The tensile strength of the dermis is primarily conferred by an extracellular matrix that is rich in collagen, which is a family of connective tissue proteins with a rigid and durable structure. In response to wounding, fibroblasts migrate into the wound bed and deposit new collagen, which aids in normal scar formation and strengthens the healed wound. Once sufficient collagen has been produced, the expression of this critical matrix protein is shut off. Thus, in the wound-healing response, collagen production is under precise spatial and temporal regulation. Using an in vitro cell culture model, we have begun to characterize the processes which control collagen synthesis by fibroblasts, and our results indicate that mechanical forces mediated by cell contact with collagen itself can signal dermal fibroblasts to cease their deposition of new matrix. These findings suggest that normal healing is controlled, in part, by forces generated during wound contraction and by feedback mechanisms within the pericellular environment, and implies that aberrant regulation by these processes may be involved in poor healing associated with ulcers or hypertrophic scars.