hydrotherapy to dogs with OA include:
• Relief of pain, swelling and stiffness
• Improved muscle mass and tone
• Increased joint range of motion
• Improved circulation
NSAIDs and adjunct medications
NSAIDs have been the foundation for treating symptoms of OA in dogs. They have anti-inflammatory, analgesic and antipyretic properties. However, serious adverse effects can occur, some of which are fatal, especially with chronic use. These most commonly include gastrointestinal, renal, hepatic and coagulation disorders. The goal is to use the minimal effective dose when other treatments are not successful. Because of these potential adverse reactions, screening to identify high-risk candidates should be performed and include a physical and chemical examination, and identification of concurrent disease or conditions. It is important to educate owners on the proper dose, administration and potential side effects of NSAID therapy. This information should be provided both verbally and in writing. Most adverse affects are seen in the first 48 to 72 hours of administration. A call to the owner at this time and reassessment within ten to 14 days is recommended. For chronic therapy, routine rechecks are recommended. GI protectants may be needed in some patients.
Adjunct medications can be used for “break through” pain or if discomfort cannot be controlled by other means.
Commonly used adjunct medications include:
• Tramadol • Gabapentin • Amatodine • Codiene
Disease modifying agents and corticosteroids
Details on these conventional medications are readily available in veterinary literature. Adequan® Canine is polysulfated glycosaminoglycan (PSGAG) prepared by extracting glycsaminoglycans (GAGs) from bovine trachale cartilage. It has been shown to inhibit certain catabolic enzymes that degrade collagen, proteoglycans and hyaluronic acid in inflamed joints. In addition, Adequan stimulates the synthesis of protein, collagen, proteoglycans and hyaluronic acid.
Hyaluronic Acid (HA) is a form of viscosupplementation, which has been shown to slow the progression of osteoarthritis and decrease inflammation within the joint. Specifically, it increases joint fluid viscosity, increases cartilage (GAG) formation, and decreases degradative enzymes and cytokines. The injections must be given under sterile conditions with the dog under sedation or general anesthesia. Reportably, over 70% of dogs respond well to HA and improvement can be noted for over six months following administration. The author’s clinical impression is that HA used alone is useful for synovitis and mild to moderate OA, but in the treatment of severe OA, an intra-articular corticosteroid is recommended.
When dogs have not responded to other treatments, intraarticular injections of corticosteroids can provide pain relief for dogs with end-stage osteoarthritis. Arthroscopic debridement of the arthritic joint may offer improved comfort and mobility. Salvage surgeries such as joint replacement and arthrodesis may also be considered.
Canine osteoarthritis is an incurable condition, but with early intervention, when possible, and a multimodal approach, we can extend longevity and quality of life for our canine patients.