Canine osteoarthritis is a common chronic degenerative joint condition that affects the whole joint but the most prominent symptom is the loss of articulate cartilage.
OA causes pain, lameness, decreased mobility, and if not managed on time and correctly the symptoms will escalate to muscular atrophy, joint effusion, incorrect joint articulation, etc. Dogs that experience chronic pain often develop other conditions such as fear, depression and anxiety, moreover, OA becomes a contributing factor to the decision of euthanasia, especially in older dogs. There are two types of OA: primary, cause of which is unknown but could be associated with the animal’s age and weight, and secondary, which is a result of trauma, inflammatory arthritis, abnormal development of the joint, like in hip or elbow dysplasia, or metabolic diseases with the pathogenesis possibly having a genetic component to it.
Studies on the prevalence of OA in the UK reported that between 2.5% to 6.6% of dogs in primary veterinary care will develop the disease (1, 2). A similar study in the US from 1997 by Johnson et al. (3) estimated the number to be 20%. However, the real prevalence numbers might be much higher. Considering the total number of dogs in these countries (12.5mln in UK and 77mln in US respectively), canine OA represents a welfare problem with a significant number of pet owners affected and the overall cost of a life-long treatment and management of the symptoms.
OA risk factors.
Since secondary canine OA is the most prevalent type, it is important to consider the risk factors in order to diagnose and manage OA at early stages. Some dog breeds are especially prone to developing OA at as early as several months old due to their genetic factors as well as body features which are required by the breed standards such as size, joint angles, leg size. Among the breeds that have an increased risk of cruciate ligament rupture are Golden Retriever, Rottweiler and Labrador Retriever (4-7); German Shepherds, Golden Retrievers, Labrador Retrievers, Mastiffs, Bernese Mountain dogs have an increased risk of hip and elbow dysplasia (8-11), while smaller breeds like Pomeranians, Chihuahua, Yorkshire Terrier might develop a condition called luxating patellar or a tricking knee (12). Diet might also be a contributing factor. For example, it was found that high-fat diet and unrestricted diet during the growth period are associated with higher risk of elbow and hip dysplasia (13).
Diagnosis of OA
The diagnosis of canine OA includes physical examination, radiography, synovial fluid analysis, arthroscopy and CT or MRI scans for more accurate visualization of joints. The main strategy of conventional OA management is to slow down disease progression, pain alleviation and anti-inflammatory therapy. The ABCDE approach which stands for analgesia, bodyweight control, disease modification and exercise can also be applied for the management of canine OA. Analgesia, or pain management, is especially important because it improves the quality of life of a dog suffering from OA.
Current treatment strategies:
NSAIDs are quite effective at addressing both pain and inflammation, so among most commonly prescribed medicines are meloxicam, carprofen, firocoxib, maxacoxib. However, prolonged treatment with NSAIDs can cause damage to the GI tract and in extreme cases lead to liver and kidney failure and even death of an animal. Other drugs such as an anticonvulsant medication gabapentin, an antiviral amantadine or an opioid tramadol can be prescribed alongside NSAIDs. However, these compounds might also have behavioral and physiological side effects.
Nutraceuticals, despite the lack of scientific evidence of their efficacy can also be prescribed together with pain relief medication and other measures. Among the most commonly used supplements for OA are glucosamine, chondroitin, methylsulfonylmethane (MSM). A study on the effect of Omega-3 fatty acids demonstrated that 127 dogs fed a diet rich in Omega-3 had a significant improvement of mobility and the tests showed reduced levels of arachidonic acid in the blood serum which indicates lower inflammation of the joints (14).
Physical therapy and surgery
Appropriate exercise and physiotherapy are also critical for OA patients once the acute phase of the disease has passed, since reduced mobility further exacerbates the symptoms and can lead to muscle atrophy. Other types of physical rehabilitation such as cryotherapy, extracorporeal shock wave therapy, transcutaneous electrical nerve stimulation, therapeutic laser treatment can be offered to the owner. In cases when no other therapy is effective, surgical intervention can also be performed, which can include complete joint replacement, osteotomy or arthrodesis (joint fusion).
It is important to remember that the traditional treatment strategies of OA only slow down (at best) the disease progression and alleviate the symptoms, but do not provide tissue regeneration, neither stop the degradation of the damaged cartilage. Currently some veterinary clinics offer experimental treatment of OA which includes the use of biologics, such as structure modifying OA drugs (SMOADs), platelet-rich plasma, gene therapy and mesenchymal stem cells (reviewed in 15). SMOADs are supposed to stabilize and repair OA lesions (pentosan polysulphate, polysulphated glucosaminoglycans, hyaluronic acid, etc) however, there is little robust scientific evidence of the efficacy of this class of OA medication. Platelet-rich plasma (PRP) is obtained from the OA affected dog by drawing blood and then injecting the processed plasma into the joint.
Growth factors released by platelets can stimulate chondrocyte proliferation and inhibit chondrocyte apoptosis. Anti-inflammatory cytokine plasmid DNA therapy is aimed at increasing the levels of anti-inflammatory cytokines which can inhibit the production of inflammatory cytokines and hence reduce the chondrocyte apoptosis, however, there have been very few studies on this therapy and further investigation is required. Studies on using mesenchymal stem cells for reverting canine OA showed very promising results. You can refer to these studies by our group (16, 17) as well as published studies from others (18-20) to learn more about our technology and benefits of stem cells for treating OA.