The Rheumatoid nodule: peripheral or central to rheumatoid arthritis?

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Abstract
When asked as a medical student how to treat a patient with rheumatoid arthritis (RA) who was not doing well the immediate answer was gold. The question was not hard since a flick through a short textbook prior to the clinic had not indicated many alternatives. How should the modern medical student answer this question? What might be the best of many treatment options for an individual patient? At least in the case of the newer biological agents their use is based on some understanding of the basic processes involved in the pathogenesis of RA. Can we therefore apply this understanding in making a choice of treatment? Unfortunately any current review of the pathogenesis of RA reveals a situation at least as complex as the therapeutic choices. This has lead Cornelia Weyand [1] to suggest that one way forward would be to develop a string theory of autoimmunity. A corollary might be that there is a minimum requirement of a rheumatoid lesion to cause tissue destruction. Identifying this requisite might get us to the core mechanism of rheumatoid pathogenesis with other mechanisms serving as disease modifiers and amplifiers, thereby explaining the heterogeneity of the disease. One rheumatoid lesion that deserves attention for this reason is the nodule as it seems to be ‘more simple’ than the synovial lesion.

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