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 Table of Contents  
Year : 2022  |  Volume : 9  |  Issue : 1  |  Page : 4-13

Dermoscopy of disorders of hypopigmentation

1 Department of Dermatology, Venereology and Leprosy, Government Medical College Srinagar, Jammu and Kashmir, India, India
2 BRLSABV Memorial Government Medical College, Rajnandgaon, Chhattisgarh, India
3 SKIMS Medical College Srinagar, Jammu and Kashmir, India

Date of Submission20-Feb-2022
Date of Decision24-Feb-2022
Date of Acceptance06-Mar-2022
Date of Web Publication16-May-2022

Correspondence Address:
Dr. Yasmeen Jabeen Bhat
Department of Dermatology, Venereology and Leprosy, Government Medical College Srinagar, University of Kashmir, Jammu and Kashmir 190010
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pigmentinternational.pigmentinternational_

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Dermoscopy has traditionally been used to diagnose neoplasms and, more recently, to evaluate inflammatory conditions. Recent observational studies have suggested a role for dermoscopy in identifying and differentiating various hypopigmentary disorders. This comprehensive review will summarize the growing literature on the use of dermoscopy for hypopigmentary disorders.

Keywords: Dermoscopy, hypopigmentation, pigmentary network

How to cite this article:
Bhat YJ, Khare S, Nabi N. Dermoscopy of disorders of hypopigmentation. Pigment Int 2022;9:4-13

How to cite this URL:
Bhat YJ, Khare S, Nabi N. Dermoscopy of disorders of hypopigmentation. Pigment Int [serial online] 2022 [cited 2023 Mar 28];9:4-13. Available from: https://www.pigmentinternational.com/text.asp?2022/9/1/4/345295

  Introduction Top

Depigmented and hypopigmented lesions are increasingly common dermatoses encountered in day-to-day practice. Hypopigmentary disorders constitute a large and heterogenous group of diseases that are clinically characterized by hypo- or depigmented macules. Dermoscopy is a noninvasive imaging technique that allows for appreciation of subtle, distinctive features invisible to the naked eye aid in the differential diagnosis of hypopigmentary disorders.

Dermoscopy findings depend on the amount and location of melanin in the skin layers, which makes evaluation of dermoscopic pattern in depigmented/hypopigmented lesions difficult owing to decrease or absence of melanin in the epidermis.

Various hypopigmentary disorders with dermoscopic features are discussed below:

  Vitiligo Top

Clinically, it presents depigmented macules in localized, segmental, generalized, or universal distributions. The role of dermoscopy in vitiligo is assessment of disease activity, pattern of repigmentation, the extent of repigmentation, evaluating response to treatment, and clinical improvement of vitiligo.[1] The dermoscopic evaluation may act as an aid in selecting appropriate candidates for surgeries. The characteristic features on dermoscopy of vitiligo are diffuse white glow, alteration in the pigment network, perifollicular pigment changes, satellite lesions, micro-Koebnerization, and leukotrichia. The absence of pigment network or white structureless areas appears to glow as a result of the complete loss of melanocytes. This loss of epidermal melanin leads to the formation of an opening through which the light-induced autofluorescence caused by dermal collagen can be observed, appearing as the bright white glow.[2]

Characteristic dermoscopic findings to assess disease activity of vitiligo can be grouped under the following parameters conveyed by the acronym BPLeFoSK criteria [Figure 1]A and scored:
  1. Border: sharp, ill-defined, trichrome
  2. Pigment network: can be reticular, absent, reduced, or reverse. The absent reticular pigment network indicates stability, whereas the reverse pigmentary network is a white reticulate pattern with pigmentation in between, indicating evolving vitiligo.
  3. Perilesional hyperpigmentation
  4. Perifollicular hyperpigmentation
  5. Satellite lesion
  6. Micro-Koebner phenomenon
Figure 1 (A) Schematic diagram of vitiligo showing features of BPLeFoSK criteria: (a) reverse reticular network, (b) absent reticular network, (c) reticulated pattern, (d) reduced reticular pattern, (e) well-demarcated border, (f) ill-defined border, (g) trichrome border, (h) polka dot pattern/satellite lesions, (i) perifollicular pigmentation, (j) perifollicular depigmentation and leukotrichia, and (k) comet tail appearance/micro-Koebnerization. (B) Schematic diagram of vitiligo showing features of stable and unstable vitiligo; (1B1) Schematics of stable vitiligo showing well defined border, absent or reticular network and perilesional and perifollicular hyperpigmentation, (1B2) Schematics of unstable vitiligo showing ill defined margin, white glow, comet tail appearance, satellite lesion, negative and broken pigment network, leukotrachia and perifollicular hypopigmentation. (C) Dermoscopy of vitiligo showing absent pigmentary network, white glow, and satellite lesions (DermLite DL3, polarized, ×10).

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A macule of vitiligo can be considered stable when the border is sharp, pigment network is absent or reticulate, presence of perifollicular pigmentation, perilesional pigmentation, and absence of micro-Keobner phenomenon and satellite lesions. Border (sharp), pigment network (absent/reticulate), perilesional hyperpigmentation, and perifollicular hyperpigmentation are given +1, whereas satellite lesions and micro-Koebner phenomenon present −1.5 and 2, respectively. A cutoff score of ≥1.5 (sensitivity 90% and specificity 94.37%) by the “BPLeFoSK criteria” indicates the lesion stability of vitiligo.[3] On dermoscopy, progressive vitiligo patterns include trichrome, comet-tail, polka dot, confetti-like, starburst, nebulous, and salt and pepper patterns. Perifollicular pigmentation is a more frequent dermoscopic feature of repigmenting or progressive vitiligo than stable vitiligo.

Reverse pigment network, a feature of melanocytic nevus and melanoma, can also be noted in early evolving vitiligo. It represents the inverse of a typical pigment network in which the hyperpigmentary lines are replaced by white lines with hyperpigmentary holes in a net-like fashion. This is contrasting to what we observe in a typical pigment network.[4] Leukotrichia is a marker of stable lesions refractory to treatment [Figure 1]B,C. Another feature, “tapioca sago,” first described by Jha et al., is reported around the lesion with active disease; on dermoscopy, they appear as 1-mm white, structureless macules, which are inapparent clinically.[5]

Trichrome pattern: darker perilesional along with perifollicular repigmentation or depigmentation.[6]

Dermoscopy can be used to compare and assess the efficacy of various treatments. The patches of vitiligo with perifollicular pigmentation on baseline dermoscopic evaluation had a 12 times higher probability of getting clinical improvement after NB-UVB phototherapy, indicating that we can predict the therapeutic responses based on certain dermoscopic features.[7]

  Pityriasis alba Top

Pityriasis alba is a type of eczema or dermatitis which presents as hypopigmented, dry macules, or patches with mild scaling, more commonly observed over the face in young children. The dermoscopy features include fairly ill-demarcated white areas with brownish-white background color. A faint pigment network is observed in the background. Hairs within the lesion are normal [Figure] 2a,b. The scales in pityriasis alba are focal in distribution and not along the skin creases, which helps in differentiating from pityriasis versicolor.[6]
Figure 2 (a) Schematic diagram of pityriasis alba showing focal white scales, ill-defined margin, and hairs are normally pigmented. (b) Dermoscopy of pityriasis alba showing white scales, faint pigment network, and brownish-white background (DermLite DL3, polarized, ×10).

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  Pityriasis versicolor Top

Pityriasis versicolor is clinically characterized by hyperpigmented or hypopigmented or erythematous, round to oval lesions with mild scaling commonly found on the upper chest, back, the upper part of arms, neck, and face. The dermoscopic features are nonuniform pigmentation, presenting as focal light brownish areas with prominent reticular pigmentary network and white structureless areas with faint pigment network. Radial distribution of lesions from the hair follicle is noted. Marginal hyperpigmentation can be seen in hypopigmented lesions and marginal hypopigmentation in hyperpigmented lesions, the features being described as “contrast halo sign.”[8] In hyperpigmented lesions, scaling in the furrows is more frequent dermoscopically. Perilesional and perifollicular scaling can be observed. Folliculocentric scaling is a conspicuous feature.[9] Follicular invasion by the yeast causes hypopigmentation of the involved hair follicle [Figure 3]a,b.
Figure 3 (a) Schematic of pityriasis versicolor showing ill-defined margin, normal hair colour with perifollicular hypopigmentation and scales along the skin creases. (b) Dermoscopy of Pityriasis versicolor showing Perifollicular hypopigmentation (red arrow) and increased scales along the skin creases(green arrow) (DermLite DL4, Polarised, ×10).

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The detached scale from skin furrows may break into two parts as a result of scratching, referred to as “double-edged” scales.[9]

  Idiopathic guttate hypomelanosis Top

Idiopathic guttate hypomelanosis is a hypopigmentary disorder which is benign in nature, and its prevalence increase with age. It commonly occurs on the extremities with small, well-defined, hypopigmented macules. The dermoscopy features include homogeneous white macules with well/ill-defined borders. Hair follicles in the lesion appear normal with no perifollicular hyperpigmentation. Multiple macules coalesce to form a polycyclic border. A hyperpigmented reticular network may be observed in and around the macule, giving it a cloudy sky appearance.[10] Four patterns described in skin of color are namely amoeboid, feathery, petaloid, and nebuloid. The amoeboid pattern has pseudopod-like projections in the macule margin, the most common type. Less frequent patterns are the feathery pattern with feather-like margin, petaloid showing a well-defined rounded border with inward projection resembles petals, and nebuloid pattern showing indistinct margins [Figure 4]A,B.[11]
Figure 4 (A) Schematic diagram of idiopathic guttate hypomelanosis showing whitish structureless areas with well demarcated hyperpigmented border in (a) petaloid, (b) feathery, (c) nebuloid, and (d) amoeboid pattern. (B) Dermoscopy of idiopathic guttate hypomelanosis showing cloudy whitish structureless areas with well demarcated hyperpigmented border (DermLite DL4, polarized, ×10).

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  Progressive macular hypomelanosis Top

Clinically progressive macular hypomelanosis presents as hypopigmented macules, which are nonscaly that coalesce to form larger macules. They are distributed symmetrically to involve the trunk and back. In progressive macular hypomelanosis, dermoscopy shows diffuse or focal whitish areas with subtle reticular pigment which may be broken at places in the background. Minimal white scales are observed and limited to skin creases [Figure 5].[12],[13]
Figure 5 Schematic diagram of progressive macular hypomelanosis showing faint reticular network and few white scales limited to skin creases.

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  Nevus depigmentosus Top

Nevus depigmentosus is a nevoid disorder caused due to the defective transfer of melanosomes to epidermal keratinocytes. The dermoscopic features show a whitish area containing a uniform but faint pigment network and irregular serrated border.[6],[14] Diffuse white glow is absent, which helps differentiate from vitiligo as the pigmentary network is faint but not wholly lost, and melanocytes present still absorb some of the incident light.[15] Leukotrichia is not observed [Figure 6]a,b.
Figure 6 (a) Schematic diagram of nevus depigmentosus showing faint reticular network throughout, perifollicular hyperpigmentation, and irregular/serrated margin. (b) Dermoscopy of nevus depigmentosus showing faint reticular network throughout (DermLite DL4, polarized, ×10).

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  Nevus anemicus Top

Nevus anemicus is a rare congenital vascular malformation caused due to localized sensitivity of cutaneous vasculature to catecholamines. It presents clinically as hypopigmented macules as a result of localized vasoconstriction. The dermoscopy shows focal areas of decreased vascular structures and preserved pigment network in the lesion with or without surrounding skin showing compensatory flare of cutaneous vasculature [Figure 7]a,b]. Lesions may merge with the surroundings during contact dermoscopy.[16]
Figure 7 (a) Schematic diagram of nevus anemicus showing a focal area of decreased vascular structures, normal pigmentary network, and compensatory flare in the perilesional areas. (b) Dermoscopy of nevus anemicus showing a focal area of decreased vascular structures and compensatory flare in the perilesional areas (DermLite DL4, polarized, ×10).

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Borderline tuberculoid leprosy shows broken, and diminished pigment network, white areas with decreased follicular openings, absent/decreased hair density and diffuse white scales in the lesion on dermoscopy. Yellow-orange areas are another important dermoscopic feature representing well-formed granuloma [Figure 8]a.[17],[18] Hypopigmented lepromatous leprosy lesions show broken pigment network, linear chrysalis-like structures, dry xerotic skin, white scales, partial loss of hair follicles, and absence of yellow-orange areas [Figure 8]b,c]. White areas were noted in most leprosy lesions, except in reaction, corresponding to decreased melanocytes in the affected patches of leprosy, differentiating it from other granulomatous infections.[19]
Figure 8 (a) Schematic diagram of hypopigmented patch of borderline tuberculoid leprosy showing broken reticular network, reduced density of hairs (circle and broken hairs seen), decreased follicular openings, diffuse white scales, and yellow-orange areas. (b) Schematic diagram of hypopigmented patch of lepromatous leprosy showing broken reticular network, reduced appendages, focal white areas. (c) Dermoscopy of leprosy showing broken pigment network, wide skin creases, absence of appendages, chrysalis-like structures (DermLite DL4, polarized, ×10).

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  Lichen sclerosus et atrophicus Top

Extragenital lichen sclerosus, also known as white spot disease, usually presents as asymptomatic lesions and clinically start as polygonal, bluish-white, slightly elevated papules, which coalesce into plaques and with time become increasingly atrophic and get a wrinkled surface. The dermoscopic features of lichen sclerosus et atrophicus demonstrates different features in early inflammatory and late sclerotic lesions. Early inflammatory lesions show white structureless areas, pink background, linear telangiectasis, comedo-like openings, and peppering of blue-gray and brown dots are observed. Late lesions show white structureless areas, chrysalis-like streaks, occasional linear vessels, and blue-gray dots [Figure 9]a,b.[20],[21] The chrysalis strands observed on dermoscopy are refractile white structures resulting from collagen in the dermis and visible only under polarized light.[22]
Figure 9 (a) Schematic diagram of lichen sclerosus et atrophicus showing pink background, red globules, linear vessels, white structureless area, and brown peppering in early inflammatory stage. In later stage, showing white background, chrysalis structures, few linear vessels and peppering of blue-gray dots, shiny white streaks, and chrysalis structures. (b) Dermoscopy of lichen sclerosus et atrophicus showing structureless white areas with brown peppering (DermLite DL3, polarized, ×10).

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Ash-leaf macules are one of the earliest manifestations of tuberous sclerosis complex and clinically present as oblong hypopigmented macules, usually on the trunk. The dermoscopic features include areas of faint pigment network and areas with complete loss of pigment network [Figure 10]a,b. The hairs in the plaque normally have pigment. The pigment network is present focally and utterly absent in other areas and has a normal brown color (faint brown color in nevus depigmentosus).[23],[24]
Figure 10 (a) Schematic diagram of ash-leaf macule showing reticular network varying from dark brown to light brown to absent with normal pigmented hair. (b) Dermoscopy of ash-leaf macule showing reduced pigment network (DermLite DL3, polarized, ×10).

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  Piebaldism Top

Piebaldism is a congenital depigmentary disorder that presents at birth as well-demarcated depigmented macules with irregular margins present over the central anterior trunk, mid-extremities, and central forehead. The dermoscopic evaluation of the depigmented lesions reveals a distorted pigment network with reduced intensity and may also be absent at places. The depigmented areas may have islands of hyperpigmentation or normal skin and an absence of perifollicular pigment [Figure 11]. The lack of perifollicular pigment may be due to the defect in the transfer of melanosomes from the melanocytes in the hair bud to the surrounding keratinocytes.[24]
Figure 11 Schematic diagram of piebaldism showing diffuse white glow, absent reticular network and normal pigmented hairs.

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  Postinflammatory hypopigmentation Top

Dermoscopy in postinflammatory hypopigmentation reveals features similar to the parent dermatosis with white structureless areas over pink background, for example, nondotted vessels/orangish structureless areas in pityriasis lichenoides [Figure 12], dotted vessels in guttate psoriasis, star-like depigmentation in prurigo nodularis, lichen simplex chronicus with chronic steroid abuse shows prominent skin markings, white structureless areas along with red background, hypertrophic lichen planus after intralesional steroid injections shows white structureless areas with pink background and yellow follicular plugging (comedo-like openings), depigmented lesion post-trauma shows white structureless areas in the area of trauma.[25],[26]
Figure 12 Dermoscopy of postinflammatory hypopigmentation following pityriasis lichenoides chronica showing structureless white areas with background orangish areas (DermLite DL4, polarized, ×10).

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  Hypopigmented mycosis fungoides Top

Hypopigmented mycosis fungoides commonly affect adolescents and young adults of Asian descent, most commonly involving the head and neck. Dermoscopy shows a broken reticular network and spermatozoa-like vessels, a highly specific feature [Figure 13].[27]
Figure 13 Schematic diagram of hypopigmented mycosis fungoides showing distorted reticular network and spermatozoa-like vessels.

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Post-kala-azar dermal leishmaniasis clinically presents as hypopigmented macules, papules, and plaques. Dermoscopic findings vary according to the type of lesion being evaluated. Patch lesions show focal areas of loss of pigment network and a yellowish structureless area representing dermal granulomas [Figure 14]. In contrast, plaque lesions show yellowish-orange areas and unfocussed vessels akin to other granulomatous dermatoses.[28]
Figure 14 Schematic diagram of post-kala-azar dermal leishmaniasis showing absence of pigment network focally and yellow structureless areas and few out of focus vessels.

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  Conclusion Top

Hypopigmentary disorders are difficult to diagnose and treat. Dermoscopy can help in providing additional clues to identify and differentiate hypopigmentary disorders and can help in improving the yields of biopsy. Furthermore, it also plays an important role in assessing the severity of the disease and response to therapy. Although histopathology remains the gold standard for the diagnosis, the utilization of dermoscopy in hypopigmentary disorders is promising and can bean adjunctive tool that can be utilized in the diagnostic assessment and treatment process.

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There are no conflicts of interest.

  References Top

Gutte R, Khopkar US. Dermoscopy: differentiating evolving vitiligo from a hypopigmented patch of Leprosy. In: Khopkar U, ed. Dermoscopy and Trichoscopy in Diseases of the Brown Skin: Atlas and Short Text. New Delhi: Jaypee Brothers Medical Publishers 2012 p. 112-3.  Back to cited text no. 1
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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14]


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Pityriasis alba
Pityriasis versi...
Idiopathic gutta...
Progressive macu...
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Nevus anemicus
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