An update on the pathophysiology of joint disease (Sponsored by Iams)

An update on the pathophysiology of joint disease (Sponsored by Iams)

Joints are highly specialized organs allowing repetitive pain-free and largely frictionless movements.1 A joint consists of bony epiphyses covered with cartilage and surrounded by a synovial membrane and the adjacent soft tissues. The surrounding ligaments, fibrous joint capsule, muscles, and tendons contribute to the integrity and movement of the joint. Muscle mass is also present to provide concussive cushioning and to limit joint movement so that it does not exceed safe anatomical boundaries. The ligaments, tendons, and muscles contain mechanoreceptors that provide proprioceptive input to allow fine motor control and prevent injury.2 Any disruption to the mechanoreceptor input, for example a deep bruise causing some bleeding into a neighboring muscle, will decrease fine motor control and predispose the joint to overload.3

Inside the joint itself, the synovium is a complex structure, with the inner lining of cells producing viscous joint fluid. Interspersed throughout the synovium are cells that have immune function, and so the synovium contributes to the inflammation that occurs in joint disease.4

Traumatic joint disease can occur following trauma from an abnormal load on a normal joint1 (a single event or repetitive microtrauma in an obese animal) or because a joint is abnormal and cannot withstand normal loads.1 An abnormal joint can arise from developmental factors (e.g. elbow incongruency), genetic factors (e.g. slope of the tibia and femur causing an upright knee prone to more concussive forces), infection (e.g. Lyme disease), immune-mediated arthropathies, and biomechanical factors such as poor muscle support.

Basic structure of articular cartilage

The architect of cartilage is the chondrocyte, which produces the extracellular matrix. The matrix is composed of glycosaminoglycans (hyaluronan and proteoglycan) and collagens (mainly type II). The collagen forms a dense network that retains the proteoglycan. The proteoglycan is highly charged and attracts water into the tissue. Thus cartilage is 75% water.

In normal cartilage, there is a very slow turnover of collagens but the proteoglycan is constantly being renewed. The proteoglycans are aggregated into large molecules ("aggrecan") with a protein core and many side chains of keratan sulfate and chondroitin sulfate. This core is in turn bound to hyaluronan chains, with each chain containing many proteoglycan molecules. Aggrecan and water provide the compressive stiffness to the tissue whereas collagen provides the tensile strength.

What is osteoarthritis?

Osteoarthritis (OA) is one of the most common diseases of dogs. Estimates suggest that 20% of the canine population is affected by OA,5 and therefore the disease's impact is very large. OA is a disease of the whole joint — the articular cartilage, bone, and synovium. The relationship between the pathology in each of these tissues is poorly understood. The articular cartilage has received most attention from researchers. Although joint biomechanics undoubtedly play an important role in disease initiation and progression, biochemical changes occur in all joint tissues and contribute to joint failure.

OA is a heterogeneous disease and assessment of the disorder is difficult. The poor correlation between radiographic and clinical data highlights this difficulty. In dogs, a typical example of this is the dysplastic hip with secondary OA — severe radiographic changes are present in a clinically silent joint. Expression of different facets of the disease seems to vary between individuals and even between different joints in the same individual. In small-animal medicine this is exemplified by differences in osteophyte expression, which clearly do not tally with the clinical picture. Most orthopedic experts agree with a model of OA that incorporates the heterogenic nature of OA and how various contributing factors interact in its development and progression. It is helpful to think of OA as a disease process rather than a disease entity.