In rats, the healing process of a full-thickness dermal freeze injury differs from that of a burn wound. Whereas burn wounds heal by wound contraction, the movement of surrounding normal skin over the defect, freeze wounds heal without wound contraction. That absence of contraction may be due to the freeze wound's lack of myofibroblasts, the cells reportedly associated with wound contraction. Myofibroblasts can be demonstrated histologically by staining the F-actin filaments of the stress fibers with NBD-phallacidin, a fluorescent reagent specific to F-actin filaments. Fibroblasts in normal dermis have no staining stress fibers. However, staining myofibroblasts are uniformly distributed in the granulation tissue of the healing burn and in the islands of granulation tissue between residual connective tissue fibers in the healing freeze wound. These residual dermal fibers were identified by their patterns of birefringence. Residual connective tissue matrix persists following cold trauma and acts like an internal splint. Burn trauma destroys cells and the connective tissue matrix, which is completely replaced with granulation tissue which undergoes wound contraction. Freeze trauma kills the cellular components of dermis, while some residual connective tissue fibers endure. This study shows that the connective tissue matrix can play an important role in the control of wound contraction.