How Do Acne Scars Form?

Acne scars are the result of tissue damage caused by inflammatory acne.


The vast majority of acne scars are caused by from persistent cases of inflammatory acne affecting the same area of skin. Individuals who suffer from frequent nodular and cystic acne outbreaks (Acne Types: 3-4) 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 for the skin to completely heal.

When an individual experiences persistent outbreaks of severe inflammatory acne, significant regions of the affected skin and underlying tissue can be damaged. Acne is an inflammatory process that usually involves an infection caused by bacteria (eg. Propionibacterium acnes).

The inflammation that occurs during severe acne prevents the body from mobilizing the cells and materials necessary for the normal healing process that is required to repair the skin. In this situation, the original (healthy) tissue can be replaced by fibrous 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 glands and surrounding tissue. These white blood cells compose much of the “pus” that comes out when you pop a zit.

The white blood cells that make up the pus in acne pimples, nodules and cysts are not uniform. Instead the pus contains a mixture of many different sub-types of white blood cells, such as macrophages, neutrophils, dendritic cells, T cells, granulocytes, mast cells and others. Neutrophils are one of the body’s front-line defenses against infection and these cells are usually the most abundant white blood cells in an acne lesion.

Many of the white blood cells (and especially neutrophils) produce powerful degradative enzymes that can damage health tissue. These cells also produce inflammatory molecules, super-oxides and free radicals. These weapons are designed to help neutralize pathogens and foreign invaders, but they can also cause damage to the surrounding healthy tissue.

In inflammatory acne, the damage caused by these white blood cells can actually cause the underlying bacterial infection to spread, leading to more inflammation and tissue damage. This can create a vicious, self-fulfilling cycle of tissue damage that leads to permanent acne scars.

Neutrophils and Acne Scars

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 can undergo apoptosis (controlled suicide) and degranulation, which releases many anti-microbial molecules, DNA and proteases into environment. These proteases that can cause tremendous damage to the surrounding tissue, which ultimately results in scarring. The proteases digest the elastin and collagen matrix that provides support and elasticity to the skin.

The Structure of Scar Tissue

Healthy skin is supported by a complex matrix (scaffolding) that provides structural support and nutrients to the skin surface. When skin is damaged, this matrix helps guide the healing process. 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. The scar tissue can permanently replace the more complex and delicate healthy 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.

Scar tissue is composed largely of collagen, which is the same material that comprises much of 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, interconnected web pattern.

In scar tissue there is much less open space than healthy tissue, and many of the essential accessory proteins and molecules that are essential for the maintenance of healthy skin are absent. This alignment of the collagen fibers and their closely packed arrangement creates a denser, less elastic tissue.

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 (without medical intervention). In some cases, the body will gradually replace some scar tissue with the healthy tissue, 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.

Fortunately, there are many different treatments available to help repair acne scar damage. The ideal type of treatment is largely dependent on the specific types of acne scarring. Acne scar treatment generally involves either surgically removing the scar tissue, or breaking it apart with laser, heat or surgical treatments.

Light and Laser treatments can be very effective treatments for many different kinds of acne scars. Invasive and non-invasive surgical treatments can also be very helpful.

Topical Retinoids may also be helpful for very mild acne scars and uneven skin tone.


Physiopathology of acne vulgaris: recent data, new understanding of the treatments. Pawin, et al. 2004.
Topical ALA Photodynamic Therapy for the Treatment of Acne Vulgaris. Hongcharu, et al. 2000.
Human b Defensin-1 and -2 Expression in Human Pilosebaceous Units: Upregulation in Acne Vulgaris Lesions. Chronnell, et al. 2001.
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.
Acne scarring: a classification system and review of treatment options. Jacob, et al. 2001.
The role of elastic fibers in scar formation and treatment. Cohen, et al. 2017.
The pivotal role of inflammation in scar/keloid formation after acne. Shi, et al. 2017.
Mechanical stress and the development of pseudo‐comedones and tunnels in Hidradenitis suppurativa/Acne inversa. Boer, et al. 2016.
Effect of basic fibroblast growth factor combined with laser on content of a variety of cytokines in acne scar wound. Dong, et al. 2016.
Scar prevention and remodeling: a review of the medical, surgical, topical and light treatment approaches. Kerwin, et al. 2014.
Post acne scarring: a review. Goodman, et al. 2003.
The molecular basis of keloid and hypertrophic scar formation. Tuan, et al. 1998.
Postacne scarring: a review of its pathophysiology and treatment. Goodman, et al. 2000.
Acne scar treatment. Rusciani, et al. 2015.
Acne scar treatment: a multimodality approach tailored to scar type. Zaleski-Larsen, et al. 2016.
Atrophic scar formation in acne patients involves long‐acting immune responses with plasma cells and alteration of sebaceous glands. Carlavan, et al. 2018.
The pivotal role of inflammation in scar/keloid formation after acne. Shi, et al. 2017.
Prospective Study of Pathogenesis of Atrophic Acne Scars and Role of Macular Erythema. Tan, et al. 2017.
Expression of inflammatory and fibrogenetic markers in acne hypertrophic scar formation: focusing on role of TGF-β and IGF-1R. Yang, et al. 2018.
The role of elastic fibers in scar formation and treatment. Cohen, et al. 2017.
Current Concepts in Acne Pathogenesis: Pathways to Inflammation. Tan, et al. 2018.