Wound healing and closure are terms that are universal in the clinical wound care space. However, there are few discussions about what constitutes healing sufficient to have useful anatomical and biomechanical function of the cicatrix, or scar. The International Classification of Diseases, Tenth Revision, Clinical Modification taxonomy lists cicatrix (adherent) (contracted) (painful) (vicious-aggressive) L90.5. Wound healing is characterized as the proliferation of new epithelium covering the wound. In reality, it is the restoration of the tissues, including the formation of a cicatrix that is ready for function and weight bearing.1
It is critical to contextualize wound and scar maturation and its relationship to anatomical function in terms of the cicatrix. Take, for example, the joints and areas of the body that provide flexibility. After injury, the extracellular matrix (ECM) achieves re-epithelialization through synthesis of immature type III collagen.2 This is different from the ECM of the unwounded skin, which is produced by type I collagen.3 Remodeling occurs when type III collagen transitions back to type I collagen: Its cross-linking forms the last stage of wound healing, resulting in a pliable, functional, and mature scar. The goal in wound healing, especially around a joint, is to gain and maintain this flexibility allowed by type I collagen.3,4
In the natural course of wound healing, we know that the tensile strength of healing tissue is precarious during epithelial resurfacing. Wound healing is based on a cascade of complex events, all of which should culminate in the resurfacing, reconstitution, and proportionate restoration of the tensile strength3 of the functional barrier of the skin, which transitionally remains a cicatrix for some time after the wound is “functionally closed.” Moreover, collagen remodeling and other events that lead to maturation of the scar tissue occur for months or years after epithelialization is complete, with the ultimate goal of decreasing the bulk of the scar and enhancing its tensile strength through realignment of the collagen fibers.3
The initial stages of collagen formation in wound repair produce a fragile layer of almost translucent collagen. As healing progresses, more collagen is produced, and more cross-links are established. Concomitantly, the blood vessels and ECM recede and are replaced by increased levels of type I collagen. In time, the damaged area becomes stronger than the original tissue. If the damage is significant enough, the replacement collagen will contract, making the damaged area smaller. However, any tension or undue strain can damage or dehisce the scar. The wound’s long axis is thought to correspond to the highest static tension of the skin.5 Therefore, the pull is primarily determined by the protrusion of the underlying bone, cartilage, and tissue bulk that the skin covers.
So, if we conceptualize the end stages of wound closure as a friable, functional cicatrix, how do we protect and enhance the functional barrier of the skin from aberrant scarring that can deter function? Aberrant scarring is explained in this month’s CME, “Insights into the Pathophysiology of Hypertrophic Scars and Keloids: How Do They Differ?” Aberrant cicatrices can occur in the form of keloids, which are massive, bulging, tumorous scars caused by abnormal ratios of collagen in connective tissues.2,6 Hypertrophic scar tissue can also manifest during the remodeling phase of wound healing.1,2,6
Rehabilitation of the cicatrix is essential for full weight bearing. Immobilization of the wound is desirable while at the same time moving the patient thorough progressive mobility. Because the cicatrix is trying to increase the tensile functionality of the wound, the use of reinforcement dressings, pressure relief, and repetitive cyclic loading versus impact loading methods are useful, especially in areas subject to the highest tensile strain. These methods may be particularly useful in patients who are wheelchair dependent or ambulating on a recently closed diabetic ulcer.
There remains a paucity of literature regarding the remodeling phase of wound care, especially functional outcome measures, including long-term follow-up on the recidivism rates for wounds in clinical trials. We need more studies that measure success using the terminal end of the remodeling phase as the final end point of wound closure.5
1. Mahdavian Delavary B, van der Veer WM, Ferreira JA, Niessen FB. Formation of hypertrophic scars: evolution and susceptibility. J Plast Surg Hand Surg 2012;46(2):95–101.
2. Gabbiani G. The myofibroblast in wound healing and fibrocontractive diseases. J Pathol 2003;200(4):500–3.
3. Kelangi SS, Bei M. Developmental biology of skin wound healing: on pathways and genes controlling regeneration versus scarring. In: Yarmush ML, Golberg A, eds. Bioengineering in Wound Healing: A Systems Approach. Toh Tuck Link, Singapore: World Scientific; 2017.
4. Sharma A, Zakka LR, Mihm MC Jr. Anatomy of the human skin and wound healing. In: Yarmush ML, Golberg A, eds. Bioengineering in Wound Healing: A Systems Approach. Toh Tuck Link, Singapore: World Scientific; 2017.
5. Salcido RS. The cicatrix: the critical functional stage of wound healing. Adv Skin Wound Care 2008;21(9):402, 404.
6. Gauglitz GG, Korting HC, Pavicic T, Ruzicka T, Jeschke MG. Hypertrophic scarring and keloids: pathomechanisms and current and emerging treatment strategies. Mol Med 2011;17(1-2):113–25.