The expression of type I, III and VI collagens was studied in nine normal and two hypertrophic scars using slot-blot and in situ hybridization techniques. Slot-blot hybridization indicated that the steady-state levels of pro alpha 1(I) and pro alpha 1(III) collagen chain mRNAs were moderately elevated in two of the nine normal scars, whereas the two hypertrophic scars analysed displayed markedly elevated mRNA levels when compared with normal skin. The mRNA levels of alpha 2(VI) collagen chain were only slightly elevated in both types of scars studied. In situ hybridization was most informative when applied to hypertrophic scars. These lesions were characterized by the presence of intense hybridization signals for type I and III collagen mRNAs, and a moderate signal for type VI collagen mRNA, in nodules which were located in the upper dermis on each side of the original wound. This may explain, in part, why hypertrophic scars rise above the level of the surrounding skin. The results of the present study are in marked contrast to our previous findings on collagen gene expression in keloids and neurofibromas, in which the steady-state levels of type VI and I collagen mRNAs in particular were shown to be elevated. Thus, our results emphasize that distinct molecular mechanisms are operative in the development of clinically different dermal fibrotic conditions, such as normal and hypertrophic scars, keloids and neurofibromas.