By Dr David Platt BVSc., PhD., DEO., FRCVS

There have been many products marketed to the medical profession to treat degenerative

joint disease (arthritis) in patients. Arthritis is characterised by slowly progressive deterioration of the articular cartilage, capsular fibrosis reduced joint mobility and pain. It is particularly prevalent in middle aged and older patients and is considered to be one of the major causes of disability in the older patient.

It has been considered for many years that arthritis is an irreversible disorder. This is certainly the case when the condition is identified in the terminal stages of a major joint pathology. If a diagnosis can be made at an early stage of the development, before massive disruption to the articular cartilage surface has occurred, it may be possible to limit to the progress of the arthritic process. By arresting further degradation and stimulating a limited repair response by the articular chondrocytes a clinical improvement can often be achieved.

The aims of any treatment regime in patients suffering from DJD / arthritis are to relieve the symptoms of pain and discomfort, prevent further degradation and restore as much joint function as possible. Treatment options that have been postulated include both surgical and non-surgical medical management. Surgical options are not considered as a first line therapy unless a specific intra-articular fracture has been identified as the primary pathology. Non-surgical management includes rest, reduced joint mobility, controlled physiotherapy, and various medical therapies.

Current medical management of DJD is largely palliative aimed at suppressing pain and inflammation primarily through the use of analgesics and/or steroidal and NSAIDs drug therapy. Uncertainty has been raised about the effects of NSAIDs on the progress of DJD. Data suggests that suppression of prostaglandin’s may have deleterious effects on the progress of cartilaginous degradation seen in DJD. These new concerns regarding the use of NSAIDs in addition to their known pattern of systemic side-effects has prompted research for new agents that relieve pain and inflammation and limit or reverse cartilaginous degradation without side-effects.

The current focus of much medical interest are substances capable of slowing the process of cartilage degradation and promotion of cartilage matrix synthesis. These compounds have been termed "chondroprotective agents" and provides the following attributes:

• Stimulate chondrocyte synthesis of collagen and proteoglycans.

• Stimulate production of hyaluronic acid.

• Inhibit cartilage degradative enzymes.

Sulphated glycosaminoglycans (SGAG) such as chondroitin sulphate are found in the matrix of cartilage and have been shown to achieve some of the above objectives. No single macromolecule, however, appears capable of accomplishing all the stated objectives. A recent approach combining compounds with complimentary effect may provide a more effective therapy. Glucosamine/chondroitin sulphate/super oxide dismutase combination as an orally bioavaiable food supplement, is one such product that has become commercially available (Cortaflex). Glucosamine (GlAm) is an aminomonosaccharide nutrient with high absorption from the gut. GlAm is a precursor of hyaluronic acid found in synovial fluid and cartilage, tendons and ligaments. GlAm stimulates GAG and hyaluronic acid production and has been shown to improve the clinical signs of DJD/arthritis in human patients. Chondroitin sulphate (CS) is the predominant GAG found in articular cartilage. CS stimulates GAG synthesis whilst also being a competitive inhibitor of PG destructive enzymes. One of the most potent group of these agents are thought to be oxygen free radicals. Superoxide dismutase is a potent agent capable of neutralising these oxygen metabolites.

There is strong evidence that oral administration of chondro-protective agents containing CS/GlAm, such as Cortaflex, can be extremely beneficial in the medical management of cases of stiff joints and may also be of benefit during the repair phase of musculoskeletal soft tissue injuries such as tendon or ligament strains.

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