Osteoarthritis
Commentary: Is It Useful to Subset “Primary” Osteoarthritis? A Critique Based on Evidence Regarding the Etiopathogenesis of Osteoarthritis

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OA is Not a Discrete “Disease”

People present with health problems (illnesses), not with what we call “diseases.” Doctors try to categorize patient presentations to give order to what they do, which would otherwise be chaotic. They have used many different approaches to classifying what they see. Historically, disorders were first categorized on the basis of the symptom complex alone (a “syndrome”)—gouty podagra, for example, was a well-recognized “disease” in the time of Hippocrates (7). With better understanding of

Evidence Supporting the Belief That OA Is Mechanically Induced

Almost 200 years ago, Brodie made the observation that cartilage destruction in OA is not primarily inflammatory (42). Laennec is credited with invoking the French term “usure” (which is equivalent to the English, “wear and tear”) to describe the changes (43). The differentiation of OA from rheumatoid arthritis may be attributed to Adams in 1857 (44). As noted, it has since been shown that the synovitis in OA is secondary to damage to the articular cartilage and subchondral bone (45, 46, 47, 48

Importance of the Viscoelasticity of the Cartilage and Bone

In the unloaded state, the opposing surfaces of a normal joint are incongruent. With loading, the cartilage and bone on both sides of the joint space deform, maximizing the contact area and thereby minimizing the stress within the cartilage (66). Because the cartilage is viscoelastic (a fluid/matrix composite that permits the movement of water through its matrix), when it is loaded, interstitial fluid flows away from the load and leaks (weeps) from the surface at the periphery of the loaded

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    Some of the thoughts expressed in this article are included in the chapter, “Neuromuscular Aspects of Osteoarthritis,” by KDB that is to be published in 2009 by Wiley-Blackwell in the book, Osteoarthritis Pain, edited by DT Felson and H-G Schaible, and the chapter, “Etiopathogenesis of Osteoarthritis,” by KDB, PD, and ELR that was published recently in Rheumatic Disease Clinics of North America (2008;34:531-59).

    Sources of support: None.

    The authors have no conflicts of interest to disclose.

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