Richard C. Nap, DVM, PhD, DECVS, DECVCN
1. Diagnosis of Osteoarthritis
Osteoarthritis (OA) is a painful, disabling condition that can affect all joints. The onset can be induced by an acute traumatic incident but in most cases it is a slowly progressing condition. The focus of this abstract is on OA of the elbow joint in the dog from the perspective of the veterinary practitioner, veterinary surgeon or veterinary GP. Elbow OA in the dog in the majority of cases is the result of elbow dysplasia (ED) which can be one of 4 conditions: ununited anconeal process (UAP), osteochondrosis dissecans of the (in most cases medial) humeral condyle (OCD), fragmented medial coronoid process (FCP) and or elbow incongruency (EI). The EI is caused in most cases by the Radius being longer (higher) than the Ulna, or in some cases the semi-lunar joint of the ulna not being congruent with the humeral intercondylar joint surfaces. The anatomy and pathogenesis of elbow dysplasia is outside the scope of this abstract.
The patients are typically presented with signs of lameness in one of the front legs. However, some dogs may be presented for an annual health check and especially when belonging to one of the breeds at risk, special attention to lameness and elbow function is indicated. Some owners will not notice signs of subtle lameness or bilateral balanced lameness.
Dogs with bilateral lameness might not present any gait imbalance because both elbows are affected to the same extent. As a result, the patient does not favor one leg over the other as is the case in one leg lameness or in the case the elbows are affected to different degrees. The bottom line is that young large- and giant-breed dogs with front leg lameness always have to be carefully checked for both legs, even when one leg is favored over the other (one side lameness). In case of bilateral lameness, the owner may report the dog to be less interested to make (longer walks) and have start-up stiffness, or needs to warm up into exercise. This is especially the case when also the hips are affected. In many cases, breeds at risk for elbow disease are also on the risk list for hip dysplasia (HD).
At presentation, the signalment and history already offer valuable information regarding the diagnosis. From the author's perspective, dogs belonging to breeds at highest risk for ED are suspected to have elbow problems, unless they are proven not to be affected (to be clean). Examination starts with carefully observing the dog to sit, walk en trot (pace) for at least 10 meters on the leash in a straight line. It is not unusual for owners to report the lameness to be in the wrong leg. They easily misinterpret the gate anomaly and don't know that "the head drops" while pacing when the dog puts weight on the (most) healthy leg. So the problem is in the other leg. If possible, also observe the dog from the side, in order to evaluate the range of motion of the elbow joints. Bilateral problems can be masked by a bilateral stiff gate and short strides with insufficient elbow action. It is advised to train the eye of the observing clinician by examining normal dogs on a regular basis until a good sense and perception of the "normal" for the different age and breeds has been established. The same is true for the rest of the clinical exam. The veterinarian cannot expect the skills of the clinical exam to be achieved without many hours of training to develop the full expert capacity to distinguish normal from abnormal. One has to train the eyes and the fingertips. This cannot be learned from the book.
One can obtain valuable information for ED by just observing the dog while sitting. Many dogs that have FCP have the tendency to rotate the foot slightly outward (15 to 20 degrees).
In case of OA, the clinical exam of the front leg in standing position may reveal joint effusion at palpation over the lateral aspect of the elbow, just caudo-proximal of the humeral lateral epicondyle, under the M. anconeus. Some fluctuation might be noticed by skilled fingers. In lateral recumbency, both legs are examined and problems in other areas are excluded while working from distal to proximal. Elbow problems might be confused with shoulder problems when passive motion and especially joint extension is done. One reason for this confusion is that the shoulder joint cannot be extended without also extending the elbow. OA can be characterized by joint effusion, broadening of the joint due to secondary degenerative joint disease (DJD); the joint feels less dry, and the structures can less clearly be identified compared to the normal situation in the healthy joint. In serious cases, crepitation can be felt under the anconeal muscle and sometimes even heard! However, these are the serious and obvious OA cases. Many times the changes are subtle and the clinician has to be well trained and pay full attention to all details. In case of OA, the range of motion (ROM) of the joint can be restricted and the full flexion and especially extension of the elbow can be painful. Elbow extension while at the same time creating slight endo-rotation may result in the dog giving signs of discomfort. The objective of the exam is not to cause the dog pain. The objective is to discover when discomfort starts and whether this is normal or abnormal. Prudence during all parts of the exam is an obvious condition. It is important to talk to the owner during the physical exam to explain what is done and why. Most owners and their pets perceive the physical orthopedic exam as stressful.
When the lameness problem has been localized in the elbow joint, the next step is to confirm and objectivize the degree of changes and the presence and degree of OA by radiographic examination (x-ray). The standard x-ray exam includes the AP and ML views. AP extended and ML flexed at 90 degrees. At least 2 additional views are advised to support the diagnosis of the individual conditions behind ED. The extended AP with 15 degrees exo-rotation and the ML extended with 15 degrees endo-rotation. These techniques and logic behind these views have been described and published by G. Voorhout and HAW Hazewinkel and are the standard in the ED screening program for breeding by the Dutch Kennel Club.
The development of OA starts subtle and in young animals at the age of 1 year, can be absent despite the presence of an ED condition. Especially in case of FCP the changes can be absent or minimal at 1 year of age. In case of FCP the location where changes can be first observed is on the medial aspect of the distal humeral condyle and the proximal part of the distal ulna (IEWG location g and h). Typically in case of UAP, OCD and EI the OA changes are more pronounced. The first and most prominent presence is often over the dorsal ridge of the anconeal process (IEWG location a). These are also present at a younger age in general. It is not unusual that OA in case of FCP shows up well after the age of 1 year, while for the other three it might be diagnosed as early as 6 to 7 months of age. However, exceptions to these rules of thumb are common and sometimes can be the results of combinations of forms of ED that go undiagnosed.
When the clinical signalment, history and clinical exam all point towards elbow problems and no diagnosis can be made, other noninvasive methods of diagnosing might be available in selected veterinary facilities. These include a bone scan (using radioactive calcium), CT and MRI scanning. In addition, invasive techniques like arthroscopy can show changes that were not visible without direct visualization. Detailed description of these techniques is outside the scope of this abstract.
2. Treatment of Osteoarthritis
OA is by nature a progressive pathologic condition for which today there is no cure. The good news is that dogs have shown to be able to live a (according to their owners) happy life with significant OA changes (based on radiographic evaluation) present in their major articulations including the elbow joint. In other words, the clinical prognosis of dogs with OA is not directly or linearly correlated to the degree of radiographic changes. The other good news is that there are various ways in which to influence the course of disease. The surgical therapies for the various ED conditions are outside the scope of this abstract. Several studies have shown that most dogs after surgery will continue to develop OA changes and sometimes the degree of OA at longer-term follow-up does not differ between surgical and nonsurgical therapy.
Nonsurgical treatment options of OA, available to the veterinary practitioner today, which can be and should be practiced in combination include 1) client education, 2) nutritional support, 3) physiotherapy and exercise, and 4) medication. Nutritional support includes a) energy intake, b) fatty-acids intake, as well as c) chondroprotective nutraceuticals such as glucosamine and chondroitin-sulphate. Physiotherapy includes a) home care as well as b) professional support with the aid of in and partly underwater exercise as well as training schedule advice and encouragement to the owner/caretaker. The medical support for dogs suffering OA can include the classic NSAIDs as well as the more recent drugs classified and COX-1 and COX-2 inhibitors.
Classic long-term studies in growing Labradors (Kealy et al.) have shown that the development of OA changes in joints is linked to the relative overweight of the growing pups. Puppies with overweight while growing up while affected by ED will develop more and more severe OA changes resulting in more clinical problems. The first (preventive) action with regard to the OA development in dogs at risk for ED and consequent OA is to raise them lean while immature. This will help them to develop less ED and as a result less OA. Also when OA is present based on ED, it has been shown that reducing body weight significantly increases mobility, reduces clinical signs of lameness, and increases owner satisfaction. So both in growing as well as adult dogs the total nutritional intake (read daily energy intake) has to be regulated in a way that the body condition score does not exceed the 3 out of 5 (or 5 out of 9). It has to be remembered that owners (and veterinarians) have a tendency to underestimate overweight due to the high prevalence of the conditions. Society has gotten used to overweight people and their pets and may consider a score 4 on a 5-point scale as normal because dogs scoring 7 on a 5-point scale are no longer an exception. Restricting food intake is one of the most simple and most powerful ways to treat OA. It is available to the veterinary practitioner at no extra costs and it has the potential to significantly impact the wellbeing of the canine patient and the owner. The importance of the role of the veterinarian and other members of the healthcare team in managing overweight in the dog population cannot be underestimated.
The second group of nutritional components with relevance to OA include the fatty acids in the diet and more specifically the unsaturated fatty acids. It has been proven that omega-3 fatty acids positively influence the inflammatory conditions (reduce inflammation) including those in the joints. The amount of omega-3 fatty acids and the relative amount compared to the omega-6 fatty acids (the omega-6/omega-3 balance) have been proven to be important. The two groups of fatty acids act in competition for metabolic pathways. The amount of omega-3 fatty acids in the diet can be increased by adding it to the food as a supplement or by providing prepared (industrial complete and balanced) foods that have increased levels according to producer specifications. The effect of these fatty acids should not be overestimated or exaggerated. They should be used as one of the available therapeutic options to influence the OA condition, in combination with others. The same applies for the use of chondro-protectives like glucosamine and chondroitin sulphate. Clinical response is reported to be individual. It has been shown in multiple species that providing these cartilage building blocks via different routes may have a positive effect on the development of OA, meaning a reduction of inflammatory and degenerative OA process and improved clinical status. However, significant controversy continues as to the impact that adding these ingredients to the daily diet may have on the condition of the patients and the levels needed in the diets to provoke an impact (if any). These kinds of diets include foods for large breeds, overweight and senior dogs. A dose response curve for the nutraceuticals has yet to be established. Maybe the best way to state their clinical relevance today is to position them as factors that may be beneficial without offering anything like a guarantee. Dogs at risk for OA and dogs suffering (early stage) OA are both candidates for the use of these nutraceuticals.
Physiotherapy and Exercise
The second important factor to influence OA together with weight management is exercise. Owner education has to increase understanding of the nature of OA changes and the commitment to work on managing the condition. Excess and peak loading of joints has to be avoided. This means that dogs should be walked several times per day and for a shorter period to begin with. It is better to walk 6 times 5 to 10 minutes than to walk 1 time for an hour and have 2 or 3 minimal P-breaks after that. The exercise should also be the same for all days of the week. Not an excessive long walk during the weekend while minimal exercise is practiced during the week. Every day of the week the same schedule. It has been shown that dogs with significant OA can run up to 5 or more kilometers (or miles) per day with their jogging owner, as long as the distance has been increased gradually and is practiced daily. Because when this daily exercise is interrupted for whatever reason (such as the owner being sick or traveling), it might show that after a period of 1 or 2 weeks of inactivity the dogs are hardly able to move! Training has to start from zero.
Together with the veterinarian and the hospital staff, the professional physiotherapist plays an important role in the education of the owner and support of the owner during the training. The physiotherapist may also play an important role in the initial phase of the treatment. Getting the dogs to start moving again. In principle, movement is good for any joint, and immobility negatively impacts joint health. Movement is one of the important factors to supply nutrients via the process of diffusion from the synovia to the avascular joint cartilage. In-clinic hydrotherapy and gentle passive movement of the joints by trained staff can help to get the dogs started and bring them back to a more active lifestyle. This can be done in combination with the use of medication to overcome initial painful reactions and limit the amount of inflammatory mediators generated in the reactivated joints. Excess mobility (more than the usual duration and intensity) increases the risk of increased release of inflammatory mediators with increased pain and clinical signs of lameness as a result. Movement is good, but overflexion and -extension and peak loading should be avoided in joints affected by OA.
The medical component of the OA treatment plan should be aimed at temporary intervention with the objective to give support in the initial phase to get the dogs moving again preferably for no longer than 2 weeks or maximum 1 month supporting the exercise and nutritional components of the treatment. The classical medical support for the treatment of OA included the nonsteroidal antiinflammatory drugs (NSAIDs). The treatment with nonsteroidal antiinflammatory drugs (NSAIDs) is designed to reduce pain and inflammation, both hallmarks of the disease. The NSAID effects include antipyretic, antiinflammatory and analgesic effects. Dosage should be kept at a minimum and the response might differ significantly between patients. The long-term use of NSAIDs, notably with complications of inappropriate use has been associated with adverse effects including gastrointestinal ulceration, hepatic toxicity, renal failure and, in some cases, negative effects on chondrocytes and cartilage. Older OA patients may suffer hepatic and renal compromise and are at higher risk for the NSAID side effects.
The NSAIDs can be classified as COX-1 and/or COX-2 inhibitors. COX-1 is mainly physiologic (gastric protection, renal blood flow, clotting activity). Some inflammatory activity has also been described in certain situations. COX-2 is mainly inflammatory. Some physiologic activity has been described (renal fluid balance, uterine implantation, wound healing including gastric ulcer healing). The older-generation NSAIDs are characteristically less COX-2-selective (potent) and at a higher risk for gastrointestinal complications, due to less COX-1-sparing effects. These include acetyl salicylic acid (aspirin), phenylbutazone, acetaminophen/paracetamol [acetaminophen is not a true NSAID, as it has analgesic features but is not antiinflammatory], diclofenac as well as flunixin and naproxen. Contemporary NSAIDs are more COX-2-selective or specific and are inferred to be safer due to their COX-1-sparing feature. These include agents such as carprofen (Rimadyl) [carprofen is more COX-2-selective but is not COX-1-sparing. The same is true for ketoprofen, etodolac, mefenamic acid, tolfenamic acid (Tolfedine) and tepoxalin (Zubrin). Higher specificity for COX-2 (more COX-1 sparing) is obtained using Veda Profen, firocoxib, mavacoxib, meloxicam, deracoxib and robenacoxib. Tramadol is primarily a tricyclic (TCA) rather than opioid and is used in combination with NSAIDs. An estimated 60% of its activity is TCA, while 40% is opioid at the mu receptor. Lab animal studies suggest concurrent use with an NSAID can increase the risk of GI adverse events. The concurrent use of tramadol with NSAIDs is only advocated when 'justified' but not as 'routine' practice in a cavalier manner (Dr. Steven Fox 2014, personal communication).
Intra-articular administration of chondroprotectant agents that 'protect' the cartilage against destruction can include polysulfated glycosaminoglycan (PSGAG) (Adequan Canine®), as well as a pentosan polysulfate (PPS) (Cartrophen V®) and a hyaluronic acid product (LegendTM). Studies showed comfortable angle of extension and lameness scores were both improved following PSGAG (Adequan®) administration at both 4 and 8 weeks following anterior cruciate ligament transection, while the concentration of neutral metalloproteinase was reduced relative to controls. The licensed PSGAG (Adequan®) is most appropriately administered in the early stages of OA, since once hyaline cartilage is lost, it is lost forever! The strategy in administering this chondroprotective is to delay the time during progression of osteoarthritis at which medically aggressive treatment is required (Dr. Steven Fox 2012). The administration of corticosteroids, both systemic and intra-articular, has to be used very conservatively because of the well-known side effects.
The discussion of cytotoxic immune-mediating agents for the treatment of arthritis (such as azathioprine, cyclophosphamide, mercaptopurine, gold salts, auranofin, sodium aurothiomalate and ciclosporin) is outside the scope of this abstract. More recent developments for OA treatment include the use of mesenchymal stem cells (MSC). These may offer interesting opportunities for the future but today are outside the therapeutic portfolio for the practicing veterinarian. Some owners and veterinarians report excellent results for OA treatment using acupuncture or homeopathy. The majority of these reports have to be classified as case reports or personal communications which do not qualify for a high ranking in terms of quality of evidence by the standards for evidence-based medicine. The golden standard to measure effects of an OA treatment protocol is a force plate gait analysis with a double-blind study design under controlled conditions. However, in the real world most owners have one dog with OA, and they see and interpret the results of veterinary intervention through their own eyes, turning their perception into reality.