The effects of chitin [(1-->4)-2-acetamido-2-deoxy-beta-D-glucan] and its partially deacetylated derivatives, chitosans, on the human dermal fibroblast-mediated contraction of collagen lattices were examined in vitro as a model for the contraction of cutaneous wounds in vivo. Chitosan CL313A, a short-chain-length 89% deacetylated chitosan chloride, inhibited fibroblast-populated collagen lattice (FPCL) contraction at higher initial concentrations (500 and 1,000 microg/ml) in FPCLs fabricated with responsive dermal fibroblasts, while in FPCLs containing non-responsive fibroblasts inhibition of contraction was reduced. The responsive and non-responsive phenotype of human dermal fibroblasts to treatment with chitosan CL313A has been reported previously by us. The inhibition of fibroblast-mediated collagen lattice contraction by chitosan appeared to be strongly correlated with whether the cells were responsive or non-responsive. The effect of chitin-50A on fibroblast-mediated collagen lattice contraction was also examined to investigate whether the level of deacetylation was important for its inhibitory effect on contraction. However, this had no effect on contraction at the concentrations tested, supporting previous work that only chitosan samples with higher levels of deacetylation showed any biological activity. This work indicates that highly deacetylated chitosan inhibits fibroblast-mediated contraction of collagen lattices and may therefore be useful as a therapeutic agent to reduce contraction and therefore scarring in wound healing in vivo.