Depigmentation and Vitiligo

What is Depigmentation?

Depigmentation refers to pigment loss in the skin. It is the lightening of the skin which can be due to a skin pigmentation disorder or deliberate cosmetic change of skin color.

When the skin is depigmented, it turns white. Such depigmentation can be complete (as in the case of generalized vitiligo) or partial (caused by injury to the skin). Depigmentation can also be permanent (for example, albinism) or temporary (for example, the yeast infection called tinea versicolor).

The specialized skin cells responsible for skin color are called melanocytes. Therefore, depigmentation involves melanocytes.

Melanocytes are found in the epidermis and produce melanin, the pigment that gives the skin its color.

Depigmentation can result from one of the following basic presentations:

• Reduced production of melanin from normal population of melanocytes – this is the case in albinism, tinea versicolor and pityriasis alba
• Reduced or no production of melanin from no or sparse melanocyte population – this is what happens in the case of vitiligo and piebaldism

How Depigmentation Occurs

To understand how depigmentation occurs, it is necessary to first understand how the skin is pigmented.

Melanin is produced by melanocytes in the melanosomes of the epidermis. This is usually in response to the penetration of the skin by ultraviolet light either from sunlight or special UV lamps and other such sources.

Melanin is therefore a photosensitive compound that protects the skin from the harmful effect of UV radiation.

The released melanin is transported from the lowest layer of the epidermis to the surface by another type of skin cells called keratinocytes.

Therefore, when the population of melanocytes is reduced or the production of melanin falls, the skin loses its color. Depending on the size of the area of the skin affected, depigmentation may leave white spots or large white patches all over the skin.

Each depigmentation spot (especially vitiligo spot) is made up of 3 color zones.

The widest zone is the central one. It is usually white and, usually, there are very few melanocytes in the skin around there. Therefore, melanin production would have dropped to zero.

Surrounding this zone is a small zone with tan, lighter color. This area is experiencing rapid hypopigmentation with melanocyte population and melanin production falling off. It represents the expansion of the central depigmented zone.

The third zone is a border between the depigmentation spot or patch and normal, pigmented skin. It is usually of a darker color than the first 2 zones and the melanocytes there are only just experiencing diminishing productivity.

Causes of Depigmentation

There are different causes of depigmentation although they all involve the destruction or desensitization of the melanocytes. Some of these causes are discussed below.

Autoimmune Disorder

Depigmentation is often the result of autoimmune attack on melanocytes. In fact, the autoimmune theory of vitiligo is regarded as the most common cause of the skin pigmentation disorder.

When the cells of the immune system sees melanocytes as foreign bodies, they attack these specialized skin cells. There are clinical evidences that show that vitiligo patients have high levels of freely circulating melanocyte-specific antibodies and even CD8+ T cells.

Therefore, depigmentation involves both cellular and humoral immune responses.

This cause is also the reason vitiligo often presents along with other autoimmune disorders such as thyroid dysfunction, alopecia areata and diabetes mellitus.

By progressively destroying melanocytes, the autoimmune attack causes a sharp reduction in the production of melanin and a rapid spread of white, depigmentation patches all over the body.

Defective Melanocytes

Another cause of depigmentation is attributed to intrinsic defects in melanocytes.

Defective melanocytes do have shorter lifespans than normal melanocytes. There are a number of structural or functional defects that could leave melanocytes vulnerable.

For example, cellular metabolism is affected by the abnormal, rough reticulum found in some melanocytes.

Another common defect in melanocytes can be found in surface proteins serving as homing receptors. The cells of the immune system may fail to identify these malfunctioning surface proteins and then attack the defective melanocytes thus reducing melanin production and causing depigmentation.

Oxidative Stress

Oxidative stress is another important cause of depigmentation. It describes the cumulative effect of harmful free radicals and reactive oxygen species such as hydrogen peroxide.

These oxidative compounds are produced from cellular metabolism and they are normally removed from the skin by antioxidants such as the enzyme called catalase.

However, if the levels of antioxidants in the skin are reduced or if the oxidative stress overcomes these antioxidants then the cells of the skin such as melanocytes are directly affected.

These oxidizing agents can break down melanocytes and shut down the production of melanin.

The presence of oxidized compounds in depigmented skin can be detected by bluish or yellow-green fluorescence of vitiligo patches under special lamps.

Toxic Chemicals

Toxic chemicals also cause depigmentation by mechanisms similar to oxidative stress. The only difference is that the oxidizing agent is introduced to the skin instead of produced from cellular metabolism.

Phenolic compounds which are commonly found in household and industrial solvents are important examples of this cause of depigmentation. Therefore, repeated and prolonged exposure to materials containing this group of compounds should be avoided.

Furthermore, some active ingredients of cosmetic products can depigment the skin.

Hydroquinones are skin-whitening agents that reduce melanin production. However, monobezone is the most powerful skin-bleaching product commonly sold. It is mostly used to deliberately cause skin depigmentation.

Nerve Damage

There are recorded vitiligo cases which developed soon after nerve damage.

The changes in the neurochemicals released at nerve endings following nerve damage are responsible for the depigmentation of the skin around the area of injury. The released neurochemical factors from the endings of damaged nerves may kill off melanocytes.

Fungal Infection

Some forms of depigmentation are also due to fungal infections on the skin itself.

A prime example of skin diseases associated with this form of depigmentation is tinea versicolor. Tinea versicolor is caused by the fungi, Malassezia globosa and Malassezia furfur. This is an even more common kind of skin depigmentation than vitiligo.

Unlike vitiligo depigmentation which is mostly a cosmetic change, depigmentation caused by fungal infections requires the elimination of the causative fungi for melanin production to resume.

Genetic Disorder

Genes play a strong role in pigment disorders. For example, albinism is a genetic hypopigmentation disorder.

However, even vitiligo has some genetic components. There are specific polymorphic genes that determine the susceptibility of individuals to depigmentation.

For example, the alleles of Apa-I gene are associated with varying risks of depigmentation.

Genetics can also determine skin pigmentation in other ways. In fact, some of the above factors including the autoimmune theory, intrinsic defects in melanocytes and oxidative stress can be explained in part by genetic differences in the population.

Classification of Vitiligo Depigmentation Spots

The appearance and distribution of depigmentation spots and patches are used to classify vitiligo.

When classified by distribution of depigmentation, vitiligo can be one of localized, generalized or universal.

The area affected by depigmentation is restricted in localized vitiligo. Examples of such cases are focal vitiligo in which depigmentation is found only on the face; and mucosal vitiligo that affects only mucosal surfaces.

Generalized vitiligo affects more body parts and the distribution of the depigmentation spots is scattered. Universal vitiligo refers to full body or near complete depigmentation.

Depigmentation as a Vitiligo Treatment Option

While depigmentation is the cause of vitiligo, sometimes it is deliberately done as a last resort in the treatment of vitiligo.

Since the contrast between depigmented patches and the normal, pigmented skin is the aesthetic problem of vitiligo, full body depigmentation is sometimes recommended for vitiligo patients when the vitiligo patches cover more than half of the body surface.

The rationale for the depigmentation of the normal skin still left is to achieve an even color tone for the whole body.

Depigmentation should only be considered when repigmentation is unachievable following repeated treatment failure with repigmentation therapies.

Even then any patient opting for depigmentation should be fully briefed on the treatment.

Although concentrated phenol solutions have been used to depigment the skin, monobenzone is the recommended medication for depigmentation.

What is Monobenzone?

Monobenzone is the monbenzyl ether of hydroquinone. It is available as a cream in 20%, 30% and 40% strengths.

Monobenzone stops the production of melanin by destroying melanocytes and causing permanent depigmentation of the skin. However, since monobenzone can only kill the melanocytes in the epidermis and not in the follicles, dark patches of pigment may appear on the skin later. These can also be removed with monobenzone.

Still, patches of color may persists along with rashes and itching which are side effects of monobenzone.

Therefore, patients opting for full body depigmentation must be prepared to camouflage and treat rashes and occasional spots of melanin.

When using monobenzone for the first time, the 20% concentration is recommended. It should be applied on one arm once daily for a week. If this well tolerated, then other exposed parts of the body should be covered with the cream twice daily.

Thereafter, other parts of the body should be depigmented too.

The entire monobenzone therapy usually takes 1 – 2 years and may even take longer. The general advice is not to apply monobenzone to every part of the body at once. This is because it is usual for depigmentation to occur in another part of the body different from where monobenzone is applied.

Other precautions to take including avoiding skin-to-skin contact for at least 2 hours after application. Contact with the eyes and mucosal surfaces should be avoided. Therefore, bed time application of monobenzone is not recommended.

When the 20% strength produces unsatisfactory results, 30% and 40% monobenzone should be used.

Lastly, since depigmentation stops the production of melanin, the skin is placed at greater risks of ultraviolet damage including sunburns. Therefore, sunscreens should always be worn over depigmented areas of the skin.