Melanocytes reside at the basal layer of the epidermis, they sit amongst the basal parent keratinocytes and are not attached to the dermal epidermal laminate membrane as basal keratinocytes are. Approximately 1 in every 10 cells are melanocytes, which are smaller than keratinocytes.

Our allotted number of melanocytes in our lifetime is finite, unlike keratinocytes. We have a limited number and up to the end of our teens we can renew melanocytes, but then you will not get anymore. Damaged melanocytes will not be replaced for the rest of your life and in fact as we age the numbers of melanocytes reduce by around 10% per decade and if uncared for this can be faster.

There are various types of hyperpigmentation, and it can develop in all different skin types – that’s why we have multiple agents, peels, needling devices, and products which target seven different depigmentation processes. Below is information on our different types of chemical peels that can be used to treat them.

Pigmentation fundamentally is caused by inflammation which can be internal or external and is as a defensive response to damaging energy. Melanocyte cells manufacture melanin and transfer it to surrounding epidermal keratinocytes where the pigment wraps around the nucleus of accepting keratinocytes.

Hormonal changes such as drops in oestrogen can make otherwise previously stable skins become more reactive to minor inflammation. Normally the inflammation is from UV rays, but injury or skin treatments can also trigger the same response. When produced in excess, this is known as a hyper response, and while there are various ways to slow down this production, it is important to control inflammatory triggers that may be driving it. This is typical of sun damaged skin.

Sources of inflammation can come from many sources; these include our own cells and our own immune system. One such source is via senescent cells, particularly melanocytes but also fibroblasts. Melanocytes are long lived, and DNA damage can lead to irregular cell function. This can happen when programmed cell death pathways are ignored or not initiated and melanocyte metabolism enters a feedback loop where they remain alive but cease their primary function of producing and distributing melanin or with fibroblasts, they stop extruding collagen and elastin and hyaluronic acid fibres and instead these cells initiate inflammatory processes impacting on their surrounding cellular environment. Therefore, the source of inflammation can be local and from our own cells. Senescent cells become more prevalent as we age and can be a key driver of melasma development especially when coupled with depreciating hormonal control. Seno therapeutics and Senolytics describes an area of research in reducing senescence either preventing initiation but also to interrupt the feedback loop once activated and override it leading to cell death of senescent cells. This latter area is borderline anti-cancer research.  Going into senescence is beneficial in preventing tumorigenesis and could be characterised as a defensive cell strategy.

Late stage (stage 4) aged melanocytes often accumulate melanin within the melanocyte and contain a structured matrix and highly dense melanin deposits.

Melanocytes are cells that synthesize melanins within melanosomes. Various factors related to melanin over and under production within melanocytes can be divided into three parts:

1. Structural proteins of melanosomes

2. Enzymes required for melanin synthesis

3. Proteins required for melanosome transport and distribution

There are multiple and I mean many different pigmentation issues, triggered by so many processes and a list of them all would take pages. 

Each melanocyte in the basal layer has dendrites; long cellular extensions reaching up into the epidermis. Each melanocyte via their dendrite’s contacts with around 30 plus keratinocytes. Excess UV exposure leads to lengthening of dendrites to transfer pigment higher into the spinosum layer, leading to uneven deposition of pigment in the spinosum layer, resulting in uneven skin tone. Dendrites can become less flexible which results in them shrinking and distribution of melanosomes becomes impaired. Imagine a bulbous bloated melanocyte packed full of melanosomes with shortened stubby dendrites. In this scenario melanosomes fail to transfer to the surrounding mobile keratinocytes, and some will drop down and be taken up by basal keratinocytes. These pigmentation packages will not migrate up as these basal keratinocytes are attached to the basal membrane. So, this pigmentation is fixed or trapped. Loss of flexibility and shrinkage of dendrites seems to be linked with low levels of omega 3 acids such as alpha linoleic acid in the cell membrane. Loss of linoleic acid due to hormonal sensitisation of the skin can lead to a 90% reduction in sebum linoleic acid which also increases our sensitivity to the androgen hormone dihydrotestosterone which can trigger increased TEWL, resulting in thickening and keratinisation of the stratum corneum resulting in blockage of follicles and maturity onset acne.  

In other situation melanosomes ‘drift down’ between basal cells and become wedged in crevices and spaces in the dermal epidermal laminate membrane. Again, this is trapped pigment which builds up over time. Some of these ‘released’ melanosomes, especially where the dermal epidermal junction is damaged can also be released into the lower dermis, where they maybe engulfed by melanophages but then they just sit there adding to the accumulation of trapped ‘pigment packages.’ Many pigmentation problems are a combination of epidermal and dermal. Companies claim great results in dermal pigmentation like melasma but on examination, they have only reduced the epidermal component, meaning the skin appears lighter but the dermal pigmentation remains. Topically applied tranexamic acid serums are popular for deeper pigment but for this molecule to work it needs to reach the dermal epidermal junction and most topical serums on the market, if not all, do not penetrate below the stratum corneum, hence intradermal injection or oral tranexamic acid is more effective. SkinMed are trialling a topical tranexamic acid which uses technology to get this molecule to where it can have a significant impact on deeper seated pigment deposition.

DNA damage from UV exposure is a key cause of excessive pigmentation. If the DNA has been damaged, then can permanently lead to excessive melanosomes and pigment granules, creating a high level of oxidative free radical stress.

Melanin-stimulating-hormone (MSH) production is increased by exposure to UV light. UV triggers an MSH cascade, which accelerates the melanogenesis process. Following UV exposure MSH receptor numbers on melanocytes tripled resulting in continuous formation of melanosomes. Pituitary stimulation is triggered by UV hitting the retina and even sunglasses, even wraparound polarised sunglasses will not stop all UV rays from getting in, but better than no sunglasses.

Keratinocytes on exposure to UV release a chemical factor called Endothelin which can also stimulate increased melanogenesis by triggering tyrosinase activation.

Another source of inflammation is out own immune system. Irritation of the skin over time can increase the activity of enzymes which covert a molecular precursor into the antimicrobial peptide cathelicidin. This peptide in normal levels is protective, but when the Kallikrein enzymes 5 and 7 become hyperactive then excessive amounts of cathelicidin are produced with some defects in the molecular structure. This can trigger inflammatory processes such as inflammasomes and cytokine cascades and damage to the barrier function of the skin, increasing inflammatory exposure, but also can cause neutrophil chemotaxis (white blood cells being drawn to the excessive levels of cathelicidin), as they believe it is an ‘intruder’. So, they initiate extreme inflammation and pus. This immune dysregulation leads to papules and pustules in rosacea for example

Although EnerPeel® Jessner forms the core of the pigmentation solution, we understand each case of pigmentation can be different. When you combine other skin issues like dark marks and lines and wrinkles around the eyes, or chrono and photo ageing, as well as the many different ethnicities and Fitzpatrick types, it’s clear to see that there is no such thing as a one-size-fits-all treatment.

We also use dermal needling and tranexamic acid to target trapped pigmentation, and we utilise 4 ingredient Tebiskin® Lightening Cream, SkinVital® Retimitate and SkinVital® CE Ferulic B5, B3, Tebiskin® PLC and Tebiskin® UV SOOTH. These are used in conjunction with Enerpeel® Jessner.

These target numerous processes for a multifactorial approach to pigment control which between them targets tyrosinase activation, tyrosinase inhibition, tyrosine degradation, faster corneocyte turnover, tyrosine production, melanosome transfer, Antioxidant reduction, VEGF, targets numerous inflammatory processes and triggers, factor 50 SPF UVa and UVb control, supply Ectoins to strengthen microbiome, and also to boost keratinocyte UV resistance, increase resistance to photodamage and actinic keratosis.

Examples of numerous Inflammatory pathways

Kallikrein Cathelicidin Inflammation

As part of the advanced medical SkinMed® training every clinic goes through to be able to supply our treatments, clinics learn how to provide bespoke treatments to clients for a range of issues and skin types.

Here are some other EnerPeel® systems in combination with, or instead of, the EnerPeel® JR, providing maximal results, with minimal downtime for every kind of patient that walks through the door.

EnerPeel® Jessner Revised (JR)

EnerPeel® JR utilises 20% lactic acid as well as 15% salicylic and 14% resorcinol, suspended in a patented EnerPeel® carrier solution. This EnerPeel® carrier solution enables us to deliver the ingredients deep into the skin to target melanocytes directly for maximum efficiency. 

How does EnerPeel® JR work?

Tyrosine is the raw material used to make melanin and is an amino acid created by the skin as and when it wants to make melanin. Inflammation causes it to be produced and the enzyme tyrosinase which lies dormant activates and facilitate the increased conversion of tyrosine to melanin, resulting in dark marks. Resorcinol attracts tyrosinase away from converting tyrosine as the enzyme has a much greater affinity to bind with resorcinol.

Lactic acid blocks the tyrosinase active part of the molecule so the enzyme cannot bind with tyrosine to melanin. Salicylic acid is used to reduce surface oil on the skin, further increasing the delivery of resorcinol and lactic acid. The solution also acts as an exfoliant, breaking down the darkened skin and bringing lighter skin to the surface.

EnerPeel® JR utilises 20% lactic acid as well as 15% salicylic and 14% resorcinol, suspended in a patented EnerPeel® carrier solution. This EnerPeel® carrier solution enables us to deliver the ingredients deep into the skin to target melanocytes directly for maximum efficiency. 

EnerPeel® Mandelic Acid (MA)

Some skin types are hyperreactive to low levels of inflammation and in these skin types, the Enerpeel JR ingredients’ inflammatory properties may overwhelm it, and the pigment reducing properties and could exacerbate the pigmentation.

This is where Enerpeel MA comes in; ideal for mild pigmentation, it is the peel to be used on darker skin types as it is a superficial peel.

MA, containing 40% Mandelic acid and calming MSM, was designed to target pigmentation in hypersensitive skins and in skins with a high post-inflammatory pigmentation risk. We recommend a course of two to six MA peels, or to use MA on potentially reactive skins before moving onto a JR, to treat:

·      Inflammatory pigmentation

·      Build skin tolerance before the JR

This is the most widely used peel in the Indian sub-continent, and we have a variety of techniques in using it in pigmented skin. We also combine it with dermal needling for deep dermal pigmentation, using the needling to break up the deep-seated pigmentation to stimulate the body to remove it and take it away.

EnerPeel® Pyruvic Acid (PA)

Pyruvic acid, encapsulated in an Enerpeel carrier, goes deep into the skin and is less inflammatory than glycolic but is still very effective at skin remodelling. It penetrates oil and so is ideal for those who also suffer from oily skin as well as pigmentation, targeting two skin issues with one peel. Pyruvic acid converts to Lactic acid in the skin and so can have a powerful impact in slowing down pigmentation. It tends to be used in lighter skins with resistant pigmentation whose skin is not hyperreactive to inflammation, to improve:

·      Resistant pigmentation

·      Mild actinic keratosis

·      Chrono and photo ageing

To find out more about all our different peels and protocols, or to ask any questions about pigmentation, please call us on 0333 247 2474, or email clinical1@skinmed.co.uk