Understanding the causes of abnormal pigmentation is crucial for treatment success, as this is a condition that depending on the cause will require a specific or combined approach to deliver results. There are a number of phases in the development of pigmentation but the various treatment modalities currently available will generally work only on one of those phases.
The “one solution fits all” mentality will ultimately deliver poor results and may cause either hyper or hypo pigmentation, particularly in skins that are of multiple genetic pigmentation we need to understand the anatomy and physiology of the cells and systems that create melanin and why and how things can go wrong. Let’s dispel a few myths regarding the difference between dark and fair skin. We now know that between these two skin colours:
. The number of melanocytes are similar
. There is a differing ratio of red to brown pigments
. There is a differing size of the melanosome that carries the pigment
. There is a differing size of the pigment granule
It is also important to note that the length of the dendrite of the melanocyte affects skin tone.
What type of skin?
We have historically used Fitzpatrick skin type classification (six skin types) to differentiate skin colours and their reaction to sun exposure, and it was a common assumption that the skin’s burn time correspond to the skin colour. This initial research was carried out in the 1930s. Since then, a rich mix of ethnicities has been developed and the six skin tones once used are no longer an accurate or useful tool. This is mostly relevant in skin that appear dark, but carry the red head (MC1R) gene.
Understanding burn time
When exposed to UVR, melanocytes produce two types of melanin: Brown pigment (eumelanin) and red pigment (pheomelanin). Eumelanin tans the skin and provides cells with some UV protection. It is part of the cell’s barrier defense systems.
Pheomelanin makes the skin more responsive to the effects of UV light (burn time) and if the ratio of red to brown is high, the skin becomes extra responsive to the effects of sunlight or other UV generating devices such as sunbeds. It is this ratio of red pigment to brown pigment that provides a greater indicator of susceptibility to sun damage.
MC1R red head gene
Red head family history types have a gene known as the Melanocortin-1 Receptor (MC1R) and with this gene the pheomelanin is altered in such a way to allow it to be more easily converted into a free radical upon exposure to UV light, generating the superoxide anion which can damage nearby skin cells, including the DNA of melanocytes. Consequently, individuals with the red head gene face a higher risk for skin cancer and related anomalies. The MC1R gene can be well hidden, thus genealogy should always be checked when in doubt.
Darker skin tone
Healing efficacy becomes an issue in darker and blended skin tones. These skin types often look fair but have hidden darker skin tone and/or red head gene, and is most susceptible to pigmented skin disorders and anomalies. It is also these darker and blended skins that will more readily suffer from post inflammatory pigmentation. This can occur from trauma caused by skin disorders as well as therapeutic interventions, infections, allergic reactions, etcetera.
Keratinocyte/ melanocyte health
An often overlooked factor when investigating the cause of abnormal pigmentation is the health of the two main cells responsible-keratinocyte and melanocyte. When contemplating pigmented skin disorder, always attempt to link cause to the effect on cells and systems. Try to think three dimensionally about the health and efficiency of the keratinocyte, melanocyte, dermal epidermal junction, and cell membrane permeability / strength, as these all play a role in the formation of pigmentation. For example, Essential Fatty Acid Deficiency (EFAD) will impair melanocyte cell dendrite development and affect the melanosome transfer to keratinocyte. EFAD will also affect the cell membrane of keratinocyte, fostering lipid peroxidation and poor formation of the bilayers of the stratum corneum , resulting in poor quality ceramides of low quantity, consequent fast TEWL and a reduction of the free water in the epidermis. Epidermal skin cells work in synergy, particularly the keratinocyte and melanocyte, and the health of one cell may affect another. Never think of a cell as a standalone unit.
Understanding cause and effect
Understanding what has happened to the epidermal cells and systems will ensure that the correct modality is chosen and determine if the condition will even respond to treatment. There are a number of causes of pigmentation including:
Melanocyte cellular senescence (cellular alzheimer’s) can be termed as the twilight state of cellular old age, where the cell is very much alive but distorted in form and function. Melanocytes are long living and slow cycling. This can mean that cellular senescence can continue for a long time, as there is no major resource of new cells. Melonocyte cellular senescence will cause the melanocyte to behave erratically, producing pigmented areas of varying sizes and shapes. They are more often found in older clients, who generally have a history of extensive sun exposure, chemical abuse, or possess the red head gene.
DNA damage is a condition where cell memory is impaired resulting in a continuing cellular replication with the same damage. This is the most difficult type to repair and the attempted prevention by the use of antioxidants is vital with individuals possessing the red head gene as it is genetic and can’t be easily avoided (except avoiding sun exposure). Solar lentigos and vitiligo are examples of a DNA damaged melanocytes.
Dendrite shortening is the result of cell membrane damage, and as previously mentioned, essential fatty acids are required for cell membrane health. Healthy cell membranes ensure active and passive transfer of nutrients, oxygen and cell waste, and are essential for dendritic cells. EFA’s are not metabolized and must be obtained via diet.
Lipid peroxidation or lipofuscin is the only form of pigmentation that does not involve the melanocyte as it is a yellow-brown pigmented waste material deposited in many nerve and skin cells. It is believed to interfere with cellular metabolism, and composed of cross-linked, peroxidised lipids and cross-linked proteins. Deposits of lipofuscin debris increase with age as the body’s ability to repair itself decreases. Tyronaise inhibitors would not help in treating this type of pigmentation.
The MSH Cascade is uncontrolled chemical stimulation of the pituitary gland causing a cascade of the melanin-stimulating hormone, resulting in continual formation of the pigment carrying melanosome. MSH accelerates the melanogenesis process. Hormonal melasma and chlosama are examples of the MSH cascade, where the hormones are either naturally or artificially stimulated (contraceptives, fertility programs, peri pause medication of pregnancy) to initiate melanin stimulating hormone (MSH) production. In some cases a hereditary predisposition may exasperate the condition.
The red head gene (MC1R) is genetic and can often be hidden . The red pigment pheomelanin can oxidize and create super oxide anion free radical, causing DNA damage of melanocyte nucleus and mitochondria. Actinic and solar keratosis are prime examples of problems caused by the red head gene, and the scrutiny of client’s sun burn history or repeated exposure areas will help diagnosis.
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