Melanin and post-inflammatory hyperpigmentation.

The skin is the largest organ of the human body and the most exposed to the environment, being the first protective barrier against external factors.

In the previous article we talked about how the microbiota was able to form “a protective shield”; well, pigmentation is also an essential element in skin protection. The color of our skin is the result of a mixture of pigments that protect us against the harmful effects of ultraviolet (UV) rays from the solar spectrum. And when the production of these pigments is altered, imbalances in skin tone can appear, an example of this is post-inflammatory hyperpigmentation.

If you continue reading this article, you will discover:

  • What melanin is and how does the melanogenesis process work.
  • What post-inflammatory hyperpigmentation is and why it occurs.

Melanin production and function.

The pigments that give color to our skin are known as melanin and are produced by specialized epidermis cells, the melanocytes. These cells have organelles inside them, called melanosomes, where the synthesis of melanin, or melanogenesis, takes place.

Melanogenesis is a process which depends on a cascade of reactions mediated by the tyrosinase enzyme and can give rise to two types of melanin: eumelanin and pheomelanin. Thus, the skin tone of each person does not depend on the number of melanocytes present in our epidermis, but on the type and amount of melanin that they synthesize. In lighter skin, pheomelanin predominates, and in darker skin, eumelanin. In this way, with the different possible combinations, a wide spectrum of skin tones is achieved.

Once synthesized, melanin is stored inside melanosomes. Then, the migration and transfer of these organelles to the keratinocytes occurs. It is estimated that each melanocyte is in contact with an average of 36 keratinocytes to which it provides pigmentation.

When melanin reaches these cells (keratinocytes), its main function is to protect keratinocytes cells from UV radiation, since it can cause damage to the genetic material. Therefore, melanosomes are positioned around the cell nucleus and thus absorb radiation.

UV radiation is the best-known factor for inducing melanogenesis, but it is not the only one. The tyrosinase enzyme can also be activated for other reasons: hormonal factors, the presence of certain vitamins, such as D, or inflammatory molecules present in the skin. This last case is the cause of the process known as post-inflammatory hyperpigmentation.

What is post-inflammatory hyperpigmentation due to?

Post-inflammatory hyperpigmentation (PIH) occurs due to an overproduction or abnormal release of melanin in response to inflammation caused by some pathology, such as acne, atopic dermatitis or psoriasis.

When an injury, rash, eczema or other internal or external factor causes inflammation in the skin, tyrosinase is activated and triggers melanogenesis. The excessive number of pigment granules changes the color and darkens the injured area beyond the time needed for recovery from the initial injury.

In addition, although post-inflammatory hyperpigmentation is not caused by solar radiation (unlike other cases of hyperpigmentation), sun exposure can worsen the spots and longer their presence in the skin. Therefore, it is more common to find these types of marks in areas exposed to the sun and in people with darker skin phototypes.

Although this condition does not prevent the development of a normal life, it can have a physical and psychological impact on the lives of those who suffer from it. The spots caused by post-inflammatory hyperpigmentation tend to disappear over time, being more persistent the difference with the natural tone of each skin and, above all, if they have been increased by sun exposure.

How to prevent post-inflammatory hyperpigmentation.

Knowing that post-inflammatory hyperpigmentation is caused by the presence of an inflammatory environment in the skin, one way to prevent it from getting worse is to avoid promoting inflammation by scratching or touching the lesions that may be the source of hyperpigmentation.

In addition, another preventive key is to protect the damaged areas from the sun so that it does not excessively stimulate the production of melanin.

In short, although melanin is a skin protection system against UV radiation from the sun, its production can be uncontrolled and lead to the formation of spots in response to inflammatory processes caused by conditions such as atopic dermatitis.

Therefore, it is important to avoid inflammation and protect yourself from the sun. And with the first thing we can help you: if you suffer from sensitive skin, more susceptible to inflammation, we recommend you visit our store and learn about our products!


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Keywords: post-inflammatory hyperpigmentation, melanin, melanogenesis, atopic dermatitis


Baumann L. (2009) Cosmetic Dermatology: Principles and practice. Mc Graw Hill

Baumann L. (2009) Cosmetic Dermatology: Principles and practice. Mc Graw Hill

Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthetic Dermatology, Jul 2010; 3(7):20-31.

Chaowattanapanit S, Silpa-Archa N, Kohli I, Lim HW, Hamzavi I. Postinflammatory hyperpigmentation: A comprehensive overview: Treatment options and prevention. J American Academy of Dermatology. Oct 2017; 77(4):607-621.


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