Clinica, histopathological and dermoscopic features along with the gist of treatment modalities.

1. Made by: Dr. Jaspreet Kaur
APPROACH
TO A
PATIENT
WITH
FACIAL
MELANOSIS
1

2. •Anatomy and physiology of melanocytes
Fitzpatrick’s skin types
Types of hypermelanosis
Classification of facial melanosis
Causes of facial melanosis
Management of Facial melanosis

3. • The human skin colour is determined primarily by
The type and amount of melanin synthesised within
melanosomes
The pattern of melanosome distribution within the
melanocytes.
• Haemoglobin (both oxygenated and reduced state) and
carotenoids also contribute to skin colour
• Melanocytes to keratinocyte ratio in basal layer: 1:4 to
1:10
• Highest density: facial and genital skin
• Lowest density: trunk and extremities
• Epidermal melanin unit: one melanocyte and each
keratinocyte that is physically in contact with its
dendrites: 1:36 to 1:40 (irrespective of anatomical
location)
• Estimated mass of all pigment cells in the body: 1.5g
Melanocytes
3

4. • Distribution of melanocytes:
• Interfollicular epidermal melanocytes
• Follicular melanocytes
• Acral melanocytes
• Extracutaneous melanocyte
• After depletion of interfollicular melanocytes,
melanocytes repopulate by hair follicle derived
melanocytic stem cells (in permanent bulge or
secondary germ area of hair follicle)
• Special stains for melanin( ability of
eumelanin to become impregnated with silver):
• Fontana Mason stain
• Warthin starry silver stain
Fontana Mason stain
4

5. • Tyrosinase is the key enzyme in the melanin
biosynthetic pathway.
• Three major forms of epidermal melanin
pigments:
Eumelanin (Brown-black)
Pheomelanin (Yellow-red)
Trichochromes (A variety of
sulphur‐containing phaeomelanic
pigments with a well‐defined structure)
5

6. Skin type and tanning ability based on the Fitzpatrick skin pigmentation scale
6

7. • Facial melanosis is a group of heterogeneous entities, sharing a common clinical feature
of altered pigmentation of face.
• It is a common presentation of darker skin type: Fitzpatrick types IV-VI.
• Three types of hypermelanosis are identified:
1. Brown hypermelanosis:
• Excess melanin is in basal and suprabasal (rarely throughout epidermis including the
horny) layers
• Pigmentation is accentuated under Wood’s lamp.
• The increased epidermal melanin can be:
• Melanotic hypermelanosis:
• Due to increased melanin production by normal number of melanocytes.
• Melanocytic hypermelanosis:
• Due to increased number of melanocytes.
7

8. 2. Blue hypermelanosis (ceruloderma):
• Excess melanin is in dermis
• Pigmentation is not accentuated under Wood’s lamp.
• Ceruloderma is due to:
• Increased transfer of melanin from epidermis to dermis (pigmentary incontinence):
• Melanin granules accumulate within melanophages
• May be free in the extracellular matrix of the dermis.
• Production of melanin by ectopic dermal melanocytes.
• Binding of melanin to exogenous pigments deposited in the dermis.
3. Mixed hypermelanosis:
• Due to increased epidermal and dermal melanin.
8

9. Systemic disease
Cutaneous
• Melasma
• Freckles and Lentigens
• Periorbital melanosis
• Seborrheic Melanosis
• Frictional Melanosis
• Exogenous onchronosis
• Pigmentary demarcation
line(F,G,H)
• Peribuccal pigmentation of
Brocq
• Nevus of Ota/Hori’s
• Erythromelanosis
follicular facei et coli
• Poikiloderma of
civatte
• Dermatosis
papulosa
nigra(DPN)
• Lichen planus
pigmentosis
• Riehl’s melanosis
• Chikangunia Fever
• Drug Induced
pigmentation
• Post inflammatory
hyperpigmentation
• Verrucae
• Pigmented BCC
• Actinic LP
Facial involvement
(predominantly)
Face+ Exatrafacial
involvement
Face+Neck
involvement
• Addison disease
• Cushing disease
• Hyperthyroidism
• Nutritional
deficiencies
(Based on primary site of involvement)
Facial Melanosis
9

10. Physiologic:
Pigmentary demarcation lines
Sun tanning
Genetic and developmental:
Lentigines
Freckles
Melanocytic nevus
Cafe-au-lait spots
Post inflammatory:
Eczema
Psoriasis,
Lichen planus
Lupus erythematosus,
Scleroderma
Morphea
Vagabond’s disease
Infections:
Tinea nigra
Nutritional:
Kwashirkor
Pellagra
Vitamin B12
deficiency
Vitamine C
deficiency
Folic acid deficiency
Physical:
Trauma,
Radiation dermatitis
Epidermal
Endocrine:
Melasma,
Addison’s disease
Cushing syndrome
Pheochromocytoma
Acromegaly
Hyperthyroidism
Neoplastic:
Malignant melanoma
Seborrhoea keratosis
Pigmented basal cell
carcinoma
(based on depth of pigmentation)
10

11. Genetic and developmental:
Mongolian spots,
Nevus of ota/ito,
Incontinentia pigment
Inflammatory:
Post inflammatory to eczema
Fixed drug eruption
Chemical and drugs:
Antimalarials,
OCP
Minocycline
Clofazamine
Topical hydroquinone
Tattoos
Endocrine:
Melasma
Physical:
Thermal burns
Post traumatic
Infection:
Syphilis
Yaws
Pinta
Neoplastic:
Metastasis of melanoma
Nutritional:
Chronic nutritional deficiency
Metabolic:
Hemochromatosis
Alkaptonuria
Macular/lichen amyloidosis
Miscellaneous:
Purpura
Dermal
Based on depth of pigmentation
11

12. Tanning
• Physiological pigmentary response of skin following exposure to UVR
• 3 phases
• Immediate pigmentary
darkening
• Low dose UVA
• Appears within
minutes of exposure
• Fades within 10-20
minutes
• Grey brown
pigmentation
• Oxidation and
redistribution of
preexisting melanin
• Persistent
pigmentary
darkening
• Higher dose UV
• Appears within
minutes of exposure
• Fades within 2-24
hours
• Brown pigmentation
• Oxidation and
redistribution of
preexisting melanin
• Delayed tanning
• UVB>UVA
• Appears 72 hrs after
exposure
• Persists for 1-2weeks
then gradually fades
• New melanin formation
due to increase in
melanocyte number and
activity.
12

13. Melasma
• Most common cause of facial melanosis
• Hyper pigmented macules on face which become
more pronounced with UVR exposure.
• More commonly seen in:
• Pregnant women( normal physiological
change)
• Females on OCP
• Light brown skin (Latinos, middle eastern,
asians)
• 20-40 years of age
• 30% patients have positive family history
• Patients with thyroid disease
13

14. • Pathology:
• Number of melanocyte unchanged but they
increase in size and become more dendritic
(hyper metabolic state)
• Melanosomes both within melanocytes and
keratinocytes are increased.
• Increased melanin deposition in the dermis and
the epidermis.
• Clinical features:
• Lesion is brown, bilateral and symmetrical.
• Common sites of hyper melanosis—Upper lips,
malar region, forehead, chin
• Less commonly also involves —extensor
forearm, mid upper chest.
• Etiology:
Estrogens stimulate melanogenesis through
estrogen receptors present on melanocytes
(pregnancy, OCP)
Begins or worsens after profound emotional stress
(raised MSH). MSH level are also raised in
pregnancy.
UVR and visible light cause per-oxidation of lipids
in cellular membranes, leading to generation of
free radicals, which stimulate melanogenesis
Constituents of cosmetics
Drugs (phenytoin, griseofulvin, and NSAIDs) can
cause melasma- like pigmentation.
Melasma
14

15. A.Depending on the location of melanin,
melasma is classified into:
Epidermal type: in which the pigment is brown
and margins of the lesions are well defined and
geographical
Dermal type: in which the pigment is grey-brown
and the margins of the lesions are poorly
defined.
Mixed or epidermo-dermal type: in which
melanin is present both in epidermis and dermis.
All melasma are now considered as mixed
melasma with the dermis showing solar
elastosis and increased vascularity
additionally.
Indeterminate type: in which it is difficult to
classify melasma, even with Wood’s light as
melasma in dark skinned individuals.
B. On the face, three patterns of melasma are
recognised:
• Centro-facial: the most frequent (63%) pattern,
with pigmentation on cheeks, forehead, upper
lip, nose, and chin.
• Malar: constituting 21%, with pigmentation
present only on cheeks and nose.
• Mandibular: the least common (16%), with
pigmentation on ramus of the mandible.
C. Natural history of melasma:
• Transient type: which disappears within a year
of withdrawal of hormonal stimulus.
• Persistent type: which persists for more than a
year after withdrawal of hormonal stimulus.
Classification of melasma
Melasma
15

16. Melasma
Malar
Centrofacial Extra facial
Mandibular
16

17. • Investigations:
1. Wood’s lamp:
• Epidermal melasma: shows
enhanced colour contrast with
woods’s lamp.
• Dermal melasma: less colour
contrast.
17

18. 2. Dermoscopy:
• Epidermal:
• Light brown pigment
• Pseudoeticular pigment network, annular and
arcuate structures
• Dermal
• Dark brown to black pigmentation
• Diffuse/ pseudo reticular pigment
• Black dots
• Perifollicular and peri-appendageal sparing
• Vascular prominence in some cases and
telangiectasia resulting from steroid abuse
Dermoscopy of melasma:
• Pseudoreticular pattern
of brown pigment (red
arrow)
• Perifollicular sparing
(blue circle)
• Vascular prominence
(blue arrow)
18

19. Freckles/ Ephelides
• Light‐brown pigmented macules on the light‐ exposed skin of fair‐skinned individuals,
typically of Celtic origin.
• Freckling is significantly associated with certain polymorphisms of the melanocortin 1
receptor gene and is transmitted in an autosomal dominant fashion without any
significant abnormality.
• UV exposure is responsible for the exacerbated pigment production by melanocytes that
results in the development of freckles.
• Several disorders are associated with freckling:
• Hereditary symmetrical dyschromatosis
• Xeroderma pigmentosum
• Neurofibromatosis (non exposed site freckling)
• Progeria
19

20. Freckles
20

21. • Pathology:
• The basal cell layer appears
hyperpigmented, without alteration
of the epidermal architecture.
• Dermoscopy:
• Uniform pigmentation
• A moth‐eaten edge
Freckles
21

22. Lentigens
• A lentigo is a benign pigmented macule in which there is an increased number
of melanocytes.
• The subtypes include
• Simple lentigo
• Actinic (or solar) lentigo
• PUVA lentigo
• Ink‐spot lentigo.
22

23. • Solar lentigines:
• Not associated with any particular skin
type
• Well defined smooth or irregular borders
• Light to dark brown( darker than freckles)
• Non uniformly distributed over sun
exposed area
• Lentigines persist even without UV
exposure, and tend to appear more
frequently in older ages (marker of
photoaging)
• Larger than freckles (few mm to few cm)
Lentigens
23

24. • PUVA lentigines:
• Develop after treatment with psoralen and UVA.
• Ink spot lentigines:
• Develop after intense sun exposure.
• Simple lentigines:
• Smaller, <5mm
• Fair skined and redhead
• Multiple lesions involving both exposed and unexposed part
• Can be associated with various syndromes involving internal organs.
Lentigens
24

25. • The term ‘lentiginosis’ is applied either when lentigines are present in
exceptionally large numbers or when they occur in a distinctive distribution.
• Generalised lentiginosis: Lentigines are commonly multiple but appear singly
or in small crops at irregular intervals from infancy onwards
• Unilateral (zosteriform) lentiginosis: Occur on one side of the body. Can be
zosteriform and occur in a dermatome‐ like or blaschko‐linear distribution.
• Agminated or segmental lentiginosis: Manifests as a circumscribed group of
lentigines arranged in a segmental pattern that develop during childhood.
• Lentiginosis
Lentigens
25

26. • Inherited patterned lentiginosis in black people: Distribution of the
lentigines included the face, lips, extremities, buttocks, palms and soles,
but not mucosal surfaces. The condition is extremely common in
light‐skinned black people, especially in combination with reddish‐brown
hair
• Eruptive lentiginosis: Widespread occurrence of very large numbers of
lentigines that develop rapidly over the course of a few months to years
• Lentiginosis profusa is a rare condition, with innumerable lentigines
present at birth or arising early in life, without systemic abnormalities or
mucosal involvement.
Lentigens
26

27. Familial Lentiginosis syndrome
27

28. • Pathology:
• Increased basal layer pigmentation due to
increase in both melanocytes and melanin.
• Dermoscopy:
• Simple lentigines:
• Dark uniform network across the whole
lesion.
• Very dark lesions are known as ink
spot lentigo.
• Blue pigmentation occurs in some lesions
due to dermal melanophages.
Lentigens
Simple lentigo
28

29. • Solar lentigo:
• Sharply demarcated and irregularly
curved Often, portions of the border are
scalloped, giving a moth-eaten
appearance.
• Light brown and structureless areas;
the term “jelly sign”.
• Areas consisting of fine parallel running
lines of light brown to dark brown colors.
They resemble the dermatoglyphics of a
human fingerprint.
• Symmetric brown follicular pigmentation[.
29

30. Periorbital melanosis
• Periorbital melanosis (POM or dark circles) is an ill defined entity of great cosmetic concern.
• Etiology:
• Dermal melanin deposition
• Superficial location of the vasculature.
• Post inflammatory hyperpigmentation (atopic or contact allergic dermatitis)
• Shadowing from lax skin
• Infraorbital swelling
• Tear trough depression.
• Familial periorbital hyperpigmentation is determined by an autosomal dominant gene
• Extension of pigmentary demarcation lines over the face (PDL-F).
• Lifestyle factors :lack of sleep, stress, smoking.
30

31. • Clinical features:
• 16-25 years (MC)
• Variegated brown to almost black
discoloration.
• Bilateral homogenous, hyperchromic
macules and patches.
• Primarily involving the upper and the
lower eyelids but also sometimes
extending towards eyebrows, malar
region and lateral nasal root.
Extension of pigmentary demarcation line-F leading to periorbital pigmentation
Periorbital melanosis
31

32. POM due to pigment deposition
POM due to hyperaemia and hemosiderin deposition
POM due to shadowing
POM due to shadowing and orbiculares prominence
Periorbital melanosis
32

33. Periorbital melanosis
Eyelid stretch test
33

34. Dermoscopic picture of mixed type of pigmentation: epidermal pigmentation along
Exaggerated pigment network dermoscopic findings (yellow arrows: Exaggerated
pigment network. Blue arrows: Normal pigment network)
Periorbital melanosis
Straight type of vessels with reticular pattern of vascular arrangement 34

35. Algorithm to diagnose clinical type using dermoscopic findings
35

36. Pigmentary demarcation lines
These are abrupt transition lines between darkly pigmented skin colour and normal skin colour.
Prevalence: 6%
Common in dark race
Pigmentary demarcation lines (8 groups):
A: Located on the anterolateral portion of the upper arm (Voigt– Futcher line)
B: Posteromedial portion of the leg
C: Hypopigmented linear bands on the mid chest in the pre‐ or parasternal region
D: A vertical line in the posteromedial area of the spine
E: Hypopigmented macules located on the chest extending from the clavicle to the periareolar
skin
F: Lines on the face- V shaped lines between malar prominence and temple.
G: Lines on face-W shaped lines between malar prominence and temple.
H: Lines on face-linear band from angle of mouth to chin
36

37. 37

38. • Etiology:
• Due to pigmentary mosaicism
• Hormones also play a role
• Histopathology
• Non
• specific with increase in melanisation.
• Dermoscopy
• Clear borders of abrupt transition between
darkly and less pigmented skin areas
• An exaggerated or prominent reticular or
pseudoreticular pattern
Exaggerated pseudo network and prominent perifollicular
accentuation of pigmentation appearing as brownish ring
(circles).
38

39. Exogenous Ochronosis
• Exogenous ochronosis (EO) is characterised by blue-black cutaneous pigmentation due to the
deposition of ochre-coloured pigment in the dermis, resulting from prolonged use of skin-
lightening creams containing hydroquinone.
• Etiology:
• Especially seen with use of hydroquinone at concentrations more than 3% for prolonged period of
time (>6 months)
• Topical use of phenol, resorcinol, picric acid, oral antimalarial and mercury have also been
implicated.
• Aggravated by sun exposure
• (Endogenous ochronosis- pigmentary changes that occur in connective tissue in patients with
alkaptonuria due to the deficiency of homogentisic acid oxidase)
• HQ> Competitive inhibition of HGO enzyme>accumulation of homogenitisic
acid>polymerisation to>ochronotic pigment in papillary dermis
39

40. Exogenous Ochronosis
40

41. Pathology:
• Comma or banana shaped ochyronotic collagen
bundles.
• Giant cells and melanophage rich granulomas.
Clinical features:
• Symmetrical diffuse/ blotchy.
• Grey brown or blue black sooty macules reticulate
pattern in HQ-treated photo-exposed areas viz cheeks,
forehead and temporal and periorbital skin with less
frequent involvement of nasal, peribuccal, and chin
areas.
• Macules are surmounted by hyper chromic, pinpoint
caviar-like papule.
(No hyperpigmentation of cartilage, sclera or conjunctivae)
Accumulation of yellow-brown pigment in the dermis.
Homogenisation and swelling of collagen fibres
41

42. Dermoscopy:
• Diffuse brown background with perifollicular
greyish blue dark amorphous structures
with some of them obliterating the follicular
openings
• Irregular, grey brown, globular, annular,
arciform structures
• Curvilinear and “worm like” structures at
places
• Fine telangiectasia
Dermoscopy of early ochronosis:
• Pseudoreticular black to brown pigment network
• Brown dots and globules (blue arrow)
• Perifollicular brown-grey amorphous structures (orange
circle)
42

43. 43

44. Naevus of Ota
• A naevus of Ota is an extensive, bluish, patchy, dermal melanocytosis that affects the sclera
and the skin adjacent to the eye
• Distributed along the first and the second branches of the trigeminal nerve.
• Extracutaneous lesions may also present in the uveal tract, dura, nasopharynx, tympanum and
palate.
• Predominantly in:
• Asians
• Females.
• Present at birth or develop during the first year of life, increasing in size and number in
subsequent years.
• Bilateral cases of naevus of Ota are sometimes associated with extensive Mongolian spots.
44

45. • Pathology:
• Elongated dendritic melanocytes are scattered among collagen bundles mainly of the
superficial dermis, and in larger numbers are compared to Mongolian spot
• GNAQ mutation
• Presentation:
• Speckled lesion
• Composed of blue and brown components that do not always coincide. This phenomenon can be
better observed in the proximal eye, where the sclera appears blue and the conjunctiva brown.
• Brown pigmentation is patchy and superficial, following a reticular or geographical pattern; blue
pigmentation is more diffuse and deeper.
• Meningeal melanocytomas of the brain, which are benign neoplasms, may complicate naevus of
Ota
45

46. Isolated dendritic melanocytes distributed among
collagen bundles of the upper reticular dermis
46

47. Hori’s Naevus
• Hori nevus, or acquired bilateral nevus of Ota like macules (ABNOM) is probably a distinct variant
seen in Koreans and Japanese.
• Late onset in adulthood
• Spares the mucosae
• Bilaterally symmetrical speckled or confluent brownish-blue or slate-grey pigmentation over the
malar regions, temples, root of the nose, alae nasi, the eyelids, and forehead.
• Without careful examination of alae nasi, forehead, and eyelids, brown ABNOM looks just like
melasma.
• Histologically, fusiform-elongated dendritic melanocytes and melanophages are scattered among
collagen bundles.
• The differentiation is essential because both are treated differently- melasma with topical agents
while ABNOM with lasers.
47

48. 48

49. Post‐inflammatory hypermelanosis
• Residual macular pigmentation resulting from prior skin inflammation.
• The intensity and persistence of the hypermelanosis are greater in dark‐skinned subjects
• The pattern and distribution of the pigmentation will sometimes allow a retrospective
diagnosis
• Various dermatological conditions resulting in PIH:
• Eczema
• Psoriasis,
• Lichen planus
• Lupus erythematosus,
• Scleroderma
• Morphea
• Vagabond’s disease
49

50. • Pathology:
• Hypermelanosis commonly follows acute or chronic inflammatory processes in the skin.
• Disorders where there is disruption of the basal layer of the epidermis frequently develop areas
of slate‐brown hypermelanosis.
• There is pigmentary incontinence with melanophages in the upper dermis.
• Hypermelanosis of the epidermis may also occur as a result of cutaneous inflammation, but
more frequently there is reduced epidermal melanin pigmentation:
• Increased mitotic rate of keratinocytes
• Diminished transfer of melanosomes from the melanocyte to keratinocytes
• Reduced transit time of the latter from the basal layer to the skin surface.

51. Seborrheic melanosis
• Seborrheic melanosis is a poorly
defined entity that has been postulated
as PIH secondary to seborrheic
dermatitis.
• It presents as localised darkening of
seborrheic areas of the face,
predominantly over the alar grooves,
angles of the mouth, and labio-mental
crease.
• More commonly in Asian, African, and
Hispanic population.
Prominent darkening of the alar grooves is appreciated with the
presence of multiple follicular plugs of inspissated sebum on the nose
Prominent darkening of the lower central area of the face, bilateral
angles of the mouth and labiomental crease
51

52. • Dermoscopy:
• The dermatoscopic findings were placed into three categories :
• Vascular: A light pink background with out of focus linear and arborizing vessels.
• Mixed presentation: Combination of pigmentation and erythema.
• Pigmented: Predominantly seen in dark-skinned individuals.Prominent hyperpigmented
pseudonetwork. Some showed annular granular structures (brown) which did not occlude
the orifices.
• The common feature in all the presentations:
• Whitish yellow excrescences of sebum coating the vellus hair shafts and prominent
follicle openings.
52

53. Yellow scales with light pink background and
linear and arborizing vessels in the nasolabial
area
Light pink erythema with linear vessels with
hyperpigmented pseudonetwork at the margin
in the nasolabial area
Seborrheic melanosis
Dermoscopy:
53

54. Prominent hyperpigmented pseudonetwork
with minimal erythema at the margins in the
nasolabial area
Whitish yellow excrescences of sebum coating
the vellus hair shafts and prominent follicle
openings
Dermoscopy
54

55. Facial Frictional melanosis
• Friction melanosis (FM) is an acquired pigmentary disorder mainly affecting young people.
• The primary skin regions affected are located over the osseous prominences,.
• Characteristic patterns of facial pigmentation following vigorous rubbing or cleaning of the face
• Resultant pigmentation leads to a paradoxical increase in the vigorous rubbing exacerbating
the pigmentation and setting up a vicious cycle of friction and reactionary hypermelanosis.
• Six chief clinical patterns of pigmentation:
1. Zygomatico-supraorbitalis
2. Metomelanosis
3. Panfacial melanosis:
4. Paranasal melanosis
5. Perioral melanosis
6. Mixed melanosis
55

56. Metomelanosis: Pigmentation over forehead.
Note the midline sparing
Zygomatico-supraorbitalis: Pigmentation
overlying zygomatic bone and temples
Facial Frictional melanosis
56

57. Facial Frictional melanosis
Panfacial : Pigmenation over the entire face
with sparing of apex of nose
Paranasal: Pigmentation on the lateral sides of
the nasal bridge and nasolabial folds
57

58. Facial Frictional melanosis
Perioral: Pigmentation around the mouth Mixed type of facial frictional melanosis
58

59. • Dermoscopy:
• Black pigment dots,
• Patchy pigment distribution on background of
acanthotic skin
• Patulous follicular openings with plugs
Facial Frictional melanosis
• Pathology:
• Epidermal hypermelanosis as well as dermal
melanosis.
• No amyloid deposits after Congo Red stain evaluation
• Irregular acanthosis of epidermis with antler-like
projections of rete ridges.
• Basal hypermelanosis and patchy melanin
incontinence
59

60. Peribuccal pigmentation of Brocq
• Aka :Erythrose peribuccale pigmentair de brocq, Erythrosis pigmentosa mediofacialis
• Diffuse brown red pigmentation around mouth but sparing a narrow perioral ring
(vermillion border)
• May extend to centre of face to forehead and in some cases may involve angle of jaw.
• Predominantly in middle aged women.
• Photodynamic substance in cosmetics is probably responsible
• Lesion has two components:
1. Erythema: Fluctuates
2. Diffuse brown pigmentation: persists but fades gradually on removal of cause
60

61. Peribuccal pigmentation of Brocq
61

62. Erythromelanosis follicular faciei et coli
• Reddish‐brown discoloration affecting the preauricular and maxillary regions, in some cases
spreading to the temples and lateral sides of the neck and trunk
• Second decade of life
• Male predominance
• Asians
• Clinical features:
• Triad of
• Hyperpigmentation
• Follicular plugging
• Erythema with or without telangiectasia
62

63. • Symmetrical distribution
• Sharp demarcation from normal skin.
• Subtype of keratosis pillars.
• Hair are lost from the majority of
affected vellus hair follicles but terminal
hair follicles of the scalp and beard are
less conspicuously affected.
• It spreads slowly, is persistent and is
not influenced by treatment.
Erythromelanosis follicular faciei et coli
63

64. • Pathology:
• Slight orthokeratosis
• Follicular hyperkeratosis
• Increased basal layer pigmentation
• Perivascular and periadnexal lymphocytic
infiltrate with vasodilatation
• Pigmentary incontinence with dermal
melanophages
Erythromelanosis follicular faciei et coli
64

65. • Dermoscopy:
• Multiple round whitish areas with follicular
plugs
• Surrounded by blue grey spots or peppering.
in a reddish-brown background
• Presence of some white scales.
Erythromelanosis follicular faciei et coli
65

66. Poikiloderma of civatte (Erythromelanosis interfollicular faciei et coli)
• Presents after years of repeated UV exposure.
• Predisposing factors:
• 30-50 years
• Female
• White skin
• Phototoxic or photoallergic reactions to chemicals in
fragrances or cosmetics.
• Clinical features:
• Symmetrically on the sides of the face, neck and upper
aspect of the chest.
• Mottled hyper- and hypopigmentation, telangiectasia and
dermal atrophy.
• The submandibular and submental areas are spared.
• Some patients experience itching, burning and flushing.
66

67. Poikiloderma of civatte
• Pathology:
• Thinning of the spinous layer
• Hydropic degeneration of the basal cell layer
• Presence of melanophages in the papillary dermis
• Dilatation of the papillary dermal capillaries.
• Investigation:
• Patch testig
67

68. • Dermoscopy:
• Dotted/globular and linear
irregular vessels (“spaghetti and
meatballs” aspect),
• Perifollicular whitish (spared) areas
• Follicular keratotic plugs (25%)
• Delicate reticular (25%)
• Structureless brownish areas (12.5%)
Poikiloderma of civatte
68

69. Riehl’s melanosis
• Riehl’s melanosis (aka pigment contact dermatitis (PCD), melanodermatitis toxica, female facial
melanosis )
• Characterised by patchy or diffuse brown to slate grey hyperpigmentation over head and neck
region predominantly affecting the lateral side of the face than the center (may involve chest,
neck, scalp, hands and forearm)
• It is considered as the non-eczematous variant of contact dermatitis
• Type 4 hypersensitivity response to repeated contact with very small amounts of contact
sensitizer (fragrances, washing materials, textiles)
• Small perifollicular pigmented macules> extend beyond indefinite margins.
• Lesions due to cosmetics and hair dye usually start over hair margins, are ill defined
hyperpigmented patches with preferential involvement of outer surface, helix and lobule of ear,
temples, periauricular areas and upper back. SITE AFFETECTED BY APPLICATION OF HAIR
DYE.
69

70. • Histopathologic:
• Basal cell vacuolar damage and pigment
incontinence
• Normal to atrophic epidermis
• Mild spongiosis
• Melanophages in upper dermis
• Patch testing is valuable in diagnosing the causative
agent.
Riehl’s melanosis
70

72. Riehl’s melanosis
72

73. • Dermoscopic features:
• Vary as per the location of the pigmentation.
• Accentuated diffuse brown pseudoreticular
network
• Regularly distributed brown dots in early PCD to
finer grey to blue dots (representing deeper
pigment incontinence)
• Follicular keratotic plugs
• Telangiectasia, and scales over an erythematous
background.
• Perifollicular keratotic plugs with perifollicular
whitish halo (corresponding to perifollicular
fibrosis) is reportedly more prominent over face than
the neck, owing to higher density of hair follicles
over the face
Riehl’s melanosis
73

75. Follicular keratotic plugs,
perifollicular whitish halo,
and flour-like scales are
described in few cases
Due to heavy melanin,
vessels and perifollicular
white halo may not be
appreciated in darker skin
types. However, pinkish
hue in the background
can be seen

76. Allergens implicated in Riehl’s melanosis
76

77. Lichen planus pigmentosus
• This is a pigmentary disorder seen in India or in the Middle East, which may or may not be associated with
typical LP papules.
• The macular hyperpigmentation involves chiefly the face, neck and upper limbs, although it can be more
widespread.
• Insidious onset and chronic course.
• Varies from slate grey to brownish black.
• It is mostly diffuse, but reticular, blotchy and perifollicular forms are seen.
• The photo-distributed or actinic pattern, which is more common, is a disease of tropics and Type IV–Type V
skin types.
• Rarely palmoplantar or mucosal involvement seen.
• Etiology:
• Sun exposure
• Photosensitizing topical agents in the actinic variant.
• Mustard oil, which contains allyl isothiocyanate, a potential photosensitizer,
• Amla oil
• Koebnerization due to friction in the flexures or due to tight clothing is thought to contribute to the inversus type
of LPP.
• Can be associated with other autoimmune diseases like lichen planus, lichen planopilaris, vitiligo, frontal
fibrosing alopecia (esp. premenopausal women) and hypothyroidism
• Can be seen blashkoid pattern 77

78. 78

79. • Pathology:
• Earliest lesions:
• Marked inflammation at the interface, which later
subsides, leaving behind the characteristic
dermal pigmentation in older lesions.
• The epidermis is usually atrophic as opposed
to acanthosis occurring in LP.
• The inflammatory phase:
• A dense band of lymphohistiocytic
inflammatory infiltrate in the upper dermis with
prominent basal-vacuolar degeneration.
• Some melanin incontinence is seen with scattered
dermal melanophages.
Lichen plans pigmentosus
79

80. • Second pattern of burnt-out inflammation:
• Minimal superficial perivascular lymphohistiocytic infiltrate and focal to absent basal-vacuolar
degeneration.
• Marked melanin incontinence with many interstitial and perivascular melanophages.
• Colloid bodies are a common finding in LPP as in LP.
• 15% of cases show immune deposits. IgM (less commonly IgG], C3, and fibrinogen deposits in
the colloid bodies (globular deposits).
• As well as linear IgM and C3 deposits along the basement membrane zone
• CD8+ lymphocytes may be a prominent component in the infiltrate
Lichen plans pigmentosus
80

81. • Dermoscopy:
• Diffuse pattern : referred to structureless
areas of brown pigmentation, probably
epidermal pigmentation.
• Dotted pattern : described fine or coarse blue-
gray dots of indicating dermal melanophages.
The presence of dotted pattern correlates with
a tendency for the pigmentation to persist.
• Mixed pattern : referred to lesions showing
both epidermal and dermal components.
Diffuse brown background, hem-like pattern of pigment (blue
arrow), grey coloured dots and globules (black circle) and
perifollicular pigment deposition (yellow star)
Lichen plans pigmentosus
Grey brown dots and globules arranged in linear interrupted
pattern( hem like) over a background pf Facal erythema
Accentuation of pseudoreticular area with dot/globules in some
areas
81

82. Perieccrine and perifollicular location of brown to bluish grey pigment globules is characteristic.
Pigment globules are very dense and course.
Frequently noted patters are:
• Diffuse
• Dotted
• Annular
• Arcuate
• Hem-like (facial and intertrigenous areas)
• Cobble stone
• Speckled (uncommon)
• Wickham striae and vascular features are absent.

83. Erythema dyschromicum perstans
• Development of persistent grey‐blue
hypermelanotic cutaneous macules for
which no specific cause can be identified
is known as ashy dermatosis.
• Erythema dyschromicum perstans be
limited to those cases in which an
inflammatory phase with erythema has
been observed.
• Commonly seen in: Young adults,
Females
83

84. • Pathology:
• The active border in cases of erythema
chronicum perstans shows vacuolar
degeneration of the basal cells.
• The epidermis contains much pigment
and there is pigmentary incontinence
• The dermal vessels are sleeved with an
infiltrate of lymphocytes and histiocytes,
and there are many melanophages
Basal hyperpigmentation (blue arrow), dermal
perivascular lymphocytic infiltrate with
melanophages (red arrow).
84

85. • Clinically:
• Numerous macules of varying shades of grey
• There may initially be signs of inflammation with a red, slightly raised and palpably
infiltrated margin (erythema dyschromicum perstans.
• The macules vary in size and tend to coalesce over extensive areas of the trunk, limbs and
face.
• Against the general greyish background are macules of hypomelanosis or hypermelanosis.
• The condition is persistent and slowly extends.
• The lesions are mostly asymptomatic, although some patients may experience mild
pruritus.
• Palms, sole and mucous membranes are spared
85

86. • Dermoscopy:
• Brown to grey dots and globules which were
observed in all of the lesions.
• The most common type of arrangement of dots
and globules is irregular linear arrangement
followed by circular arrangement
• The most common color of background is
pinkish brown background followed by skin
colored background
• The most common vessel pattern was
represented by irregular linear and coiled
vessels
Brown to grey dots and globules forming irregular lines, circles and angulated lines arranged in a
reticular pattern. A light brown background can also be observed
Widespread distributed brown to grey dots with a pinkish background
86

87. <———-—————Macular pigmentation of uncertain etiology*————————
——>

88. Facial acanthosis nigricans
• Increased prevalence of obesity and insulin resistance in patients present with FAN
• Also know as metabolic melanosis and metabolic melasma
• Clinical features:
• The brown-to-black ill defined macular pigmentation
• Present on the zygomatic and malar areas with varying degrees of textural changes especially
in overweight and obese individuals.
• Overlying skin being rough, dry, and verrucous.
88

89. An obese patient with brown-to-
black macular pigmentation with
blurred margins. Note the
characteristic involvement of the
zygomatic area, extending
downward. The skin is dry, rough,
and verrucous
Clinical picture of a middle
aged gentleman with normal
BMI with mild lesions of FAN.
Involvement of the eyelids can
be appreciated
Facial acanthosis nigricans
Classical morphology of
facial acanthosis nigricans
can be appreciated over
the forehead
89

90. • Investigations:
• In adult‐onset AN, patients should be screened for underlying endocrinopathy or malignancy.
• A sensitive test for insulin resistance is serum insulin, the levels of which may be elevated before the onset
of diabetes
• Elevation of glycosylated haemoglobin levels.
• According to the consensus statement provided by Misra et al., three out of the following five factors need
to be present for identification of metabolic syndrome:
• Abdominal obesity (>40 inches in males and >34.5 inches in females), Non-obligatory
criterion
• Fasting blood glucose ≥100 mg/dl
• Blood pressure ≥130/85 mmHg
• Triglycerides ≥150 mg/dl
• HDL (<40 mg/dl in males and <50 mg/dl in females).
90

91. Chickengunia fever
•Acute febrile illness presenting with symptoms like intense asthenia, arthralgia,
myalgia and headache
•Chikengunya is caused by alpha virus and is transmitted by Aedes aegypti and Aedes
albopictus.
•Clinical features:
•Most common cutaneous manifestation of chikungunya is an erythematous
maculopapular rash.
•Post chikungunya pigmentation:
•Develop after two weeks or more after the rash; by the time high grade fever has
subsided
•Discrete macules, freckle-like, diffuse, flagellate, Addisonian type of palmar
pigmentation, periorbital melanosis and pigmentation of pre-existing acne
lesions
91

92. •Patients do not have any preceding
erythema or eruption over the affected
areas during the acute febrile phase.
•The "chik sign": Striking pigmentation
over nose is seen in several patients of CF
•Pathology:
•Intact basal layer with diffuse
hypermelanosis of the entire
epidermis, suggesting an increased
intra-epidermal melanin
dispersion/retention triggered by the
virus. Chik sign
92

93. Systemic causes of facial melanosis

94. Drug induce pigmentation
• Several mechanisms are involved in drug‐induced changes of pigmentation of the skin.
• These include:
• Increased melanin synthesis
• Increased lipofuscin synthesis
• Deposition of drug‐related material
• Post‐inflammatory hyperpigmentation
• Amiodarone
• Antimalarials
• Clofazamine
• Cytotoxic drugs
• Hydantoin
• Psychotropic Drugs
• Tetracycline
• Fixed drug eruption
94

95. Addisons disease

97. British Journal of dermatology(2013)169 (Suppl.3). Pp41-56

98. • Amiodarone:
• Photosensitive and phototoxic reactions in
more than 50% of patients.
• < 5% -Slate‐grey or purple discoloration
due to drug induced discolouration of
mainly the sun‐exposed skin, especially
the face, with prominent involvement of the
nose and sometimes the ears.
• The discoloration is caused by UV
accumulation of amiodarone and lipofuscin
in dermal macrophages.
98

99. • Antimalarial drugs:
• 25% of patients receiving one of the four
commonly used antimalarials for atleast
four months develop discolouration of
skin.
• Yellowish pigmentation of the skin is
common with mepacrine . Pigmentation
appears to result from complexes of
melanin, haemosiderin and mepacrine, in
combination with sulphur
• Bluish‐grey pigmentation on sun‐exposed
areas, including the face.
• May involve hard palate and nails.
• Bleaching of colour of hair occurs.
99

100. • Clofazamine:
• Initial redness of the skin due to an
accumulation of the drug.
• Later, with prolonged treatment, a
violaceous brown colour develops that is
most noticeable in lesional skin
100

101. • Cytotoxic drugs:
• Common side effect of antitumour
agents used in cancer
• Busulphan
• Cyclophosphamide
• bleomycin (flagellate pigmentation)
• fluorouracil
• hydroxyurea
• daunorubicin
• methotrexate
• mithramycin
• mitomycin
• thiotepa
• adriamycin
101

102. • Hydantoin, Phenytoin:
• Melasama patterned facial melanosis
• Barbiturates:
• Diffuse brown post- exanthematous
discolouration
• Psychotropic Drugs:
• Chlorpromazine:
• Blue grey pigmentation in sun
exposed ares of skin in few patients
receiving high doses for prolonged
period.
• Trifluperazin
• Impramine
Chlorpromazine pigmentation: patchy bands of muddy
pigmentation extending across the nose to the paranasal and
preauricular skin in an elderly male receiving long‐term therapy.
102

103. • Tetracycline:
• Mainly with minocycline.
• 4 unique patterns of pigmentation that share a
similar morphology:
• Type 1: Blue-grey macules in areas of acne
scars
• Type2: At sites of previous inflammation or
distant from sites of inflammation or infection
,mostly on sun exposed areas
• Type 3: Muddy skin syndrome-diffuse brown grey
discolouration with tendency to photo
aggravation.
• Type 4: Vermillion of lower lip.
103

104. • Fixed drug eruption:
• Acute eruption characteristically leaving residual
hyperpigmentation
• Well circumscribed areas of slate-brown pigmentation.
• Melanosis may be diffuse or melasma like.
• Recurrence of lesion at the same site with
development of new ares of involvement with
repeated exposure to causative agent.
• Most commonly reported gents:
• NSAIDS
• Paracetamol
• Co-trimoxazole
• Tetracycline
104

105. Addisons disease
• The discoloration in Addison disease is typically diffuse with accentuation in sun‐exposed areas
• Also accentuated in the flexures, at sites of pressure and friction, and in the creases of palms
and soles
• Normally pigmented areas, such as the nipples and genital skin, darken.
• Pathology:
• The hypermelanosis is the result of increased secretion of melanotrophic hormones by the
pituitary.
• Affected patients have elevated plasma levels of à‐MSH‐like immunoreactivity
105

106. John Wiley and Son, Burket al. Addison’s disease, diffuse skin, and mucosal hyperpigmenation with subtle “flu‐like” symptoms — a report of two cases. Pediatr Dermatol
Diffuse hypermelanosis of gingiva
Diffuse hypermelanosis of the skin
(c) Hypermelanosis of labial mucosa (d)Hypermelanosis of tongue
Addisons disease
106

107. Hyperthyroidism
• It is usually diffuse and is broadly of addisonian pattern,
(although involvement of the mucous membranes is uncommon
and pigmentation of the nipples and genital skin is less striking).
• The eyelids are occasionally conspicuously pigmented
(the Jellinek sign).
• Some patients show melasma‐like pigmentation.
• It is speculated that the skin discoloration in
hyperthyroidism may be due to increased release of
pituitary adrenocorticotropic hormone, compensating for
accelerated cortisol degradation.
107

108. Nutritional deficiencies
• Hyperpigmentation caused by nutritional deficiencies may be of addisonian type but without
involvement of the mucous membranes
• Or may occur in well‐defined patches on the face and neck and occasionally on the trunk .
• The scaly inflammatory plaques that may develop in these syndromes are usually followed by intense
pigmentation .
• Vitamine B12 deficiency:
• Lower intracellular reduced glutathione levels, causing a decrease in its inhibitory function on
tyrosinase activity in melanogenesis- increase in melanogenesis.
• Associated with a defect in melanin transport and the incorporation of melanin into keratinocytes,
causing incontinence of pigment.
108

109. • Dappled and mottled pigmentation.
Affects the face and the dorsum of the
hands and feet (may be limited to the
fingertips and nails or, rarely, may be
generalised)
Ill‐defined hyperpigmentation of the
mucosal surfaces and hypopigmentation
of the hair may also occur.
A, Hyperpigmented macules on the face and upper
and lower lip

110. • Vitamine B3 deficiency (Pellagra):
• Inadequate dietary supply of tryptophan especially
where diets are based on maize with little animal
protein.
• Affected skin becomes hard, dry and cracked and
in extreme cases is black in colour.
•
• The sites of involvement are the sun‐exposed skin
of the face, neck, dorsum of the hands and feet,
and sometimes the forearms.
• Mucosal sites are also affected

111. • Vitamine A deficiency:
• Phrynoderma are the most
characteristic, particularly in children:
these may be associated with
hyperpigmentation of the face and
limbs.
• Vitamine B9 deficiency:
A diffuse brown pigmentation is also seen
occasionally in patients with
megaloblastic anaemia due to folic acid
deficiency, particularly during pregnancy.

112. Management of
facial melanosis
• Clinical approach to facial melanosis
• Lifestyle modification
• Sunscreens
• Removal of provoking factors
• Skin lightening agents
• Topical
• Systemic
• Other modalities
112

113. Facial
Melanosis
History of systemic
or topical drugs/
heavy metal
exposure
Red-brown patches
on lateral cheek and
neck.
Superimposed tiny
follicular papules
Atrophy,
telangiectasia
Fine scaling,
violaceous
Constant use of
cosmetics
Ashy slate grey
pigmentation
Woman, post-
pregnancy
Light to dark brown or
brown grey cheeks
Erythromelanosis follicular
Poikiloderma of Civatte
Actinic LP
Riehl’s melanosis
EDP, LPP
Melasma
Exogenous ochronosis
Photo-distributed
Reticulate, net like
Clinical Approach to facial melanosis
113

114. • Begins in the temples and then involves the side of
face and neck
• Greyish black pigmentation
• History of prolonged hydroquinone use
• History of pigment aggravation by hydroquinone use
• Micropapules or micro-pigmented papules present
• Characteristic histology
• Fine scaling over pigmented lesions
• Due to cosmetic use
• Pigmentation involving the sides of the face and
even neck or forehead
• Greyish brown pigmentation
• May be reticulate in pattern
Exogenous ochronosis
Riehl’s melanosis
LPP
Differentiating other facial melanosis from melasma
114

115. • Area of the sides of the forehead and cheeks
commonly involved
• History of application of oils or perfumed
substances on face and scalp
• Presence of inflammatory signs in early stages.
• Involvement of anterior neck
• Atrophy and telangiectasis
Poikiloderma of Civatte
• Pigmented photo contact
dermatitis
Differentiating other facial melanosis from melasma
115

116. Avoid provoking agents:
Essentail in
• Melasma
• Reihl’s melanosis
• Exogenous ochronosis
• Drug induced hypermelanosis
• Also in other facial melanosis
Lifestyle modification:
• Avoiding peak hours of sunlight (11:00 A.M. to
4:00 P.M. )
• Using shady sides for activities
• Using sunshades
• Using broad rimmed hats (4 inches)
• Sunglasses
• Tightly knit protective clothing
• Reducing itch to reduce scratching and
mechanical skin manipulation known to
contribute to PIH formation—applying
moisturizers
116

117. • Sunscreens:
• Prevent photo induced darkening
• Broad spectrum sunscreen should be
used.
• Should be applied in appropriate
amount and frequency.
• 2mg/cm2 coverage needed
• Every one hour or Teaspoon rule
(To apply 2 mg/cm2 of sunscreen the whole
body, a typical adult averaging 1.73 m2 would
require 35 ml of sunscreen)
• Tinted sunscreen containing iron
oxide (>3%) have greater protective
effect against visible light.
• Tinted sunscreen have advantage of
providing camouflage.
• Sunscreen should be used all year
round.
117

118. 118

119. Hydroquinone
• 2%-4% widely used in melasma therapy.
• Inhibits the conversion of DOPA of melanin
by inhibiting the activity of tyrosinase.
• May interfere with DNA and RNA synthesis
• Degrades melanosomes
• Destroys melanocytes
119
• Adverse reactions:
• Dose and duration dependant
• Acute reactions like asymptomatic transient
erythema and dose dependant irritation.
• Confetti like depigmentation at doses >2%
• Rarely exogenous ochronosis develops
• C/I in pregnant and breastfeeding women
119

120. Azelaic acid
• Derived from Pityrosporum ovale
• 10-20%
• Antiproliferative and cytotoxic to melanocytes
• Reversible inhibitor of tyrosinase.
• Shown to be as effective as HQ 4% but without its side effects.
• The combination of azelaic acid with 0.05% tretinoin or 15%–20% glycolic acid may produce
earlier, more pronounced skin lightening.
• Adverse effects:
• Pruritus, Mild erythema, Scaling, Burning
• Safe in pregnancy
120

121. Kojic acid
• Produced by Aspergillus oryzae and Penicillium spp.
• Inhibits tyrosinase by chelating free copper at enzyme’s active site.
• When used alone, KA, 1−4%, is only modestly efficacious.
• However, KA has a place as a combination therapy in management of FM, if the patient has
difficulty tolerating other first-line therapies.
• Known sensitizer and may cause contact dermatitis and erythema.
121

122. Retinoids
• Improves penetration of other drugs
• Increases melanin shedding by increasing keratinocyte turnover.
• Also inhibits tyrosinase transcription, interrupting melanin synthesis .
• While tretinoin may be effective in reducing melasma, it typically takes at least 24
weeks to see clinical improvement
122

123. Glycolic acid
• GA 5%–10% is an alpha-hydroxy acid.
• It decreases pigment by many mechanisms including
• thinning the stratum corneum,
• enhancing epidermolysis,
• Dispersing melanin in the basal layer of the epidermis,
• Directly inhibiting tyrosinase
• Increasing collagen synthesis in the dermis.
• Irritation is common and resolves with temporary withdrawal combined with application
of moisturizers.
123

124. Topical steroids
• Inhibit synthesis of mediators like prostaglandin and leukotriene and this may partly
explain their effect on melanogenesis.
• Used in combination as it also reduces irritation from other products like tretinoin and
hydroquinone.
• Mono therapy is best avoided due to frequent adverse effects like rosacea-like
dermatosis, atrophy, telangiectasia, acneform eruptions and hypertrichosis.
124

125. Hydroquinone 5%
+
Tretinoin 0.1%
+
Hydrocotisone 1%
Hydroquinone 2%
+
Tretinoin 0.025%
+
Mometasone 1%
Hydroquinone 4%
+
Tretinoin 0.025%
+
Flucinolone acetonide 0.01%
Hydroquinone 2%
+
Tretinoin 0.025%
+
Fluticasone propionate 0.05%
Triple combinations
This original Kligman formula employed a mild steroid, dexamethasone 0.1% in combination
with 0.1% tretinoin, and 5% hydroquinone in a cream base.
125
FDA
approved

126. N-ACETYL GLUCOSAMINE Monomeric unit of chitin Inhibits conversion of protyrosinase
to tyrosinase
OCTADIENEDIOIC ACID Structurally similar to AA Modulates synthesis of tyrosinae
mRNA
B-CAROTENE Structural analog of Vit A Saturates melanocyte receptor and
reduce melanin production
LINOLEIC ACID Derived from botanical oils Accelerate tyrosinase degradation
SILYMARIN Plant silybium marinum Inhibits melanogenesis
N-ACETYL-4-S-
CYSTEAMINYLPHENOL
Phenolic agent Tyrosinase inhibition
UNITAMURON h-22 Vegetal equivalent of hyaluronic
acid
Preservation and an increase of
skin hydration
Smoothing effect on skin
Increase skin elasticity
126

127. recommended
• 70% Glycolic acid peel is most commonly
used.
•Dermabrasion :
• Useful for patients with a prominent
dermal component that is often very
hard to treat
• Local or full-face dermabrasion up to
the upper or mid-dermis has been used
127

128. • Lasers:
• Second or third line modality.
• Melanin has a broad absorption spectrum, but longer wavelengths penetrate deeper and can
target dermal pigment, but melanin absorbs better with shorter wavelengths: given these
attributes, many light and laser sources have been tried.
• Challenging because of the high risk of damage to surrounding tissue that can lead to long
lasting and delayed PIH.
• The 1064-nm QSNY is the most widely used laser in darker skin types because of the longer
wavelengths that allow for a deeper penetration.
128

129. Systemic agents in skin lightening
129

130. • Miscellaneous agents
• Hyaluronic acid,
• green tea,
• ellagic acid-rich pomegranate extract,
• coumarin extracts from the plant
• Angelica dahurica,
• epidermal growth factor and
• combinations of multiple natural extracts namely
• natural collagen extracts,
• bearberry extract,
• Glycyrrhiza glabra extract,
• grape seed extract, lycopene,
• kelp,
• olive leaf extract,
• hawthorn,
• jujube,
• sea buckthorn,
• starch,
• coix seed,
• pearl extracts,.
130

131. Melasma

132. • Specific treatments:
• EDP
• Clofazamine: used as first line treatment in
inflammatory EDP .
• Dose: 100mg OD for 3 Months
• Dapsone: second line treatment of EDP
• Dose: 100mg OD for 3 Months
• Erythromelanosis follicular et coli
• First line topical keratolytics: urea 10-20%,
ammonium lactate 12%, tretinoin 0.05-0.1%
• Second line: salicylic or glycolic acid peel
• Third line: oral isotretinoin- 0.1-1 mg/kg/day
• Other: Lasers for background erythema and
hyperpigmentation.
• Poikiloderma of civatte
• Intense pulse dye laser with tunable dye
lasers.