Facial Melanoses Dr. Laxman Mavarkar

Conflict of Interest

• Conflict of Interest: None

IntroductionFacial Melanoses is a form of hyperpigmentation of

the face associated with increased melanin.

Normal Skin Color

• Normal skin colour is

determined mainly by

melanin.

• Haemoglobin (in both the

oxygenated and reduced

state) and carotenoids also

contribute to skin colour .

Differences in Skin ColorRacial and ethnic differences in skin color are related to the number, size, shape, distribution of melanin-laden organelles called melanosomes. These are produced by melanocytes.

Melanin Synthesis• Tyrosinase is the key

enzyme in the melanin biosynthetic pathway.

• Two major forms of melanin are produced in melanocytes: Brown-black known as eumalnin and yellow-red known as pheomelanin .

Skin Types

Causes of facial melanoses

• Melasma (chloasma)• Lichen planus pigmentosus (LPP)• Riehl's Melanosis (pigmented contact dermatitis).• Periorbital melanosis (POM) (or dark circles)• Postinflmmatory hyperpigmentation.• Exogenous ochronosis• Acanthosis Nigricans.• Poikiloderma of Civatte• Freckles• Lentiginosis

MelasmaMelasma is a chronic skin disorder that results in symmetrical, blotchy, brownish facial pigmentation.

What causes melasma?

• The cause of melasma is complex.

• There is a genetic predisposition to melasma , with at

least one-third of patients reporting other family

members to be affected.

• Known triggers for melasma include- Sun exposure,

Pregnancy, Hormone treatments, Hypothyroidism and

thyroid autoimmunity .

What causes melasma? (Cont.)

Recent study demonstrated an increased expression

of estrogen receptors on skin with melasma, as

compared to normal skin.

Who gets melasma?• Melasma is more common in women than in

men.• It generally starts between the age of 20 and 40

years.• Melasma is more common in people that tan

well or have naturally brown skin type 3 and 4 compared with those who have fair skin (skin types 1 and 2) or black skin (skin types 5 or 6).

What are the clinical features of melasma?

• Melasma presents as pigmented macules and larger patches. These are found on both sides of the face and have an irregular border. There are several distinct patterns.

• Centrofacial pattern: forehead, cheeks, nose and upper lips.

• Malar pattern: cheeks and nose.• Mandibular pattern: jawline.• Brachial type of melasma affecting shoulders and upper

arms.

Type of melasma Type of melasma Clinical features

Epidermal •Well-defined border •Dark brown colour •Responds well to treatment

Dermal •Ill-defined border •Light brown or bluish in colour •Responds poorly to treatment

Mixed

•The most common type•Combination of bluish, light and dark brown patches •Partial improvement with treatment

How is the diagnosis of melasma made?

• Diagnosis is made clinically.

• Occasionally, skin biopsy may be performed to make or confirm the diagnosis of melasma.

What is the Treatment of Melasma?

• A variety of treatments are effective only at lightening

pigment.

• Discontinue hormonal contraception.

• Use broad-spectrum sunscreens.

• Use a mild cleanser, and if the skin is dry, a light

moisturiser.

Topical Therapy• Tyrosinase inhibitors are the mainstay of treatment.• Many tyrosinase inhibitors, such as hydroquinone, kojic

acid, azelaic acid, phenols, and arbutin have been tested in pharmaceuticals and cosmetics for their capability of preventing overproduction of melanin.

• Hydroquinone(2% to 4%) is one of the most frequently prescribed ingredients among the conventional skin-whitening agents.

• It is thought to be mutagenic to mammalian cells and cytotoxic to melanocytes.

Topical Therapy (Cont.) • Hydroquinone may cause

irritant/contact dermatitis in 25% of patients.

• If used in higher concentration and longer duration causes exogenous ochronosis (a bluish grey discolouration).

Exogenous ochronosis

Banana-shaped collagen fibers covered by ochronotic pigment .

Topical therapy for melasma

• Azelaic acid 15%-20%.

• Retinoic acid 0.025%-0.1% .

• Kojic acid

• Ascorbic acid (vitamin C).

• Alpha hydroxyacids like glycolic acid and lactic acid.

• Others like arbutin and deoxyarbutin (from berries),

licorice extract, rucinol, resveratrol and tranexamic

acid.

Do lasers work for melasma?

• Lasers may be used in melasma, but they generally

produce only temporary results.

• Laser therapy is not the primary choice to treat melasma

as studies reveal little to no improvement in the

hyperpigmentation for most patients.

What is the prognosis for melasma?

• Results take time and rarely completely successful.

• Unfortunately, even in those that get a good result from

treatment, pigmentation may reappear.

Lichen Planus Pigmentosus

• Lichen planus pigmentosus is a variant of Lichen

planus that tend to occur in darker pigmented skin.

• It occurs predominantly in female in the third or

fourth decade of life.

• LPP affect mainly face and neck.

• They are slate gray macules and patches.

• In contrast to the classical lesions of lichen planus,

the lesions of LPP are usually asymptomatic.

Lichen Planus Pigmentosus (Cont.)

Lichen Planus Pigmentosus (Cont.)• This condition can

persist from 2 years to 21 years.

• The mucous membranes, palms and soles are usually not involved.

• It is typically bilaterally symmetrical.

Diagnosis of LPPFocal basal cell vacuolization with dermal melanophages, and a sparse lymphohistiocytic inflammation

Treatment of LPP• Lichen planus is a self-limiting disease that usually

resolves by its own.

• Unlike other type of lichen planus LPP is usually

resistant to treatment.

• Systemic steroids, oral metronidazole,oral acitretin and

colchicine.

• Topical steroids, topical calcineurin inhibitors.

Pigmented Contact Dermatitis(Riehl's Melanosis )

This pigmented contact dermatitis is caused by antigens

present in the cosmetics and fragrances which include

chromium hydroxide, aniline and azo dyes, mercury

compounds, formaldehyde. Sometimes occupational

allergens like coal tar, asphalt and mineral oil.

Pigmented Contact Dermatitis• The hyperpigmentation in pigmented contact

dermatitis is postulated to be caused by frequent and

repeated contact with small amounts of sensitizing

allergens.

• Many cases are preceded by mild erythema, edema,

and pruritus.

• It presents as patches of diffuse gray-brown

pigmentation on forehead, scalp, face, and neck .

Incidence of Pigmented Contact Dermatitis

• Women appear to have a greater predilection for pigmented

contact dermatitis.

• Majority of cases appear to occur in young to middle-aged

women.

Pigmented Contact Dermatitis

Pigmented Contact Dermatitis (Cont.)

UV exposure may

contribute to the

hyperpigmentation in

select cases, which is

supported by the fact that

some of the chemicals

implicated are known

photosensitizers

Diagnosis of Pigmented Contact Dermatitis

Dermal inflammation, prominent pigment incontinence

Diagnosis of Pigmented Contact Dermatitis (Cont.)

Patch test: Perform closed

patch testing with the

standard series, cosmetic

series, fragrance series, and

patient's personal products.

Treatment

• Complete avoidance of the suspected allergen is necessary,

and removal of these agents often leads to gradual

improvement.

• Mild topical steroids can be used at night.

• Sunscreens during day time.

Periorbital Melanosis(Dark circles)

Periorbital melanosis (Dark circles) Cont.

• This is a common worldwide problem.

• Complex in pathogenesis, and lacking straightforward

therapeutic options.

• Periorbital melanosis is defined as bilateral, homogeneous

hyperchromic macules and patches primarily involving the

lower eyelids but also sometimes extending towards the

upper eyelids.

Dark Circles

DC are caused by multiple etiologic factors that include

genetic,postinflammatory hyperpigmentation secondary to

atopic or allergic contact dermatitis, faulty habits,

periorbital edema, superficial location of vasculature, and

shadowing due to skin laxity, etc.

Periorbital Melanosis• Prevalence of this condition is estimated to be 30.76%.

• Studies shows that most common age group was 16-25 years .

• Higher preponderance for females over males.

• Genetic conditions are not necessarily congenital (present at

birth) may manifest later(genotype is fixed at conception, but

the phenotype may not manifest until adult life).

Periorbital Melanosis (Cont.)

Periorbital Melanosis (Cont.)

• Commonest type of periorbital melanosis in Indian

patients to be of genetic type and followed by vascular

and post inflammatory type.

• In vascular type of dark circle appears to be due to a

combination of transparency of the overlying skin and

dermal vascularity

Diagnosis

A thorough history and

clinical assessment of the

lower eyelids and cheeks.

Treatment

• Medical line of treatment is disappointing.

• Calcineurin inhibitors helpful in postinflammatory type of

periorbital melanosis.

• Lasers like Q-switched lasers and fractionated resurfacing are

more useful in treating the pigmentation.

Postinflammatory Hyperpigmentation

• Postinflammatory hyperpigmentation is caused by 1 of 2

mechanisms that result in either epidermal or dermal

melanosis.

• The epidermal inflammatory response (Ex: dermatitis) results

in the release and subsequent oxidation of arachidonic acid to

prostaglandins and leukotrienes.

PIH

• These inflammatory products stimulate epidermal

melanocytes, causing them to increase the synthesis of

melanin and subsequently to increase the transfer of

pigment to surrounding keratinocytes.

• Such increased stimulation and transfer of melanin

granules results in epidermal hypermelanosis.

PIH (Cont.)

On the contrary, dermal melanosis occurs when

inflammation disrupts the basal cell layer, causing melanin

pigment to be released and subsequently trapped by

macrophages in the papillary dermis, also known as

pigmentary incontinence.

PIH (Cont.)

• Postinflammatory hyperpigmentation is a universal

response of the skin, but it is more common in

individuals with darker skin (Fitzpatrick skin types III

to VI).

• Postinflammatory hyperpigmentation can be caused by

any inflammatory process of the skin.

Presentation of PIH

The distribution of the hypermelanotic lesions depends on the location of the original inflammatory dermatosis

Presentation of PIH (Cont.)

• Postinflammatory hyperpigmentation can occur with various

disease processes that affect the skin. These processes include

allergic reactions, infections, trauma, and phototoxic

eruptions.

• Dermatological procedures also can causes PIH.

• PIH is more common on the face than other part of the body.

Presentation of PIH (Cont.)Common inflammatory diseases that result in postinflammatory hyperpigmentation include acne excoriée, lichen planus, systemic lupus erythematosus and chronic dermatitis.

Presentation of PIH (Cont.)Furthermore, lesions of postinflammatory hyperpigmentation can darken with exposure to UV light..

Wood Lamp

• A Wood lamp examination enables distinction of epidermal

postinflammatory hyperpigmentation (PIH) from dermal

postinflammatory hyperpigmentation.

• Epidermal lesions tend to have accentuated borders under a

Wood lamp examination, whereas those of dermal lesions

appear poorly circumscribed and are not accentuated with a

Wood lamp examination

Skin BiopsyIf a history of preceding inflammatory dermatosis is unclear or absent, skin biopsy is warranted to exclude other underlying causes of hyperpigmentation.

Histologic Findings

• Epidermal postinflammatory hyperpigmentation involves

increased melanin pigment in the basal cell layer of the

epidermis. Occasionally, giant melanosomes are evident in the

epidermis.

• Dermal postinflammatory hyperpigmentation involves

melanin pigment in the upper dermis, with pigment

incontinence due to increased numbers of melanophages in the

papillary dermis.

Treatment

• The treatment of postinflammatory hyperpigmentation

tends to be a difficult and prolonged process that often

takes 6-12 months to achieve the desired results.

• Each of these treatment options potentially improves

epidermal hypermelanosis, but none is proven effective

for dermal hypermelanosis.

Treatment (Cont.)

• Daily use of a broad-spectrum sunscreen (sun protection

factor [SPF] 15 or greater) is an essential part of any

therapeutic regimen.

• A variety of topical treatments have been used to treat

epidermal postinflammatory hyperpigmentation, with

varying degrees of success. These agents include

hydroquinone, tretinoin cream, corticosteroids, glycolic

acid (GA), and azelaic acid etc.

Treatment (Cont.)

• Combination of topical creams and sunscreens may be

necessary for significant improvement. They are only effective

for epidermal hyperpigmentation.

• Laser treatment may be able to address dermal pigment

deposition(1064-nm Q-switched Nd:YAG laser).

Prognosis• Postinflammatory hyperpigmentation tends to fade with time

and therapy.

• Remnants of epidermal hyperpigmentation may persist for

indefinite periods, typically 6-12 months, after the initial

inflammatory process.

• Dermal postinflammatory hyperpigmentation may even persist

for many years.

Poikiloderma of Civatte

Presents as reticulate

spots of

hyperpigmentation and

atrophic

hypopigmentation with

telengiectasia.

Poikiloderma of Civatte (Cont.)

• Poikiloderma of Civatte is most commonly seen in middle-

aged, postmenopausal women.

• Many consider it to be a reaction pattern of the skin and not a

disease. The term poikiloderma refers to the combination of

atrophy, telangiectasia, and pigmentary changes.

Poikiloderma of Civatte (Cont.)• Patients usually complain of chronic reddish-brown

discoloration on the lateral cheeks and neck.• Lesions usually are asymptomatic, but occasionally, patients report mild itching/ burning.

Causes

• Photosensitizing chemicals in perfumes or cosmetics have

been implicated in the pathogenesis of poikiloderma of

Civatte.• Chronic exposure to ultraviolet light appears to be a primary

etiologic factor, which is supported by the finding that lesions occur on sun-exposed areas.

Histologic Findings

Epidermal atrophy, telengiectasia, and dermal fibrosis

Treatment

• No specific medical treatment exists for poikiloderma of

Civatte.

• Educating the patient about avoiding sun exposure and the

proper use of sunscreens is most important.

• Pulsed dye laser (PDL) and Intense pulsed light(IPL)

treatments seem the best way to reduce the telangiectasia and

pigmentation

Conclusion

• Facial melanoses are a common presentation causing cosmetic

disfigurement with considerable psychological impact.

• Some of the well defined causes of include melasma, Riehl's

melanosis, Lichen planus pigmentosus,and poikiloderma of

Civatte.

• But there is considerable overlap in features amongst the

clinical entities.

Conclusion (Cont.)

• Etiology in most of the causes is unknown, but some factors

such as genetic, UV radiation , exposure to chemicals,

exposure to allergens are implicated.

• The treatment includes removal of aggravating factors,

vigorous photoprotection, and some form of active pigment

reducing agents.

• Other forms treatment include chemical peeling and lasers