Arthritis is an umbrella term for more than 100 rheumatic diseases affecting joints and connective tissue. The two most common forms are osteoarthritis (OA) and rheumatoid arthritis (RA). Osteoarthritis— also referred to as osteoarthrosis or degenerative joint disease—is the most common form of arthritis. It is sometimes simplistically described as the "wear and tear" form of arthritis. The causes and progression of degenerative joint disease are still not understood. Rheumatoid arthritis is a chronic and often progressive disease of the synovial membrane leading to release of enzymes which attack, erode, and destroy articular cartilage. It is an inflammatory response involving the immune system and is more prevalent in females. Rheumatoid arthritis is extremely complex. Its causes are still unknown.
Sokoloff defines degenerative joint disease as "an extremely common, noninflammatory, progressive disorder of movable joints, particularly weight-bearing joints, characterized pathologically by deterioration of articular cartilage and by formation of new bone in the sub-chondral areas and at the margins of the joint" . As mentioned, osteoarthritis or osteoarthrosis is sometimes referred to as the "wear and tear" form of arthritis, but wear itself is rarely a simple process even in well-defined systems.
It has been noted by the author that tribological terms occasionally appear in hypotheses which describe the etiology of osteoarthritis (e.g., "reduced wear resistance of cartilage" or "poor lubricity of synovial fluid"). It has also been noted that there is a general absence of hypotheses connecting normal synovial joint lubrication (or lack thereof) and synovial joint degeneration. Perhaps it is natural (and unhelpful) for a tribologist to imagine such a connection and that, for example, cartilage wear under certain circumstances might be due to or influenced by a lack of proper "boundary lubrication" by the synovial fluid. In this regard, it may be of interest to quote Swanson  who said in 1979 that "there exists at present no experimental evidence which certainly shows that a failure of lubrication is or is not a causative factor in the first stages of cartilage degeneration." A statement made by Professor Glimcher  may also be appropriate here. Glimcher fully recognized the fundamental difference between friction and wear as well as the difference between joint lubrication (one area of study) and joint degeneration (another area of study). Glimcher said that wearing or abrading cartilage with a steel file is not osteoarthritis, and neither is digesting cartilage in a test tube with an enzyme. But both forms of cartilage deterioration can occur in a living joint and in a way which is still not understood. It is interesting that essentially none of the many synovial joint lubrication theories consider enzymatic degradation of cartilage as a factor whereas practically all the models of the etiology of degenerative joint disease include this as an important factor.
It was stated earlier that there are at least two main areas to consider, i.e., (1) mechanisms of synovial joint lubrication and (2) the etiology of synovial joint degeneration (e.g., as in osteoarthrosis). Both areas are extremely complex. And the key questions as to what actually happens in each have yet to be answered (and perhaps asked). It may therefore be presumptuous of the present author to suggest possible connections between two areas which in themselves are still not fully understood.
Tribological processes in a movable joint involve not only the contacting surfaces (articular cartilage), but the surrounding medium (synovial fluid) as well. Each of these depends on the synthesis and transport of necessary biochemical constituents to the contact region or interface. As a result of relative motion (sliding, rubbing, rolling, and impact) between the joint elements, friction and/or wear can occur.
It has already been shown and discussed—at least in in vitro tests with articular cartilage—that compounds which reduce friction do not necessarily reduce wear; the latter was suggested as being more important . It may be helpful first of all to emphasize once again that friction and wear are different phenomena. Furthermore, certain constituents of synovial fluid (e.g., Swann's lubricating glycoprotein) may act to reduce friction in synovial joints while other constituents (e.g., Swann's protein complex or hyaluronic acid) may act to reduce cartilage wear.
A significant increase in joint friction could lead to a slight increase in local temperatures or possibly to reduce mobility. But the effects of cartilage wear would be expected to be more serious. When cartilage wear occurs, a very special material is lost and the body is not capable of regenerating cartilage of the same quality nor at the desired rate. Thus, there are at least two major tribological dimensions involved—one concerning the nature of the synovial fluid and the other having to do with the properties of articular cartilage itself. Changes in either the synovial fluid or cartilage could conceivably lead to increased wear or damage (or friction) as shown in Fig. 4.9.
A simplified model or illustration of possible connections between osteoarthritis and tribology is offered in Fig. 4.10 taken from Furey . Its purpose is to stimulate discussion. There are other pathways to the disease, pathways which may include genetic factors.
In some cases, the body makes an unsuccessful attempt at repair, and bone growth may occur at the periphery of contact. As suggested by Fig. 4.10, this process and the generation of wear particles could lead to joint inflammation and the release of enzymes which further soften and degrade the articular cartilage. This softer, degraded cartilage does not possess the wear resistance of the original. It has been shown previously that treatment of cartilage with collagenase-3 increases wear significantly, thus supporting the idea of enzyme release as a factor in osteoarthritis. Thus, there exists a feedback process in which the occurrence of cartilage wear can lead to even more damage. Degradative enzymes can also be released by trauma, shock, or injury to the joint. Ultimately, as the cartilage is progressively thinned and bony growth occurs, a condition of osteoarthritis or degenerative joint disease may exist. There are other pathways to the disease, pathways which may include genetic factors. It is not argued that arthritis is a tribological problem. However, the inclusion of tribological processes in one set of pathways to osteo-arthrosis would not seem strange or unusual.
A specific example of a different tribological dimension to the problem of synovial joint lubrication (i.e., third-body abrasion), was shown by the work of Hayes et al. . In an excellent study of the effect of crystals on the wear of articular cartilage, they carried out in vitro tests using cylindrical cartilage sub-chondral bone plugs obtained from equine fetlock joints in sliding contact against a stainless steel plate. They examined the effects of three types of crystals (orthorhombic calcium pyrophosphate tetrahydrate, monoclinic calcium pyrophosphate dehydrate, and calcium hydroxyapatite) on wear using a Ringer's solution as the carrier fluid. Concentration of cartilage wear debris in the fluid was determined by analyzing for inorganic sulphate derived from the proteoglycans present. Several interesting findings were made, one of them being that the presence of the crystals roughly doubled cartilage wear. This is an important contribution which should be read by anyone seriously contemplating research on the tribol-ogy of articular cartilage. The careful attention to detail and potential problems, as well as the precise description of the biochemical procedures and diverse experimental techniques used, set a high standard.
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