4. 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 .
5. Differences in Skin Color
Racial 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.
6. 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 .
9. Melasma
Melasma is a chronic skin disorder that results in
symmetrical, blotchy, brownish facial pigmentation.
10. 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 .
11. What causes melasma? (Cont.)
Recent study demonstrated an increased expression
of estrogen receptors on skin with melasma, as
compared to normal skin.
12. 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).
13. 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.
14. 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
15. 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.
16. 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.
17. 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.
18. 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).
20. 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.
21. 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.
22. 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.
23. 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.
25. 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.
26. Diagnosis of LPP
Focal basal cell vacuolization with dermal
melanophages, and a sparse lymphohistiocytic
inflammation
27. 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.
28. 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.
29. 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 .
30. 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.
32. 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
34. 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.
35. 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.
37. 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.
38. 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.
39. 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).
41. 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
43. 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.
44. 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.
45. 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.
46. 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.
47. 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.
48. Presentation of PIH
The distribution of the hypermelanotic lesions depends
on the location of the original inflammatory dermatosis
49. 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.
50. Presentation of PIH (Cont.)
Common inflammatory diseases that result in
postinflammatory hyperpigmentation include acne excoriée,
lichen planus, systemic lupus erythematosus and chronic
dermatitis.
51. Presentation of PIH (Cont.)
Furthermore, lesions of postinflammatory hyperpigmentation
can darken with exposure to UV light..
52. 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
53. Skin Biopsy
If a history of preceding inflammatory dermatosis is unclear or
absent, skin biopsy is warranted to exclude other underlying
causes of hyperpigmentation.
54. 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.
55. 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.
56. 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.
57. 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).
58. 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.
60. 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.
61. 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.
62. 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.
64. 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
65. 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.
66. 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
