To be able to supply effective long-run treatment for Pigmentation solutions, the up to date skin treatment specialist should absolutely perceive the prevailing skin condition associate degreed have an in-depth information of the cells and systems concerned to be able to with confidence embark of a corrective program.
There is a lot of to be understood concerning what has caused the pigmentation we have a tendency to see in our shoppers and why it's a disorder that may not depart by itself. In fact, pigmentation is probably the toughest of all skin conditions to know and acquire a satisfactory result once treating.
Further adding to the confusion is that the wide range of treatment choices on the market, and despite the claims of treatment marketers, some modalities are going to be inappropriate and/or ineffective once used unaccompanied. (Depending on the reason for the pigmentation)
This is wherever the skin technician will inadvertently waste time and cash (not to say challenge skilled credibility) by taking the answer within the wrong treatment direction by victimization the modalities out of sequence.
Understanding what's occurring throughout the epidermal cell life cycle, and at what stage throughout the cycle the matter has been triggered can ultimately dictate the simplest sequence of modalities to take care of the matter.
Asking the question
We know that animal pigment production could be a basic a part of the skin barrier arms, and keratinocytes acquire their animal pigment from melanosomes, that 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 can then take around 5-8 days to molt. (Age & manner dependant)
Two queries has to be asked:
If all pigment is passed to the keratinocyte and every one keratinocytes ultimately molt why will pigmentation stay inside the skin?
If the pigment has not been past to a keratinocyte wherever 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 millimeter.
The Melanocyte is a dendritic, long lived and slow cycling cell with no major stem cell resource, this profile means that if a Melanocyte become damaged or loose 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 Alzheimers, and is caused by the cells 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 cells 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 behavior 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 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 that 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 skins essential fatty acid content
Understanding the causes of pigmentation bring 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 Sunblock .
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: Clients home care to be upgraded after desquamation
Introduce Vitamin A base creams and continue to use Vitamin C based creams/serums & antioxidants & sunblocks. Continue taking supplements.