How Do Acne Scars Form?
The vast majority of acne scars result from persistent cases of inflammatory acne affecting the same area of skin. Individuals who suffer from consistent nodular and cystic acne lesions are at a very high risk of developing permanent acne scarring. This is particularly true when a region is affected by overlapping acne outbreaks, with no opportunity to completely heal in-between.
In cases of persistent inflammatory acne vulgaris, large areas of skin and underlying tissue are damaged, but the continuing infection and inflammation prevent the body from mobilizing the cells and materials necessary for repairing those structures. As a result, the original (healthy) tissue is replaced by scar tissue.
The Role of Inflammation in Acne Scarring
What many people may not realize is that acne scarring is primarily due to the body’s own immune response to infection, and not the infection itself. A major component of inflammatory acne is the migration of white blood cells to the hair follicle, sebaceous gland and surrounding tissue. These white blood cells compose much of the “pus” or edema fluid that comes out when you pop a zit.
The white blood cells that make up the pus in a whitehead are not uniform, but rather are composed of many different sub-types of white blood cells, such as macrophages, neutrophils, dendritic cells, T cells, granulocytes, mast cells and others. Many of these cells produce powerful degradative enzymes, inflammatory molecules, super-oxides and free radicals. While these weapons are designed to help neutralize pathogens and foreign invaders, they can cause damage to the surrounding cells and tissue. In inflammatory acne the damage caused by these white blood cells actually causes the infection to spread, leading to more inflammation and damage, creating a vicious, self-fulfilling cycle.
When it comes to scarring, perhaps the most important type of white blood cell is the neutrophil. The neutrophil is one of the first responders to the infected follicle, and can accumulate in great numbers. Neutrophils are kind of like the suicide bombers of the cellular world. When they reach the site of infection they often undergo apoptosis (controlled suicide) and degranulation, which releases many anti-microbial molecules, DNA and proteases into environment. In particular it is these proteases that can cause tremendous damage to the surrounding tissue and ulimately lead to scarring. These proteases digest the elastin and collagen matrix that provides support and elasticity to the skin.
These powerful enzymes also damage many other proteins that are essential for the holding the matrix (aka: scaffolding) that provides the foundation for healthy skin tissue. Without this matrix to guide healing, the body has a very difficult time properly repairing and re-creating the damaged tissue. In cases of persistent infection and inflammation, the body is not able to repair the matrix fast enough to keep up with the damage. In these cases, the body begins to build scar tissue, which is simple and tough, in place of the more complex and delicate matrix. This process underlies not only the formation of acne scars, but of other diseases marked by chronic inflammation, such as chronic obstructive pulmonary disorder (emphysema) and rheumatoid arthritis.
The Formation of Scar Tissue
Scar tissue is composed largely of collagen, which is the same material that comprises a healthy sub-cutaneous matrix. However, unlike the healthy matrix – which is a complex, spacious and interconnected web of collagen and other proteins – the collagen in scar tissue is much different. In scar tissue, the collagen becomes tightly bundled and tends to line up in a single direction, instead of the original random web pattern.
In scar tissue, many of the essential accessory proteins and molecules are excluded and there is much less open space. This alignment of the collagen fibers and their closely packed arrangement creates a denser, less elastic tissue. In addition, scar tissue becomes impermeable to migration by many cell types, preventing the formation of blood vessels and a regrowth of complex structures, such as hair follicles and sweat glands. This is why scar tissue is generally monotone, feels tough and dense to the touch, and is hairless. It also explains why the body has such a difficult time replacing scar tissue with healthy tissue.
Repairing Scar Tissue
Once scar tissue has been generated at a site of injury, it is relatively permanent. In some cases, the body will gradually replace some scar tissue with the proper tissue type, but this process is so slow that is largely irrelevant. The single best treatment for acne scarring, is to prevent it in the first place. This means aggressively attacking the infection and treating the inflammation as it arises. Treatment after the fact generally involves either surgically removing the scar tissue, or damaging it with laser, heat or surgical treatments. The damage stimulates the healing process and creates space for new, functional tissue to form.
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References and Sources
Physiopathology of acne vulgaris: recent data, new understanding of the treatments.
Pawin, et al. 2004. For article abstract, click here.
Topical ALA Photodynamic Therapy for the Treatment of Acne Vulgaris.
Hongcharu, et al. 2000. For article abstract, click here.
Human b Defensin-1 and -2 Expression in Human Pilosebaceous Units: Upregulation in Acne Vulgaris Lesions.
Chronnell, et al. 2001. For article abstract, click here.
A prospective, randomized, placebo-controlled, double-blinded, and split-face clinical study on LED phototherapy for skin rejuvenation: Clinical, profilometric, histologic, ultrastructural, and biochemical evaluations and comparison of three different treatment settings.
Lee, et al. 2007. For article abstract, click here.