INFLAMMATION CAUSES HYPERPIGMENTATION

 After receiving the WORST facial of my life, my skin is still healing nearly six months after. This esthetician squeezed and pinched my skin until I was left with many red marks that resembled bug bites. It wasn’t until I went to another esthetician downtown NYC, who was very knowledgeable about colored skin, that she told me inflammation leads to hyperpigmentation, and the more I pinched at my skin, the more dark spots will develop.

INJURY 

Injuries to the skin include picking of the skin and the intensity of pressure placed on the skin. Melanocytes are the type of cells in our skin essentially giving color, and when the skin is inflamed these melanocytes develop. Inflammation is apart of the body’s defense system. Our skin as a whole recognizes trauma to the body and initiates healing and removal of these harmful substances. Inflammation on the skin can appear red, itchy and sore to the touch.  

The strength of the injury dictates how extensive the hyperpigmentation will be. If the clog pore you are extracting is superficial to the skin and removes easily, a dark spot will not develop. However, if the pore you are extracting is deep in the tissue and requires an immense amount of pressure, a dark spot will develop. And depending on the  amount of pressure placed, and deeper the dark spot will develop into the skin delaying the healing time. 

HOW MELNOCYTES FORM 

   All melanocytes reside in the basal layer of the epidermis, which is the deepest layer of the skin.  Pigment production starts off the pituitary gland and is regulated by Melanocyte Stimulating Hormone, which is a peptide hormone. This hormone stimulates intra melanocytic organelles. An increase of this hormone is triggered by cell injury.  The pigment is then transferred to the surrounding keratinocytes that distribute it to the superficial layers of the skin.

 Melanogenesis is a regular process that gives rise to two types of melanin, Eumelanin and melanin to protect against UV rays. This whole process is dependent on tyrosine, which is an amino acid substrate. This enzyme is then broken apart by tyrosinase to form L- 3,4-Dihydrooxphenlylalnine ( DOPA) . When DOPA is oxidized ( combined with oxygen)  it produces Pheomelanin which is seen in fair skin. Further oxidation of DOPA results in Eumelanin. Pheomelanin produces a higher concentration of free radicals in response to UVR , causing an increase of skin cancer in fair skin people. In darker skin, inflammation leading to hyperpigmentation is more common because of the skin cells activity. Melansomal pH in darker skin is neutral which is optimal for melanogenesis. 

ABNORMAL PIGMENTATION and INFLAMMATION 

 SKin injury and trauma to the skin from acne picking induce an inflammatory response. Nitric oxide ( free radical) is released after damage along with other cell mediators. Macrophages are a huge mediator in the cell injury process. The melanin that is produced from injury is engulfed by macrophages which hold the melanin in the dermis until they degrade or get shredded from the skin. This enables the dark spot to remain visible months after post injury. 

SOURCE 
Encyclopædia Britannica, inc. (n.d.). Melanocyte. Encyclopædia Britannica. https://www.britannica.com/science/melanocyte 

Chadwick, S., Heath, R., & Shah, M. (2012, May). Abnormal pigmentation within cutaneous scars: A complication of wound healing. Indian journal of plastic surgery : official publication of the Association of Plastic Surgeons of India. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495392/#:~:text=Cutaneous%20injuries%20invoke%20an%20inflammatory,to%20the%20site%20of%20injury. 

Hyperpigmentation and the sun: Sun protection. Eucerin. (n.d.). https://int.eucerin.com/skin-concerns/sun-protection/hyperpigmentation-and-the-sun#:~:text=Small%2C%20darkened%20patches%20of%20skin,by%20making%20then%20even%20darker