Melasma-spots

We often hear about Melasma, Chloasma, hormonal spots, sun spots, photoaging. But we do not distinguish well what each concept is, neither what they appear, nor their treatment.

All of these conditions are different types of hyperchromia or commonly known as skin pigmentation.

 

Hyperchromia (pigmentation) and melanin of the skin

Skin pigmentation is caused by the combination of four pigments located in the dermis and epidermis: Oxygenated hemoglobin, deoxygenated hemoglobin, carotene deposits, as well as in other exogenous pigments (medicines, metals, etc.) and epidermal melanin (which gives ethnic pigmentary differences).

Melanin is a complex chemical structure biopolymers and it’s the main pigment responsible for the normal color of the skin and hair.

It is found in all individuals forming complex combinations that give rise to the multiple shades of skin color. It is regulated by genetic, environmental, and endocrine factors, which modulate the amount, type, and distribution of melanin in the skin, hair, and eyes.

There are two types of melanin:

• Eumelanin: Blackish brown pigment that provides dark colorations
• Pheo-melanin: Yellowish or brownish-red pigments that make up a higher proportion of sulfur than the above and they are responsible for clear colorations.

 

Synthesis of melanin and its protective function:

MC1R receptors regulate skin pigmentation, UV responses and the risk of melanoma. Its activation increases the production of melanin and its deposition in the epidermis, limiting the penetration of UV rays into the skin.
The synthesis of melanin takes place inside melanosomes, from tyrosine. A succession of tyrosine oxidations catalysed by tyrosinase, leads to the synthesis of DOPA (dihydroxyphenylalanine) to produce then a common intermediate compound: dopaquinone. From this point, two distinct pathways lead to the formation of eumelanins and pheo-melanins.

The production of pheomelanin depends on the incorporation of a cysteine and the retention of sulfur after the synthesis of dopaquinone.

Tanning is an adaptive pigmentation and is a mechanism for protecting the skin against solar aggression (the MC1R receptors are activated). The more pigmented the skin, the more it is protected against negative effects such as photo aging and skin cancer.
The melanin barrier is the most effective device against solar radiation, in which the ultraviolet light spectrum is the area that affects the skin.

Ultraviolet rays are subdivided into 3 types:

UVA	Immediate pigmentation   (thanks to the oxidation of melanin present in melanocytes)
UVB	Delayed pigmentation   (tanning), thickening of the stratum corneum, solar erythema.
UVC	Retained by the Atmospheric Ozone Layer

 

Hyperchromia or Hyperpigmentation:

We can find many types of hyperpigmentation, which are classified according to their ethology:

Hyperchromia caused by melanocytic hyperactivity or proliferation:

 

Class	Characteristics
Ephelides (Freckles)	• There is an increase in melanin pigment in the epidermis • Are small in size and located in sun-exposed outdoor areas • Appears from childhood and has hereditary character

Lentigo

• They are brown or brownish-blackish spots, isolated or grouped • Can be located in any area of body surface • There is an increase in melanocytes of the epidermis and they are induced by the overexposure of the sun, in particular, the senile lentigo appear in people of 50 years that has been exposed repeatedly under the sun without the proper protection

Melasma or Chloasma

• Light brown or dark brown spots, which develop slowly and systematically • Predominantly in female and it has been associated with hormonal factors, cosmetics, sun exposure and family trend • Common during pregnancy

Nevus (Moles)

• Blackish hyperpigmentation, which may also have hair • Congenital abnormality that can also be acquired • If there are signs of oozing, itching, pain, or inflammation, it is advisable to consult your doctor.

 

Hyperchromia due to photosensitisation:

On the other hand, hyperchromias can be caused by photosensitization of solar radiation in contact with chemical agents such as perfumes, plants containing furocumarin with photosensitive properties, facial powders with alamine that can give photodermatosis. And as we have already commented, certain medicines with photosensitising properties such as psoralens or diphenhydramine, etc.

Cold, heat and mechanical rubbing, applied repeatedly, are also agents that can cause an increase in skin pigmentation

 

Post inflammatory hyperchromia (BPH):

In skin disorders such as acne, eczema, herpes, burns, among others. A process of inflammation of the skin is typical of these conditions, which, as a consequence, after this inflammatory process can lead to hyperpigmentation.

 

How can radiation affect our skin? SKIN PHOTOAGING

The sun is a good ally for capturing Vit D, to have a beautiful skin tone and makes us feel better mentally. But it is one of the main factors of premature aging.

Photoaging is an acceleration of the natural intrinsic aging of the skin induced by the damage caused by ultraviolet radiation from the sun. It is characterized by the appearance of wrinkles, roughness, laxity and unequal pigmentation of the skin. And it can take decades to manifest.

In the short term, when there is excessive exposure of ultraviolet radiation, it can produce an augmentation of pigmentation or melanogenesis, inflammation and erythema caused by sunburn. After exposure of ultraviolet rays, the skin undergoes histopathological changes. Among them a thickening of the epidermis, especially of the stratum corneum, and to the dermis. This thickening causes a higher production of keratinocytes, and at the same time an increase in the biosynthesis of DNA, RNA and proteins, and as a consequence there is a greater degradation of these.

Epidermal DNA is highly susceptible to structural modification by solar UV radiation even in exposures that do not produce erythema. If the damaged DNA is not repaired, it can result in characteristic mutations that lead to skin mutations and later to the possibility of skin cancer. The sun’s UV rays also cause a degradation of the main components that give stiffness, turgidity and elasticity to the skin such as collagen and elastin, and an inhibition of their synthesis. This impairs the structural integrity of the skin during photoaging, causing wrinkles and other signs of age.

It also produces an immunosuppression, where the Langerhans cells (in charge of the defense) are exhausted in contact with UV rays, therefore the skin is more exposed to external aggressions.

 

Depigmenting treatments
Two of the main methods to lighten the color of the skin by reducing skin pigmentation are: bleaching the melanin already formed, and preventing the formation of new melanin.

The results of the discoloration of the skin spots are visible after long periods of treatment and, above all , if appropriate photoprotection precautions are taken.

Depigmenting substances slow or retard this process of melanogenesis or melanin formation by several pathways or stages.

• Destruction of melanocytes (Rucinol (4-n-butyl resorcinol, N-acetyl-4-S- cysteaminophenol)
• Inhibition of formation and alteration of melanosome structure (lipyl acid, ellagic acid)
• Inhibition of the biosynthesis of tyrosinase: blocking of the factors that induce its synthesis or its enzymatic activity (lactic acid and placental extracts), inhibition of its enzymatic activity (as in the case of plant extracts), formation of a substrate that inhibits the activity of tyrosinase activity and inhibition of glycosylation (some amino sugars such as glucosamine or galactosamine).
• Inhibition in the formation of melanin, by a reduction of the dopamine reaction to dopa. ( Vit C , reduced glycation and cysteine , albatin )
• Interference with melanosome transfer ( Tetrinoine
• Increased degradation of melanosomes in keratinocytes. (glycolic acid, phenol, paraaminobenzoic acid and paraphenylenediamine)
• Stimulation of cellular activity (Vit c, albatin )
• Discoloration of the formed melanin. (AHA, BHA)

 

How WHITEPRO’s whitening agents work?

 

AZELAIC ACID

Azelaic acid as a tyrosinase inhibitor reduces melanin production and helps to reduce pigmentation, especially in dark skin whose acne spots leave persistent brown marks (postinflammatory hyperpigmentation) or which have melasma. It also has a direct anti-inflammatory effect due to its oxygen-free radical removal activity indicated for post-inflammatory pigmentations.
It is also characterized by inhibiting DNA synthesis and mitochondrial oxidoreductase activity.

 

ARBUTIN
Alpha arbutin is a natural derivative of hydroquinone, an active with great depigmenting power. Unlike hydroquinone, Alpha Arbutin has a good tolerance in the skin and does not require a medical prescription.
Its natural origin derives from fruits such as blackberries or blueberries, but especially is found in a great concentration in the leaves of the Gayuba.
It is a powerful depigmenting agent by directly inhibiting the tyrosinase enzyme and the maturation of melanosomes, involved in the production of melanin. Therefore, it is a great ally against the spots and unifies the tone of the epidermis.

 

SKIN BRIGHT ACTIVE (Helianthus Annus Seed Oil, Dimethylmethoxy Chromanyl Palmitate)

Skin Bright active is one of the main active ingredients with depigmenting properties thanks to the Dimethylmethoxy Chromanyl Palmitate, which inhibits the tyrosinase enzyme and digests the L-DOPA substrate, which are involved in the production of melanin. In high doses, it has been shown to act like some powerful aggressive depigmentants such as hydroquinone.

Dimethylmethoxy Chromanyl Palmitate has also been shown to have a very significant photoprotective effect on keratinocytes (skin epidermal cells), and can therefore prevent the harmful effects of ultraviolet radiation on the skin.

 

AMLA

Phyllanthus emblica, commonly known as Amla , is used in Ayurveda ( traditional medicine of India ).
It has cosmetic applications due to its antioxidant and anti-inflammatory properties, as it effectively protects the skin against irritation induced by reactive oxygen (ROS) substances caused by ultraviolet (UV) sunlight, responsible for sunburn and photoaging.
Phyllantus emblica also protects from collagen degradation and fibroblasts from free radicals generated by exposure to solar UVB, and thanks to its activity as a precursor of type I collagen and its anti-colagenase activity.

 

MELACARE (CAMELLIA JAPONICA SEED OIL, OXALIS TRIANGULARIS OIL, EREMANTHUS ERYTHROPAPPUS BRANCH/LEAF OIL)

Melacare is a compound of three essential oils with great depigmenting, antioxidant and anti-inflammatory power.
Melacare contains Oxalis triangularis oil as the main depigmenting agent since it prevents melanogenesis (melanin production), inhibiting the enzyme tyrosinase and the production of cAMP essential for this process.

 

NIACINAMIDE

Niacinamide plays a very important role as a depigmenting agent, as it decreases the transfer of melanosomes, which transport melanin to the most superficial layers of the skin. In addition, it inhibits the maturation of tyrosinase and prevents ultraviolet radiation from reducing ATP levels and inhibiting glycolysis, thereby improving DNA repair and reducing UV-induced immunity suppression.

 

VITAMIN C (Ascorbyl Glucoside)
Vit C is a powerful depigmenting agent, since it inhibits the action of the tyrosinase enzyme responsible for the formation of melanin, and therefore the spots on the skin. It can also prevent post inflammatory hyperpigmentation as it is responsible for a reduction of the macrophages involved in the inflammation processes.

 

LIQUORICE EXTRACT (Glycyrrhiza Glabra)

The main active ingredient in liquorice extract is Glabridin. It has a structure similar to dihydrobenzene and therefore stands out for its great depigmenting power, not only inhibits tyrosinase, but also reduces melanin.