Common Causes of Pigmentation
To be able to offer effective long-term treatment solutions, the contemporary skin treatment specialist must fully understand the prevailing skin condition and have an in-depth knowledge of the cells and systems involved to be able to confidently embark on a corrective program.
There is much to be understood regarding what has caused the pigmentation we see in our clients and why it is a disorder that will not go away by itself. In fact, pigmentation is possibly the hardest of all skin conditions to understand and get a satisfactory result when treating.
Further adding to the perplexity is the wide variety of treatment options available, and despite the claims of treatment marketers, some modalities will be inappropriate and/or ineffective when used unaccompanied. (Depending on the cause of the pigmentation)
This is where the skin technician can unwittingly waste time and money (not to mention challenge professional credibility) by taking the solution in the wrong treatment direction by using the modalities out of sequence.
Understanding what is going on during the melanocyte life cycle, and at what stage during the cycle the problem has been triggered will ultimately dictate the best sequence of modalities to deal with the problem.
Asking the question
We know that melanin production is a fundamental part of the skin barrier defense system, and keratinocytes obtain their melanin from melanosomes, which originate from Melanocytes. After receiving the pigment, the keratinocyte continues its journey of differentiation and ultimately desquamates. This journey takes around 8-10 days and will then take around 5-8 days to desquamate. (Age & lifestyle dependent)
Two questions need to be asked:
1. If all pigment is passed to the keratinocyte and all keratinocytes ultimately desquamate, why does pigmentation remain within the skin?
2. If the pigment has not been past to a keratinocyte, where is it?
These questions have been posed ever since it was understood that these two cells work in synergy with one another, and no doubt will continue to be the subject of controversy for some time yet to come.
Melanocytes make up approximately 10% of the viable epidermis, or around 1300 Melanocytes per square millimetre.
The Melanocyte is a dendritic, long lived and slow cycling cell with no major stem cell resource. This profile means that if a Melanocyte becomes damaged or lose efficiency in any way, then it would be unable to correctly deposit or distribute the pigment-carrying melanosomes to the keratinocytes. Localised hypo or hyper pigmentation will be the result.
Let us look at the most common forms of abnormal keratinocyte/melanocyte and explore what is happening in each.
In some forms of pigmentation, (generally in people over 40) the Melanocytes in the affected areas are suffering from cellular senescence. Put simply, this is cellular Alzheimer’s, and is caused by the cell’s ageing. In this scenario, cells are still functional but in an abnormal manner. This abnormal activity can manifest itself in either loss or over production of the pigment-carrying melanosomes, resulting in abnormal distribution of pigment to the keratinocytes.
Understandably, there will be no quick fix with this as a primary cause, as the effected melanocyte is a long-living and slow-cycling individual with no major source of new cells to draw from.
Modes of treatment such as Assisted desquamation (Microdermabrasion, peeling) will unfortunately have limited effect on pigmentation issues with this cause. Why?
In the case of Microdermabrasion or peeling, the shortening of the desquamation part of the cycle by removing the top layer of abnormally pigmented keratinocytes does not change the behaviour of the donor Melanocytes in any way.
Subsequent generations of keratinocytes will still carry abnormal pigment profiles. At best, these methods will provide temporary reduction.
Similarly, Laser or Intense Pulsed Light can only denature the melanin granule in the keratinocyte, which will offer an excellent result but will not address the cellular senescence of the melanocyte and not change the way the melanin is distributed.
If incorrectly used, these technologies may not only denature melanin pigment, but also destroy the errant melanocyte, and is this what we wish to achieve? Remember that the melanocyte is a long-living and slow-cycling entity with no major source of new cells to draw from. We could easily make the problem far worse.
Cellular old age may be improved by improving the overall health of the melanocyte, to get a more normalized action from them. Essential Fatty Acids like Omega 3 and Vitamin-based treatments will yield the best results, with Vitamin A and C being the obvious choices.
In the forms of pigmentation that are caused by DNA damage, the cell’s memory is impaired with the resulting replicated cells duplicating the damage and appearing the same as their predecessors. As with Melanocytes suffering cellular senescence, DNA damaged cells are more difficult to treat. They are however easier to prevent.
The common cause of the DNA damage is (surprise, surprise) UV radiation, however there is frequently a genetic disposition to this damage in the form of the MC1R gene (Red head gene). This gene is more susceptible to free radical damage than most others, so prevention is paramount.
A three-pronged attack to correct this pigmentation can be undertaken using Antioxidants for prevention, Vitamin A for DNA damage and Tyrosinase inhibitors to slow down future melanin production.
Hormonal induced pigmentation
These forms of pigmentation are caused by the Melanocytes receiving an overload of the chemical instructions that stimulate their behaviour at the beginning of melanogenesis.
In this scenario, the pituitary gland is adversely influenced by an aggravating medication or pregnancy; this will cause a continual cascade of the Melanin Stimulating Hormone (MSH).
The melanocyte receives an overload of the Melanin Stimulating Hormone and does not know when to turn off, resulting in the continuous manufacture of the pigment-carrying Melanosome.
It takes less than 1 minimal erythema dose of UVR to over stimulate this cascade.
In the case of hormone imbalances, these incorrect messages can trigger Melanocytes to be over active in their melanin production, resulting in the classic butterfly pattern of pigmentation that is characteristic of hormonal pigmentation.
Methods to counter these instructions to over-produce melanin are the only real long-term solution with this cause, as once the melanocyte activity has been normalized, the pigment becomes less apparent. The first step to halting this chemical cascade is to remove the offending cause; this will mean the discontinuation of the medication or after pregnancy.
Modalities that chemically intercept the chain of instructions to produce melanosomes are the best solution with this cause, with Tyrosinase inhibitors playing an important role in reducing the level of melanosomes produced.
Essential Fatty Acid Deficiency = Shortened dendrites
The forms of pigmentation that are more readily treatable are those caused by cellular malnourishment. The typical scenario in this case is the dendrites of the Melanocytes have become shortened and less flexible due to essential fatty acid deficiency.
Because the dendrites are shorter, the distribution of melanin to keratinocytes is severely compromised. Even if the Melanocytes are producing the correct volume of melanin, the distribution is far more localized than it should be.
This results in the melanin being dumped in close proximity to the melanocyte instead of being spread more evenly through the 30 or so keratinocytes that surround it. A darker area is the most common outcome, and can range from a small spot to larger areas depending on localized melanocyte health.
As skin care professionals we should be well aware that Essential Fatty Acids (EFAs) are essential to the health of dendritic cells, and as they are not metabolized by the body, must be provided via topical application, diet or supplements.
Clearly, pigmentation with this cause will better respond to diet and supplemental modalities and that EFAs should be part of the preparatory phase of the treatment of any pigmentation treatment. In this scenario, we are taking steps to normalize the behaviour of the Melanocytes, thus providing a better long-term solution.
Epidermal eco system
Another aggravating factor that will cause poor deposition similar to that of the shortened dendrites is the density of the Spinosum layer.
The Spinosum layer is the largest area of the epidermis, and in a Caucasian skin the Spinosum layer is where there is the greatest interaction between keratinocyte and melanocyte. If the Spinosum layer has become atrophied in depth, there will subsequently be less area for melanosome deposition, and once again poor and irregular deposition of pigment may occur.
In this scenario, you will have to think more holistically and concentrate on raising keratinocyte strength and epidermal density before a treatment program can begin.
Keratinocyte stem cell
Keratinocytes are a hydrophobic cell and represent 80% of the cellular population of the epidermis. There is an almost unlimited supply of these cells because of the keratinocyte stem cells that reside in the very deepest parts of the rete pegs and around the bulge of the hair follicle.
In recent research it has been noted that the keratinocyte stem cell can be influenced by the melanocyte. In this situation, the melanocyte may dump pigment-carrying melanosomes onto the keratinocyte stem cell resource, and if this happens the stem cell is pigmented before it arrives in the basal cell layer.
During its subsequent journey through the Spinosum layer the keratinocyte will receive more pigment resulting in a double dose of pigment.
Another site where this melanosome dumping occurs is the dermal-epidermal junction.
Clearly treatment modalities other than Tyrosinase inhibitors will have little effect on this cause.
The Melanocyte is still the major culprit because of its dumping habit, so effective treatment still has to be in the form of slowing down the formation of further pigment. Attempting to deal with the melanin after it has been deposited will be at best a short-term solution with limited results.
We have determined the primary causes of pigmentation are:
• Cellular senescence (Alzheimer’s), which is caused by ageing cells.
• DNA damage caused by free radicals & the MC1R gene.
• Dendrite shortening & impaired cell membranes caused by EFA deficiency.
• Poor density of the Spinosum layer.
Simply knowing the cause however is not the total answer, as understanding what has happened to cells and systems will ensure that the correct modality is chosen when it comes time to treat the skin. (If in fact the particular condition will even respond to treatment)
Understanding how new cells are created and the role of the epidermal stem cell becomes importantly apparent when investigating pigmentation and as a cause needs to be considered.
Effective modalities include:
• The use of tyrosinase inhibitors
• UVR blockers
• Inhibit Melanosome maturation
• Melanin granule denaturing
• The inhibition of cell communication
• Assisting desquamation
• Raising the skin’s essential fatty acid content
Understanding the causes of pigmentation brings you to the inescapable conclusion that there is no one answer to pigmentation and that a treatment program may require all modalities for any result to be achieved.
There will still be the important skin analysis and consultation process before any treatment program is written. The outcome of that analysis will determine cause and effect on the cells and systems involved, the client Fitzpatrick and the Basic Majority Skin Type, client age and work/play lifestyle: these will dictate protocols that must be followed at all times. One size does not fit all!
It is also imperative that the client understands that without their commitment to change of work/play lifestyle, without home care and without salon treatments there will be no long-term improvement in the pigmentation.
This sequence of preparation/treatments will yield best long-term results, as it addresses the specific needs of each of the effected cell/systems.
Repair Cell Membrane of Melanocyte (Client home care for minimum of 2 weeks)
Antioxidant based creams/gels should be used with sunscreen.
Essential Fatty Acids Omega 3, 3000mg a day. Vitamin C, 1000mg a day and Magnesium Ascorbyl Phosphate or Ascorbyl Tetra-isopalmitate based cream to prepare and acclimatize skin to Vit C.
Preparatory Phase; 1st treatment (Prepare skin for the penetration of actives)
Light stratum corneum level peel with Lactic Acid or Microdermabrasion
Suitable for all Fitzpatrick skin tones, Lactic Acid is non inflammatory and hydrating. Many blends of peeling acids are now available. Remembering that this is a preparatory phase of the treatment program, not the answer. If skin requires it, do two treatments 10days apart.
Preparatory Phase: Client’s home care to be upgraded after desquamation
Introduce Vitamin A base creams and continue to use Vitamin C based creams/serums & antioxidants & sunscreens. Continue taking supplements.
Primary Treatment (Course of 10 treatments minimum)
Your choice of skin lightening program, containing Tyrosinase inhibitors. Antioxidants and Vitamin A.
Secondary Treatment (Introduce at the 5th week of skin lightening program)
Intense Pulsed Light: degrading the melanin granule.
This choice of modality is Fitzpatrick guided and is really only suitable for Fitzpatrick skin types 1-3 and perhaps bottom end 4.
As you can see there is no one treatment that will do all things for the pigmented lesion, I would like to point out that the results all vary on the individual and that this is an example of the most basic treatment program.
It would have to be repeated a number of times to achieve the best result.
Important: Clients should always be warned that it would take only one lapse of sun exposure to undo all of the improvements achieved!
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