OA is a degenerative, progressive and irreversible disease process of synovial joints characterized by the progressive loss of articular cartilage, osteophyte formation and periarticular fibrosis, leading to development of pain, lameness and loss of articular movement.
OA is the most common articular condition in the dog. It is thought that between 8 to 20% of dogs suffer from OA, being more prevalent in the older dog. OA is the seventh most common cause of canine insurance claims in the UK. In the UK alone, it is thought to affect 1.4 million of dogs.
OA can be primary (no known cause) or secondary to a primary joint disease. Primary OA is very rare in the dog, where more often than not, the OA disease can be traced down to a primary problem (e.g., hip or elbow dysplasia, shoulder osteochondrosis).
OA is a continuous disease process although the clinical pattern is characterized by periods of apparently few clinical signs followed by intermittent acute episodes of pain and lameness that can often be related to an increase in exercise levels or a change in the dog's lifestyle. OA is often recognized as an intermittent disease, as owners and clinicians tend to recognize the acute episodes of worsening known as flare-ups.
Articular cartilage is a very complex structure, formed by an extracellular matrix and a relatively low number of chondrocytes. The extracellular matrix is a mixture of water (its main constituent) embedded in proteoglycans trapped in a collagen network. Cartilage metabolism is very complex, being governed by humoral factors. The chondrocytes are in charge of the synthesis and degradation of the cartilage matrix. Under physiological conditions, there is a balance between the synthesis and the degradation. In OA, there is a marked increase of cellular metabolism and matrix turnover, with a net loss of cartilage matrix. Interleukins and growth factors are closely associated in order to regulate and activate enzymes such as collagenases and aggrecanases. The loss of cartilage matrix is closely associated with the loss of the biomechanical properties of the articular cartilage which further accelerates the rate of cartilage loss and the liberation of inflammatory mediators. The degradation of cartilage matrix and the release of inflammatory mediators within the synovial fluid will lead to the development of synovitis which in turn will accelerate the degradation process. The inflammatory mediators will activate nociceptors locally and also will be involved centrally causing OA to be painful at local level and central (brain) level.
OA is a painful disease although the exact mechanism of pain is not well understood. It is thought that pain comes from stimulation of neuroreceptors located at the level of the synovial membrane, joint capsule, intra and periarticular ligaments and from subchondral bone. The neuroreceptors are activated because of the release of proinflammatory mediators such as prostaglandins, leukotrienes and others, as well as the mechanic effect of loading over damaged and altered articular and periarticular tissues. Lactic acid release is thought to occur at the level of the subchondral bone due to venous stasis and is believed to further contribute to pain. The release of inflammatory mediators is a continuous, chronic process in OA. Pain is often the limiting factor associated with joint disease.
Even though OA is considered to be a non-inflammatory disease, the mild degree of inflammation frequently associated with this condition can result in peripheral sensitization. This results in increased spontaneous activity and decreased activation threshold of nociceptive fibers. Activity of the primary joint afferents also leads to changes within the dorsal spinal horn, resulting in central sensitization and changes in the neural structures of the dorsal horn that facilitate and amplify the nociceptive response. Changes in the periarticular tissues correspond to the neurobiologic changes, resulting in increased stimulation of nociceptors caused by mechanical and chemical alterations resulting from tissue damage. The combination of these events results in the complex dynamic of joint pain.
Nociceptive (acute) pain plays a physiological role in order to prevent further tissue damage and in order to stimulate tissue repair. Chronic pain does not contribute to tissue repair and only leads to physical and emotional distress. The pattern of distribution of pain in OA in humans is both peripherally driven (60-80%) and centrally driven (20-40%).
The painful response to joint use and the subsequent loss of joint function will lead to disuse peripheral joint tissue atrophy and the loss of joint support. In turn, this will result in further loss of joint use and will accelerate the changes within the articular cartilage and periarticular structures. There is evidence that suggests that central sensitization can actually drive the progression of the disease in the joints and that downward modulation of central sensitization can result in decreased joint pathology.
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