Abstract
Abstract
This study showed that the initiation of granuloma formation in alcoholic mice was retarded but eventually reached normal levels. The delay appears to be related to a failure of cells to migrate into the sponge as rapidly as they did in control animals. Thus, there is clear evidence to support the clinical impression of poor wound healing in alcoholics. Although repair is eventually accomplished, the initial decrease in the rate of this process may be significant enough to put the alcoholic patient at risk.
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