Contributors: Matthew Pead

 Species: Canine   |   Classification: Miscellaneous


  • Osteoarthritis (OA Arthritis: osteoarthritis ) is a familiar problem for veterinary practitioners. Numerous dogs, and an increasing number of cats, suffer from secondary osteoarthritis.
  • Many patients display signs from an early age, as their OA is secondary to a developmental joint problem.
  • The dictionary definition of arthritis is Inflammation of a joint or joints characterized by pain and stiffness of the affected parts, but it has become a word used by the healthcare professional and the public alike to encompass almost any condition involving a joint.

    Sub-dividing the disease into types of similar clinical presentation and pathophysiology provides a practical approach to dealing with arthritis Arthritis: pathophysiological classification.Print off the owner factsheet Arthritis Arthritis to give to your client.


  • OA is characterized by the degeneration of articular cartilage resulting in fibrillation, fissures, gross ulceration and finally the destruction and loss of the tissue (Martel-Pelletier, 1998). In the medium and long-term, thickening of the joint capsule and production of peri-articular osteophytes are frequently observed by the clinician.
  • The ability of cartilage to resist compression is dependent on proteoglycan molecules held within the collagen framework of the matrix. Proteoglycan molecules have a high affinity for water, and it is this retention of water within the cartilage matrix that gives the tissue its resilience to compression. Loss of the proteoglycan molecules, and the subsequent break down of the mechanical capacity of the cartilage, is common in OA.
  • Joint pain in OA is a complicated issue as it may arise from the synovitis, stretching of the joint capsule ligaments, muscle spasm, bursitis, tendonitis, interosseous hypertension, subchondral trabecular microfracture and the stretching of periosteum in the stimulation of nerve ends over periosteal osteophytes.
  • It is common to think of OA as a degenerative disease, and while the major changes are clearly degenerative, they are linked to chronic inflammatory changes within the joint. The loss of the proteoglycans is mediated by enzymes which are released from the chondrocytes, and the release of these enzymes in abnormally high quantities is related to the presence of inflammatory mediators such as; cytokines like Interleukin 1 (IL1), prostaglandins, and nitric oxide (NO) Arthritis: pathway by which chronic changes develop in OA.
  • There is also a low-grade inflammatory synovitis in OA. The synovial cells are involved with a group of inflammatory mediator substances similar to those of the chondrocytes, and are probably responsible for perpetuating the cycle of chronic inflammation and causing a component of the pain related to OA.
  • Understanding that the degeneration is unlikely to reverse, but that the processes are limited to the joint, concentrates the clinical treatment effort in preserving joint function.

    In reality this translates into the concept of promoting appropriate exercise to maintain a reasonable lifestyle without further endangering the joint.

Clinical picture

  • The clinical picture of arthritis may include sustained periods of clinical signs, occasional flare ups, and the predisposition to the early onset of joint problems in old age.
  • The secondary nature of the disease often explains the presentation; a single joint in a previously traumatized animal, bilaterally symmetrical where it arises from a developmental disease.


  • As this is a complex disease it is inevitable that effective treatment involves the co-ordination of a number of elements, and adjusting them as the disease changes over the life-time of the patient.
  • Treatment of OA must be aimed at keeping the joint in use, minimizing discomfort, and preserving the structures of the joint for as long as possible.
  • Without a doubt the most important therapy for such patients is the combination of weight control and exercise management, minimizing the load on the joint, and maximizing the range of movement and the fitness of the muscles around it:
    • Weight control is critical to minimize attrition of the joints during locomotion.
    • Controlled exercise is required both to promote joint function and the continued function of the other structures in the limb.
  • There are numerous targets for drug therapy in OA including analgesia, slowing cartilage destruction, boosting cartilage formation, and blocking any one of the numerous chronic inflammatory pathways. The treatment used will vary both from one patient to the next, and for an individual patient over time.
  • OA is truly a disease in which the clinician needs to weigh the clinical signs and diagnostic findings, understand the underlying processes and then gauge which therapy or combination of therapies may be required for the individual patient.


  • In most acute presentations of arthritis the initial focus of management is analgesia Analgesia: overview. Appropriate analgesia promotes use of the joint, and controlled use promotes many beneficial processes within the joint.
  • Analgesia alone has been shown to be beneficial in OA, with successful trials of drugs that only have an analgesic effect. The most common veterinary analgesics used in OA are the non-steroidal anti-inflammatory drugs (NSAIDs).


  • As the damage to cartilage structure is such a characteristic component of OA, antagonizing degeneration in the medium to long-term, is clearly a worthwhile goal.
  • Disease modifying agents such as hyaluronic acid, polysulfated glycosaminoglycans and pentosan polysulfate Pentosan polysulfate may reduce cartilage degeneration, promote the repair of joint structures, and have an anti-inflammatory component. Unfortunately not all of these are licensed for all species and some require intra-articular injection, but there is some solid evidence for their efficacy.
  • There has been a recent rise in the use of the so-called nutraceuticals Therapeutics: oral chondroprotectants. These substances, primarily glucosamine and chondroitin sulfate Chondroitin sulfate , are building blocks of the glycosaminoglycan chains which go together to make up the large proteoglycan molecules.
  • The theory is that providing these nutraceuticals in the diet provides a ready substrate for the repair of cartilage within the joint and that this promotes relief from the signs of OA. The evidence for the efficacy of these substances is limited but there does appear to be some case for their use in the management of long-term OA in people.
  • Tetracycline Tetracycline antibiotics appear to reduce the activity of catabolic enzymes in the joint, while some NSAIDs may have a chondroprotective effect in some patients.
  • Green lipped mussel extract with its variety of glycosaminoglycans, vitamins and omega-3 fatty acids, may have a variety of beneficial effects, including chondroprotection.

Anti-inflammatory agents

  • Medium to long-term blocking of the pathway of chronic inflammation is another avenue for treatment of OA.
  • Corticosteroids Therapeutics: glucocorticoids will block inflammation, but the widespread systemic effects of even medium-term steroid administration combined with their negative effects on repair processes, make them largely unsuitable in OA.
  • The NSAIDs Analgesia: NSAID seem ideal for OA as they have a dual action against inflammation and pain. The potential problem with these drugs is that they inhibit the enzymes that make a variety of normal and inflammatory mediator substances, and therefore have side-effects relating to the blocking of some normal cellular processes.
    These side-effects mean that there are some warnings against their long-term use in dogs, and that their use is quite restricted in cats.
  • The discovery that NSAIDs could affect different components of the cyclo-oxygenase (COX) pathway that produces prostaglandins (PGs) was thought to be a breakthrough in OA therapy. It was thought that selective COX-2 inhibitors would control the signs of OA without renal and gastrointestinal side-effects.
    It now seems unlikely that even selective COX-2 inhibitors will be free of side-effects or suitable for all manifestations of OA judging from recent experience in the human field.
  • An alternative approach is to inhibit the inflammatory pathway upstream of COX, stopping the production of inflammatory mediators, but leaving COX and other enzymes unhindered in their role in normal physiology.
  • Curcumin and the essential oils of turmeric (Asian spice) have anti-inflammatory and anti-oxidant properties. Curcumin inhibits inhibitor of kappa B kinase (ikKB), blocking the downstream inflammatory pathways such as the induction of COX-2, inducible nitric oxide synthase (iNOS) and 5 lipo-oxygenase (5LO) pathways.
  • In addition, the essential oils inhibit the production of free radicals and prostaglandins reducing inflammation of the joint. A plant based product that combines the beneficial effects of curcumin and turmeric essential oils is now available and offers an alternative approach for the management of joint disorders.

Classification of arthritis

Secondary arthritis

Immune mediated arthritis

  • Immune-mediated arthritis Arthritis: immune-mediated is not common in dogs.
  • Immune mediated arthritides are associated with body wide diseases based on an inflammatory pathology. They are often associated with a polyarthritic patient that is systemically unwell with a range of non-specific medical signs like dullness and inappetence, in addition to the locomotor effects of their abnormal joints.
  • Fortunately such patients tend to stand out from the more common osteoarthritics in terms of their presentation and history, and once recognized, a generic mechanism for diagnosis can be employed with the emphasis on routine hematology and biochemistry, accurate radiography and synovial fluid analysis Synovial fluid: culture and sensitivity in preference to a reliance on specific tests such as rheumatoid factor Rheumatoid factor which are often misleading.
  • Just as the osteoarthritics these animals require a package of care, focused around controlling their disease with steroids or cytotoxic drugs, but also employing elements of analgesia and physical therapy to minimize the effects of the disease where possible.