The closure of severe wounds where viable tissue has been destroyed by trauma involves the depositing of a new connective tissue matrix, the amount of which is dictated by the severity of trauma. That new connective tissue matrix is immature, and in some cases, can reduce itself. When this occurs in a healing wound it is called wound contraction. When it occurs in the scar of a healed wound, it is called scar contracture. Forces generated in fibroblasts organise the surrounding connective tissue matrix, and this is responsible for the contraction of wounds and the contracture of scars. The experimental work presented here supports the idea that these contractile forces residing in the fibroblast work as individual units to contract the wound. There is no evidence to support the idea of the myofibroblast, a specialised cell, being responsible for contractile forces, as reported. The morphological appearance of stress fibres, which denote the presence of myofibroblasts, may, in fact, signify the termination of the generation of contractile forces. Control of cellular contractile forces appears to be linked to the composition of the connective tissue matrix. A matrix rich in type III collagen contracts faster and to a greater degree than one made from type I collagen. It is suggested that granulation tissue and immature scar with a matrix rich in type III collagen will contract more readily than a more mature scar with less type III collagen. Evidence presented from in vitro models suggests that fibroblasts generate the forces of contraction, and collagen controls those forces in wound closure and scar contracture.