Wound healing is the body’s method for repairing damaged tissue, and a component of this is fibrosis, the process of forming the fibrous connective tissue that creates a scar. While fibrosis is a standard part of healing, its overproduction can lead to complications and pathological scarring. Understanding the difference between normal repair and excessive fibrosis is important for managing wound outcomes.
The Normal Wound Healing Process
The body’s response to injury unfolds in four overlapping phases, starting with hemostasis. This stage begins when tissue is damaged, as blood platelets rush to the site. Contact with exposed collagen prompts platelets to aggregate and form a fibrin clot that stops bleeding and provides a temporary matrix for healing.
Following hemostasis, the inflammatory phase starts. Neutrophils, a type of white blood cell, arrive to clear the area of bacteria and cellular debris. They are soon joined by macrophages, which continue this cleanup and release growth factors that signal the transition to the next phase. This inflammatory response is necessary to prevent infection.
The proliferative phase is characterized by rebuilding tissue. Fibroblasts migrate into the wound and deposit a new extracellular matrix, primarily composed of collagen. This forms granulation tissue, a fragile tissue that fills the wound space, complete with new blood vessels to supply oxygen and nutrients.
Finally, the remodeling phase begins, which can last for a year or longer. The initial, weaker collagen is gradually replaced by a stronger, more organized form. The new collagen matrix is cross-linked and realigned along lines of tension, increasing the tensile strength of the repaired tissue. This process results in a mature, less prominent scar.
The Development of Fibrosis in Healing
Fibrosis is the process responsible for creating the scar tissue that repairs a wound. It relies on fibroblasts, which migrate to the injury site during the proliferative phase. Once there, they produce components of the extracellular matrix, most notably collagen, which acts as a scaffold to fill the void left by the injury.
A primary event in fibrosis is the transformation of some fibroblasts into myofibroblasts. These specialized cells contain contractile fibers, similar to muscle cells, allowing them to grip the wound edges and pull them together. This action, known as wound contraction, reduces the size of the defect. Myofibroblasts are also particularly active in secreting collagen.
In a normal healing scenario, the fibrotic process is tightly regulated. Once the wound is closed and the matrix is established, myofibroblasts are programmed to undergo apoptosis, or controlled cell death. The remaining fibroblasts reduce collagen production, and the remodeling phase begins. This “off-switch” ensures only the necessary amount of fibrous tissue is created.
Pathological Fibrosis and Scarring
When the regulatory mechanisms controlling fibrosis fail, the healing process can become pathological. This occurs when the “off switch” for collagen production does not engage, causing fibroblasts and myofibroblasts to continue their activity after the wound has filled. The result is a disproportionate accumulation of extracellular matrix, leading to scars that can be painful, itchy, and functionally limiting.
One common form of pathological scarring is the hypertrophic scar. These scars are raised and often red but are confined to the boundaries of the original injury. They appear within weeks of the injury as a direct result of excess collagen deposition and do not invade the surrounding healthy tissue.
A more aggressive form of pathological fibrosis results in keloids. Unlike hypertrophic scars, keloids grow beyond the original wound margins, invading adjacent normal skin. They can appear months after the initial injury and may continue to expand. Keloids are formed from an overproduction of disorganized collagen, resulting in a dense, rubbery growth.
The distinction between these scar types lies in the behavior of the fibroblasts. In hypertrophic scarring, the fibrotic process is overactive but contained. In keloid formation, the process is both overactive and unregulated in its growth. Both conditions represent a failure to properly conclude the healing phases.
Factors Influencing Fibrotic Outcomes
Several factors can influence whether a wound heals with a normal scar or develops a pathological fibrotic state.
- Genetic predisposition is a significant factor. Individuals with a family history of keloids are at a much higher risk, and this is particularly prevalent in populations with darker skin tones.
- The location and mechanical forces on a wound play a part. Wounds over joints or on areas with high skin tension, like the chest and shoulders, are more prone to pathological scarring because constant tension can stimulate fibroblasts.
- The initial healing environment is another determinant. A wound that becomes infected or experiences prolonged inflammation is more likely to result in significant scarring because chronic inflammation continuously signals fibroblasts to remain active.
- Age and hormonal factors can affect scar formation. Younger individuals, between 10 and 30, tend to have a more vigorous healing response that can become excessive. Hormonal fluctuations, such as during puberty or pregnancy, also influence scarring.
Managing and Treating Fibrotic Scars
The approach to managing fibrotic scars involves both prevention and active treatment. Preventative measures begin with proper wound care immediately after an injury. Keeping a wound clean, moist, and covered helps to prevent infection and reduce the inflammatory response, lowering the risk of an excessive fibrotic reaction.
For existing hypertrophic scars and keloids, several non-invasive treatments are used. Silicone gels or sheets are a primary option, believed to work by hydrating the scar tissue and reducing collagen production. Pressure therapy, using custom-fitted garments, applies steady pressure to the scar, which can help flatten it and is useful for large burn scars.
When conservative measures are insufficient, medical interventions may be necessary. Corticosteroid injections directly into the scar are a frequent treatment, as they reduce inflammation and break down excess collagen fibers. Cryotherapy, which freezes the scar tissue with liquid nitrogen, can also be effective in reducing the hardness and size of keloids.
More advanced treatments include laser therapy, which can reduce the redness of scars and improve their texture. Surgical excision may be considered to remove the scar tissue, although for keloids, there is a high risk of recurrence. Often, a multi-modal approach combining several of these treatments provides the most effective outcome.