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Canine arthritis (degenerative joint disease)

Osteoarthritis (OA) is a slow progressive disorder of synovial joints (Hegemann et al., 2002). OA specifically involves the imbalance between catabolic and anabolic processes (metabolism) resulting in erosion of joint cartilage, remodelling of subchondral bone, osteophyte formation and variable degrees of synovial membrane inflammation (synovitis).

OA is the most common form of arthritis and is present in 20% of dogs over one year of age (Hegemann et al., 2002). OA is also referred to as degenerative joint disease (DJD).

These changes in the metabolic balance in the joint lead to the following changes in the pathology of the arthritic joint.

  • Decreased synovial fluid quality (viscosity) – Due to defective synoviocyte metabolism the major component of synovial fluid, hyaluronan, has reduced molecular weight reducing its lubrication qualities (Francis et al., 1993). Additionally there is hypoxia, decreased pH and lactate accumulation in the synovial fluid.
  • Cartilage failure – Cartilage failure is both a primary cause of OA and a secondary outcome of the arthritic process, discussed further in 'What is the arthritis cycle?'. Cartilage failure is characterised by softening, fibrillation, fragmentation and degradation of the cartilage matrix reducing its functional capacity (Gardner, 1983).
  • Heightened inflammation (synovitis) / Immune response – Cartilage degradation products elicit t an immune response that provokes subsequent inflammation in the synovium, synovitis (Hamerman, 1993). The inflammatory response causes a release of noxious substances which subsequently affect cartilage, bone and synovial fluid.
  • Vascular engorgement - The immune response can lead to lipid deposition and fibrin clots in synovial tissues and subchondral blood vessels (Arnoldi, 1996). Subsequently, OA affected patients have hyperlipidemia, hypercoagulability and hypofibrinolysis (Cheras et al., 1997). It has been shown that 60-70% of OA patients have hypercoagulability and hypofibrinolysis (Ghosh and Ceras, 2001).
  • Cell necrosis, bone remodelling, bone necrosis. – Blood flow and nutrition to bone and synovial cells is compromised by lipid and fibrin occlusions resulting in ischaemia, cell necrosis, bone necrosis and joint pain (Ghosh and Cheras, 2001).

Below is a comparison of the changes in an osteoarthritic joint next to a normal joint.

Coagulation, immune system and bone, the forgotten elements of OA

OA is widely associated with irregularities in cartilage, synovial fluid, synovial tissue and related inflammation. As outlined in the pathology description above, OA has other key elements involved in the OA process such as the elements of the coagulation system, bone failure and the immune response. These are elements that are often not considered in the treatment of OA. In order to undertake a proper OA treatment a holistic view of all underlying elements is required.

Normalisation and balance in a range of metabolic activity is required and is vital to successful treatment of OA.

To develop drugs specifically for osteoarthritis...... the thinking that has gone into the antirheumatic drugs should be discarded; the evidence suggests that the early changes in the cartilage matrix are not inflammatory. But pain and secondary inflammation are common late results of the early changes in the cartilage (Gardner, 1983).

Contributing factors to OA?

Key contributing factors to OA include

  • Breed Size - Large or giant breeds have a higher incidence of OA
  • Age - OA is more common with older dogs
  • Weight – Overweight dogs are more prone to OA
  • Breed inherited traits – Which cause or encourage OA such as hip dysplasia or elbow dysplasia
  • Stress Activity - Levels of high stress or abnormal activity for long periods of time, such as excess athletic activities can initiate the OA process
  • Joint injuries and trauma – injuries to the joint incite the OA process and encourage the 'arthritis cycle', discussed further in What is the 'arthritis cycle'?

 

REFERENCES

Arnoldi CC (1996) Development from osteoarthritis and nontraumatic osteonecrosis to osteoarthrosis. ARCO Newsletter 8(1):4-27

Francis DJ, Hutadilok N, Kongtawelert P, Ghosh P (1993) Pentosan polysulphate and glycosaminoglycan polysulphate stimulate the synthesis of hyaluronan in vivo. Rheumatol Int 13:61-64

Gardner DL (1983) The nature and causes of osteoarthrosis. Br Med J 286:418-424

Hamerman D (1993) Aging and osteoarthritis: Basic mechanisms. J Am Geriatr Soc 41(7):760-770

Hegemann N, Kohn B, Brunnberg L, Schmidt MF (2002) Biomarkers of joint tissue metabolism in canine osteoarthritic and arthritic joint disorders. Osteoarthritis Cart. 10, 714-721

McLaughlin R (2000) Management of chronic osteoarthritic pain. Veterinary Clinics of North America: Small Animal Practice 30, 933-949