Cn-04-pigmentation

Pastiche Advanced Education; Specialist training class: Cause and Effect of Pigmentation

Welcome to your next unit of learning about the skin condition pigmentation. Today's lecture cover the leading
causes of pigmentation and the effect those causes would have on the cells and systems of melanogenesis.
Student resources for today can be downloaded from the student resources folder. They are today's class notes
"cause and effect", the oxidative stress flow chart and the two hormonal and two genetic flow charts. Keep all
previous class notes with you for reference.
We ended the last unit of learning on Melanogenesis asking the question, why does the skin condition
pigmentation exist? If all pigment is passed to a keratinocyte and all keratinocytes desquamate.
This question and many more must be answered before one can fully understand the challenges of treating the
difficult skin condition pigmentation, so I thought a page of Q&A would be helpful in answering those questions
that have been so difficult to answer in the past.
First, you must remember all steps of melanogenesis learnt in the previous unit of learning. Just in case you have
forgotten have your previous class notes close by for reference. Then consider all things that could go wrong
during that complicated melanogenesis process. If you’re ready we shall begin.
Question: Why would there be an abnormal increase in the pigment carrying melanosomes?
Answer: the main reason that we know of is linked to an event such as pregnancy or medications such as the
oral contraceptive, in‐vitro fertilization medication or progesterone based medication. These cause the pituitary
gland to make too much melanin stimulating hormone. When this happens the MSH is continuously adhering to
the receptors of the keratinocyte and in turn, the melanocyte creating an uncontrolled manufacturing of
melanosomes.
This uncontrolled release of the melanin stimulating hormone is called the MSH cascade and will be reflected in
the butterfly pattern of pigmentation that is commonly seen in the center of the face, across the upper lip, and
forehead.
Question: What would stop the keratinocyte from picking up melanosomes?
Answer: This may happen because the keratinocyte cell membrane is not viable or flexible enough to practice
the endocytosis method of picking up the melanosomes that have been released into the extracellular space.
Essential fatty acid deficiency is a leading cause of poor cell membrane health and will influence cell membrane
viability.
This would reflect in an unhealthy epidermis that may be indicating other keratolytic disorders, and have
Essential Fatty Acid Deficiency. This can be recognized by dry skin, flakey, ridged finger nails and scaly body skin
and scalp.
What also needs to be remembered is that if the keratinocyte cell membrane is unviable so will be the
melanocyte cell membrane, a combination of both will lead to poor dispersion of pigment across the spinosum
layer.

Question: Where will the melanosome fall if not picked up by a keratinocyte?
Answer: Our base knowledge of skin tells us that the keratinocyte mother cell and melanocytes are attached to
the basal lamina of the dermal‐epidermal junction by keratin filaments called hemi‐desmosomes, this junction is
made up of 3 layers of collagen connective tissue and is permeable, and in some literature is referred to as the
dermojunction.
The dermojunction is made of sinusoidal connective tissue, so named, because it is filled with holes, pockets and
channels that allow the movement of fluids, and immune cells to move through from the dermis to epidermis.
The epidermal side of this junction is called the basal lamina, and it is onto this that the melanosome would rest
after not being picked up by the ascending keratinocyte. If this is an ongoing problem then large amounts of
pigment could accumulate into this junction.
Question: What would happen to the dermal epidermal junction as it deteriorates with age or injury?
Answer: Pigment can accumulate in the dermal epidermal junction for many years before it becomes noticeable
as pigmentation. The aged skin will lose the strength and integrity of the junction and this will result in looseness
and separation of the epidermis from the dermis.
All of the accumulated pigment that was in the junction will be released into the dermis as a result of the dermal
epidermal junction collapse. This is called dermal pigmentation.
Question: What will be the result if the spinosum layer were not viable enough for the even dispersion of
pigment?
Answer: Accumulation of pigment into smaller areas of the spinosum layer, which may reflect as pigmentation.
Question: What will be the result if the melanocyte to keratinocyte ratio were not the normal 1 to 30?
Answer: One has to understand that the melanocyte is programmed to make a specific amount of melanosomes
relative to the strength and length of sun exposure it has experienced. These melanosomes should be released
across to thirty keratinocytes for pickup.
If the melanocytes dendrites are not long enough to reach thirty keratinocytes, or there is a lesser number of
keratinocytes to pick up the melanosomes then it is likely that the thirty cells worth of melanosomes will be
released out to perhaps only 10 cells.
This would reflect in a heavy deposition of pigment into a very small area, with the chances of many
melanosomes spilling into the dermal epidermal junction.
I hope that by my answering these few questions it has helped you to understand a little more about the
melanocyte and its very close partner the keratinocyte.
There are still a few more facts that have to be covered in relation to the causes that lead to the skin condition
pigmentation, apart from the skins exposure to UVR.
These causes will be found during the consultation process if care is taken to ask the right questions, and it must
not be forgotten that UVR plays a role when combined with any of the following influences.
There are more causes that lead to the skin condition pigmentation. Many will be outside influences such as
photo sensitizing chemical and medications.
1.
Hormones that may be altered due to the contraceptive pill or pregnancy. Hormones that may be altered due to I V F and peri pause medications. Medications that are progesterone based. We have discussed this briefly in the previous Q&A and have learnt that the chemicals stimulated by pregnancy or some medications cause an uncontrolled release of the melanin stimulating hormone, sometimes referred to as MSH cascade. This results in the facial butterfly pattern of pigmentation commonly seen in the centre of the face. There are a few more interesting facts to learn about these hormonal events. 1. The oral contraceptive pill and pregnancy have both been seen to have a genetic component to them, and mothers or sisters often show the same pattern of pigmentation during pregnancy or when taking the pill. The IVF, progesterone based, and peri pause medications have shown to cause the same pattern of pigmentation but without any genetic history of other family members showing the same. This pattern of pigmentation seems to be directly related to the medications taken. It is advised that the client must avoid getting sun burnt whilst on the medication or when pregnant. This is to avoid the risk of permanent cellular damage to the melanocyte whilst it is under the duress of creating a large amount of pigment. If, "by chance", cells were irreparably damaged when making such a large amount of pigment, in the future it may continue to make many melanosomes even under the influence of very weak UVR. All of the following medications or chemicals have the ability to reduce the natural burn time and in doing so cause the skin to sun burn in less time than the natural Photo type usually allows. Not all will result in pigmentation unless of course the skin has been assessed as "high risk" for pigmentation, however, a sun burnt cell may result in a rogue cell, and cause skin cancer. 1. Medications that are cortisone or steroid based. Medications that are photosensitisers such as oral or topical chemotherapy medications that include immuno‐modulators such as Aldara or Zyclara or 5‐Fluorouracil. Medications that reduce burn time such as antibiotics, and antifungal medications. Medications that reduce burn time such as those for by‐polar disorders (Chlorpromazine and Lithium). Photosensitising chemicals including emollient esters such as bergamot essential oil. Research has brought to light, products commonly used by skin treatment therapists and their clients that also are known to be photo‐sensitizers. For further study: Read pages 71 & 72 of my Advanced Skin Analysis book or page 133 of my Cosmetic Chemistry book. If the established cause of the pigmentation is induced by medication, be it topically applied or orally taken, no guarantee of improvement can be made, until the medication has been discontinued. We have covered some of the medications and chemicals that cause or aggravate the formation of the skin condition pigmentation, or cause cellular inflammation of the melanocyte and keratinocyte. In addition to these causes, the level of cellular damage, and cell membrane health, must also be taken into consideration. These causes will also be discovered during the consultation process and include the nutrition and genetic history. Knowing what a cell requires to function is a key to finding the “leading cause” of a skin condition. This is because a cell will only make as good as what it receives nutritionally or the health of the surrounding cells that it works in synergy with. You may remember from a previous lecture that the health of the keratinocyte cell membrane is paramount in the formation of the ceramide component of the bi‐layers. Ceramides are the emulsifier of the sebaceous and sudoriferous secretions that make up the acid mantle. There are several nutrients that the keratinocyte requires that it cannot metabolise; they are E.F.A’s and Choline. Both are essential in preventing lipid peroxidation and controlling cellular inflammation. Essential Fatty Acid Deficiency (E.F.A.D) is a common nutritional deficiency that will result in many skin cells being compromised and unable to practice efficient, active and passive transfer of nutrients and cell waste. This may result in a keratinocyte that will be unable to build the skin barrier defense systems required to protect the inner layers of skin. In addition, a poor quality spinosum layer will mean poor deposition of pigment throughout the epidermis resulting in pigmentation. The innate immune system may also become compromised leaving the skin more susceptible and sensitive to outside influences. We will now discuss another leading cause of pigmentation, Genetics and the ability to tan. We each have a colour of skin that has been roughly divided into 6 categories. With the mixed ethnicities of today that could be expanded into 18 categories. Knowing the skins burn time during exposure to UVR has become of increasing importance for the skin treatment therapist of today. We learnt in an earlier class that a significant difference between black and white skin is in the length of the dendrite of the melanocyte. Enabling the melanocyte in a black skin to place pigment higher into the spinosum layer, thereby affording earlier protection from extreme sun exposure. It has recently been observed that some white skin melanocytes are showing a change in the length of dendrite. These are skins, that have been living in hot sunny climates, for a period of time and it is thought that the melanocyte is compensating for extended sun exposure by trying to place pigment higher into the spinosum layer offering earlier protection. The resulting malformed dendrites, will definitely be responsible for uneven deposition of pigment throughout the spinosum layer. Knowing the skins burn time and risk for pigmentation during exposure to UVR has become of increasing importance for the skin treatment therapist of today. So many of the treatment modalities used today involve chemicals, heat, and light or electrical impulses all of which if not controlled can burn, pigment or scar skin. Therefore, the clarification of the skin Photo Type, Risk for pigmentation, and Burn time should be established early in the skin analysis process. This classification will dictate the treatment protocols chosen at the end of the consultation and when preparing a treatment program for the client. The original Fitzpatrick chart, established the “minimal erythema dose” also known as the M.E.D. One MED was the point of reference used to describe the time it took for a skin colour to burn, and it is still used as an indication of a sunscreens sun protection factor also known as the S.P.F. What now must be taken into consideration is the Risk for pigmentation, skin cancer and keloid scarring. Every skin colour comes with risk. What we have learnt more recently about skin colour is called the “minimal melanogenic dose” or MMD. MMD is the terminology used when describing the melanocytes ability to protect skin. It has been proven, that even the fairest skin can accumulate melanin within the epidermis over a period of a summer. We refer to MMD as the melanocytes ability to make melanin and as a result the skins ability to tan. With the mixed ethnicities of the world today there are many hidden dangers and hair and eye colour as an indication of photo type is now misleading. The melanocortin 1 receptor gene or red hair gene as it is often called can also be hidden, this means that the clients risk for skin cancer may not be obvious. If the genetic history has a combination of the ability to tan, and the red head gene, it should be considered a recipe for disaster. This is because the ability to tan often means that the skin has long hours of unprotected exposure. This could culminate into skin cancer and pigmentation as the melanocyte and keratinocyte cells age. The use of skin diagnostic equipment is one way to analyse the skins photo type and risk for pigmentation. Along with sensible questions about genetic heritage, tanning ability, red head gene and sun bed usage. Let us review those questions that are on the client consultation form, you will see I have written a brief rationale alongside each question. 1. Genetic heritage: Darker skins naturally come with risk for pigmentation (photo type 4 to 6) however, the photo type three can accumulate colour over a summer so the skin colour looks a photo type 4.This is because of minimal melanogenic dose. (MMD) Tanning ability: It is during the teenage years, when most people will have gained a tanning experience, use this time span to determine skins tanning ability. Include sun burn history into this story to gain knowledge about body areas that may have been repeatedly sun burnt. You can then check these areas for other skin anomalies. Red Hair gene: Carries the potential for the red pigment pheomelanin to oxidize and create the super oxide anion free radical which can then damage the mitochondria DNA of the melanocyte. This leads to the risk of skin cancer, because of the loss of apoptosis ability. Tanning bed usage: The bandwidth of UV that is used in many tanning beds is U.V.A.; it is a given that tanning beds will cause pigmentation, also we know that this bandwidth of light will accelerate the ageing process by increasing the enzyme collagenase. This enzyme will denature the supporting collagen fibril of the dermis and also accelerate vascular damage. It has been postulated that "for every ten tanning bed sessions" the skin will age forward by one year. The causes that have been covered in this module are the most common, and there are many more, you will have to be ever vigilant in uncovering these. Always use a reference web site or book that will give you updated side effects of medications. In addition, stay abreast of chemicals within the cosmetic industry that may be photo sensitisers, never become complacent. Pigmentation is difficult enough to treat as it is, and will not respond unless all aggravating factors have been removed. To move to the next unit of learning please complete the assessment page. When this is completed you may then move to the next unit called Visual diagnosis of pigmentation. Prior reading; to reinforce the subject of cause and effect and to help with the next unit of learning please read pages 73 to 77 in the advanced skin analysis book. Please study the flow charts to learn how to carry information across to the cells and systems affected by a leading cause.

Source: http://www.pastiche.co.nz/e-learning/CN-04-pigmentation.pdf