What Is Scar Tissue
Scar tissue is made up of fibrous collagen, which is a tough protein that is predominately made up of the 3 amino acids; proline, glycine and hydroxyproline. Fibrous collagenous scar tissue forms when normal connective tissue is altered/damaged by disease, injury, or surgery.
Scar tissue behaves differently from normal connective tissue. Normal connective tissue is mature, stable and has a small degree of pliability. In comparison, scar tissue is much more disorganized, dynamic and pliable, making it more weak and less functional.
Scar tissue formation is dependent on the severity of the wound, genetics, how much blood access the structure had pre injury, as well as the activities performed during the healing process.
Pain can be associated with scar tissue as it contains more pain receptors than the original tissue.
The health professional looking after you will determine the appropriate amount of movement whilst respecting the healing process.
Types of scar tissue:
Hypertrophic scarring: characterised as being thick and raised scarring that stays within the borders of the original wound size. There is a 3x increase of collagen production in hypertrophic scars. They form a wavy and regular pattern of collagen that is parallel to the dermis. These scars may improve over time and respond to exercise/manual therapy treatment. In normal dermal skin tissue, there are two distinct layers: the papillary and reticular layers. In hypertrophic scars, there is papillary and reticular dermal scarring which means that movement can be impacted due to the adhering of these layers to each other.
Keloid scarring: characterised as being lumpy and rigid that extends beyond the borders of the original wound size and continues to grow after the healing process has finished. There is a 20x increase of collagen production in keloid scars. The excess collagen that is produced is unhelpful to the healing process and forms disorganised pattern. This means that the tissue is not as flexible or as functional as the tissue that it is replacing. It also has poor blood flow, which limits oxygen and nutrient delivery/removal. In keloid tissue, there is no distinction seen between the papillary and reticular dermal layers, meaning that the scarring can significantly impact movement as it adheres to the surrounding structures.
Depressed/atrophic scars: characterised as small skin indentations and can be caused by chickenpox or acne due to the skin not replacing the damaged tissue.
Contracture scar: characterised by skin tightening and movement restriction, which can be caused by burns when the skin and surrounding tissue pull together during the healing process. A contracture scar can affect skin, muscles, tendons and ligaments.
In normal wound healing, there are three major phases: the inflammatory phase, the proliferative phase, and a remodeling phase.
This inflammatory phase occurs immediately after trauma, and involves blood clotting and macrophages to clear the site of injury. Immediate swelling occurs, which is a process that encourages immobilisation, thereby limiting movement and reducing risk of further tissue damage. Inflammation regulation is controlled by proinflammatory cytokines (IL-6 and IL-8),and an anti-inflammatory cytokine (IL-10). A change in expression in these cytokines may lead to an increased development of collagen and thus hypertrophic scar or keloid formation.
During the proliferative phase of healing, collagen is created to provide a new framework for the tissue to build upon and regenerate. The process involves macrophages releasing growth factors, such as transforming growth factor-beta (TGF-beta), which activates fibroblasts (which creates collagen). Collagen to collagen bonds are weak, which allows for scar tissue reshaping to occur. In hypertrophic scars and keloids, it’s proposed that there is dysregulation of TGF-beta. TGF-beta 1 and 2 manage activation of fibroblasts, while TGF-beta 3 leads to decreased fibroblast activity. This stage lasts 3 to 8 weeks, depending on the damaged structure and relative blood access of the damaged tissue.
During the remodeling/maturation phase, collagen matures, solidifies, and shrinks. Maximal stress should be placed on the tissue during this phase as risk of tissue failure is low and collagen synthesis is still accelerated. This is the time to take the scar tissue from a disorganized and weak state, to having a structure that is appropriate for its function. This is achieved through performing exercises that force the structure to behave how we want it to - eg a balance exercise to force the scar tissue to behave as a lateral ankle ligament by decelerating a lateral ankle roll. However, if immobilisation is adopted during this phase, then the collagen fibers can criss cross and the tissue can shrink significantly, resulting in reduced ROM and function. Tissue remodeling becomes significantly more difficult as time increases because the tissue becomes less adaptable. Remodelling can occur over a >12 month period, and it is important that the joint is continually loaded during this time so that the scar tissue adopts the role that is required and doesn’t resort to its natural inclination to form disorganised collagenous arrays. If it does, than it will be weak and the risk of reinjury is significantly increased.