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March 26, 1932


JAMA. 1932;98(13):1090. doi:10.1001/jama.1932.02730390044015

Arthritis as a disease of uncertain etiology is obeying the law that history repeats itself. As in the case of most other diseases, arthritis has gone through a long period of clinical observation and therapeutic trial and error. Numerous theories have been advanced concerning the etiology, some of them apparently inadequately controlled. Following Nichols and Richardson's anatomicopathologic studies1 there has been a general lapse in consideration of the fundamental pathogenesis, punctuated at intervals by a recrudescence of interest.

Because of the marked difference in anatomic endchanges between a degenerative (hypertrophic) arthritis and proliferative (chronic infectious) arthritis, many students are inclined to assign an entirely different set of etiologic factors to the two types of joint disease. Others have questioned the soundness of this view. The recent work of Klinge,2 therefore, is of considerable possible significance in determining this question. The first step in Klinge's experiments was to sensitize

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