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Hypothesis-generating for viral triggers in rheumatoid arthritis; prospective studies required before any clinical implications.
We now understand many of the immunopatho- logical processes that damage joints and other structures in rheumatoid arthritis and diffuse connective tissue diseases. Unfortunately, our progress in this direction is matched by an equal failure to identify the causes of all but a few of these disorders. Nevertheless, the stimuli which initiate these diseases are probably commonly encountered and tissue damage results when these immunopathological processes are abnormal in intensity and duration- in other words, disease follows an unusual host reaction to a variety of environmental factors. This principle is well illustrated by the degenerative disease of the central nervous system, subacute sclerosing panencephalitis, which ensues in in- dividuals who are unable to control the growth and dissemination of measles virus. An equivalent example in rheumatology is the onset of rheumatic fever and rheumatic carditis in susceptible individuals exposed to /3-haemolytic streptococci. The central theme in the connective tissue diseases is the failure of patients with these disorders to limit the extent of their response to external insults. In non- copyright.
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A. M. Denman (1978) studied this question.
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