Role of the free radical release process in the pathogenesis of morphea in contrast to systemic sclerosis

Abstract

The objective of this study was to assess the importance of the free radical release process in the pathogenesis of localized scleroderma and compare it with that in systemic sclerosis. The study was conducted on 20 randomly collected cases of morphea (4 single plaque, 7 linear, and 9 disseminated), 16 cases of systemic sclerosis, and 10 age- and sex-matched healthy volunteers. Blood samples and homogenized skin biopsies from lesional and nonlesional skin of patients and controls were examined for superoxide dismutase (SOD) activity using spectrophotometric assay, and for lipid peroxide level using the thiobarbituric acid assay. Morphea and systemic sclerosis cases showed significant elevation of blood, lesional, and nonlesional skin lipid peroxide levels and SOD activity compared with normal controls. When each of the subtypes of morphea were compared with the controls, a significant elevation of SOD was found in lesional skin in all groups, in plasma of linear and disseminated morphea, and in nonlesional skin of cases of disseminated morphea. A comparison of systemic sclerosis and morphea cases revealed no significant differences in blood or tissue SOD activity or lipid peroxide level. In both groups, the degree of skin induration could be correlated with changes in lesional SOD activity and lipid peroxide levels, respectively, but no correlation could be found between SOD or lipid peroxide and antinuclear antibody titer. The free radical release process is as important in the pathogenesis of morphea as it is in systemic sclerosis, where it appears to be involved in the development of skin induration.