|
 
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| REVIEW ARTICLE |
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| Year : 2021 | Volume
: 8
| Issue : 1 | Page : 14-24 |
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Dermoscopy of disorders of hyperpigmentation
Sunmeet Sandhu, Shekhar Neema, S. Radhakrishnan
Department of Dermatology, Armed Forces Medical College, Pune, India
| Date of Submission | 04-Jun-2020 |
| Date of Decision | 03-Oct-2020 |
| Date of Acceptance | 12-Mar-2021 |
| Date of Web Publication | 07-Apr-2021 |
Correspondence Address:
Shekhar Neema
Department of Dermatology, Armed Forces Medical College, Pune
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/Pigmentinternational.Pigmentinternational_
Disorders of hyperpigmentation are common in clinical practice and accounts for a large number of dermatology consultation in our country. These disorders, especially with facial involvement can result in tremendous psycho-social impact and are associated with poor quality of life. Disorders of hyperpigmentation are clinical diagnosis; the role of histopathology is limited by its invasive nature and reluctance on part of patient to undergo facial biopsy as well. Dermoscopy is a relatively new tool to diagnose these groups of disorders, but it has become popular due to its noninvasive nature and ability to perform the dermoscopic examination repeatedly over a period of time. Dermoscopy cannot replace thorough clinical history and histopathological examination, but it has distinct advantage in diagnosis of many disorders of hyperpigmentation. In this review, we will cover dermoscopy of disorders of hyperpigmentation and our approach to dermoscopy of these disorders.
Keywords: dermoscopy, EDP, facial melanosis, hyperpigmentary disorders, melasma
How to cite this article:
Sandhu S, Neema S, Radhakrishnan S. Dermoscopy of disorders of hyperpigmentation. Pigment Int 2021;8:14-24 |
| Introduction | |  |
Disorders of pigmentation are common in dermatology practice. Skin pigmentation is one of the predominant variable phenotypes in humans and skin tone variability is known throughout the world with some skin types being more susceptible to pigmentary disorders than others. The prevalence and psychological impact of these disorders varies as per the geographical areas and skin types. Individuals with darker skin are particularly more susceptible to pigmentary disorders because of contrast produced by lack of pigment in darker skin and tendency to develop post inflammatory hyperpigmentation. Around 10.8% adult patients attending dermatology outpatient department (OPD) in western India presents with disorders of pigmentation,[1] whereas studies from South India have reported the frequency of hyperpigmentary disorders among children attending the general OPD as 3.28 per 1000 children.[2] More than 80% of the population has heterogeneity of skin color over face irrespective of age and gender.[3]
Dermoscopy is a noninvasive and in vivo diagnostic tool to visualize subtle clinical patterns that are not visible to the unaided eyes. It was initially used to aid diagnosis of pigmented lesions and melanoma, however, its role in general dermatology is increasing. It has a role in diagnosis of inflammatory disorders, infections and infestations, and hair and nail disorders. Its use in pigmentary disorders known as “pigmentaroscopy” is a relatively new and exciting area of dermoscopy.
The first step in pigmentaroscopy is to ascertain the color of the lesion that depends upon the location of melanin at a particular depth in the skin. This has a diagnostic as well as prognostic significance. Black, brown, gray, and blue color perceived on dermoscopy represents the placement of melanin in superficial epidermis, dermo-epidermal junction, papillary dermis, and reticular dermis, respectively. Skin over trunk and extremities shows reticular pigment pattern, whereas over face shows pseudo reticular pattern due to interruption by hair follicles.
Dermoscopic findings are the mirror of underlying histopathological features. In pigmentary disorders, conditions may have overlapping histopathological features and they may vary as per the stage of the disease. The same is true for dermoscopy in these disorders where features may overlap. However, dermoscopy have certain advantages as clinician can perform dermoscopy in entire involved area, repeat dermoscopy during disease evolution and can change or confirm the diagnosis. This makes the pigmentaroscopy a dependable and valuable tool to aid in diagnosis, prognosis, and monitoring of treatment efficacy. In this study, we aim to provide an up-to-date practical overview of the dermoscopy in disorders of hyperpigmentation affecting individuals with skin of color.
Lichen planus pigmentosus
Lichen planus pigmentosus (LPP) was first described by Bhutani et al.[4] as an uncommon macular variant of lichen planus that is more commonly seen affecting the dark-skinned population (Fitzpatrick skin type IV and V). It is characterized by brown to slate gray hyperpigmented macules in the sun-exposed region of the face and neck or sun-protected flexural skin over axillae and inguinal areas. The morphological variants described in literature as per its frequency in descending order are diffuse, reticular, blotchy, perifollicular, and annular.[5] Histopathological examination (HPE) of LPP reveals an atrophic epidermis, hypergranulosis, interface dermatitis, colloid bodies, and dermal melanophages in the upper dermis.[6]
Dermoscopic examination of LPP shows following features [Figure 1]A and B.[7],[8] | Figure 1 (A) Dermoscopy of Lichen Planus Pigmentosus shows reticular pattern of pigment (blue arrow), blue gray dots and globules (blue star) and brown-gray dots and globules (orange star). The dots and globules are not distributed uniformly. (Dermlite DL4, polarized, ×10); (B) Dermoscopy of Lichen Planus Pigmentosus shows brown-gray reticular pigment pattern, peri-eccrine (orange arrow) and perifollicular (red arrow) gray-brown pigmented dots, and globules (Dermlite DL4, polarized, ×10); (C): Dermoscopy of Erythema Dyschromicum Perstans shows linear distribution of blue-gray dots and globules (green arrow) (Dermlite DL4, polarized, ×10).
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Reticular or pseudoreticular pattern of brown pigmentation representing epidermal pigmentation.- Fine or coarse slate gray to blue-gray dots or globules representing dermal melanophages.
- Other features include absence of Wickham striae and vascular features, perifollicular and peri-eccrine gray to brown to gray-blue pigment deposition and Hem-like pigment pattern.
Sharma et al.[4] has shown significant association between dermoscopic features of dots with/without globules to moderate-severe pigment incontinence on HPE. There are multiple distribution patterns of dots and globules described as “hem-like,” “arcuate,” “incomplete reticular,” and “complete reticular,” corresponding to various stages of skin pigmentary network. This possibly represents varying degrees of pigment incontinence such as severe incontinence pointing towards incomplete and complete reticular network and mild cases to hem-like and arcuate pattern.[4]
Because there is overlapping clinical and HPE patterns among LPP, pigmented contact dermatitis, erythema dyschromicum perstans (EDP), and exogenous ochronosis, dermoscopy of these conditions also show considerable overlap. However, there are subtle dermoscopic distinguishing features between LPP and these melanosis as highlighted in [Table 1] with the dotted pattern in LPP owing to eccrine involvement as one of the key differentiating features on dermoscopy.[9] | Table 1 Dermoscopic differences between Lichen Planus Pigmentosus, Erythema dyschromicum perstans, Riehl’s melanosis, Melasma, and Exogenous Ochronosis.
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Erythema dyschromicum perstans
The first description of Erythema dyschromicum perstans (EDP) also known as Ashy dermatosis was given by Ramirez[10] where the term “Ashy” signifies the ashy gray color of the lesion. Clinically, it presents as asymptomatic slate gray to blue brown macules or patches distributed symmetrical over trunk. The initial lesions may have an erythematous border. Generally, extremities and face and neck are spared. Histopathology reveals edema of papillary dermis, basal layer vacuolar degeneration, and perivascular infiltrate in the early lesions. Later lesions have lesser inflammatory infiltrate, more pigment incontinence, and dermal melanophages in the deeper dermis than seen in LPP.[11]
Dermoscopic features of EDP are based on dots and globules, background colors, and pattern of blood vessels.[12] The color and size of the dots and globules in EDP are quite relevant to differentiate it from LPP. Typical dermoscopic features of EDP has small gray-blue dots and globules over a bluish background corresponding to location of melanophages/pigment deposits and inflammatory infiltrate in deeper dermis in contrast to LPP where there are larger brownish-gray dots/globules corresponding to lichenoid inflammation occurring just below the epidermis and superficially located pigment incontinence [Figure 1]C.[13] Study by Elmas et al.[12] has shown irregular linear configuration of dots and globules as the commonest type of arrangement followed by circular arrangement and reticular arrangement. There is absence of predilection for perifollicular or peri appendageal regions or accentuated pseudoreticular pigment network as the lesions in EDP have truncal distribution that lacks pseudoreticular pigment network.[14]
Apart from the usual bluish background of the lesions, earliest lesions (<1 month duration) might have a pinkish brown background.[12] Vascular structures were seen in one-third of the lesions with irregular linear pattern as the commonest vessel pattern.[12] Telangiectasia was seen in 82.4% of the lesions in the study by Vinay et al. Vascular structures possibly correspond to superficial dermal telangiectatic vessels.
There is a significant correlation of dermal melanophage density with dermoscopic grades of disease severity and total disease duration. Vinay et al.[15] in their cohort of 51 patients of acquired dermal macular hyperpigmentation (ADMH) with LPP, EDP, Riehl’s melanosis/ Pigment contact dermatitis, idiopathic macular eruptive pigmentation, and other acquired hyperpigmentary disorders have correlated their dermoscopic features with histopathological features highlighting association with disease severity and duration. Although the early stage with focal vacuolization of basal layer and mild pigment incontinence corresponds to only pigment dots (grade 1) on dermoscopy. A further progressive disease and severe pigment incontinence shows larger aggregates of dermal melanophages observed as globules and blotches on dermoscopy. Grade 2 has dots predominantly with occasional globules, arranged as lines and semiarcuate structures that initially are broken and incomplete appearing as Chinese letter-like pattern and forms complete reticulate pattern (grade 3) on subsequent disease progression. A dense conglomerate of dermal melanophages involving the dermis diffusely hindering the normal pigment network (grade 4) is seen in patients with continued insults.[15] This highlights ADMH to be a continuous pathological process passing through various stages of lichenoid tissue damage corresponding to dermal pigmentation density.
Melasma
Melasma is a common, multifactorial hyperpigmentary disorder with a complex pathogenesis. Clinically, it presents as symmetrical hyperpigmented macules and patches over face, predominantly over malar areas and forehead. Rarely, it can involve extra facial sites over trunk and forearms. Clinical examination and Wood’s lamp aid in its classification as epidermal, dermal, and mixed variants based on the location of melanin, which can be further confirmed by dermoscopy. However, essentially all melasma are now considered as mixed melasma with the dermis showing solar elastosis and increased vascularity additionally.[16],[17]
Dermoscopy helps in diagnosis, differentiation from other facial melanosis, monitoring of treatment and follow up of treatment associated side effects such as steroid induced telangiectasia and exogenous ochronosis. Evaluation should look into the depth and arrangement of pigment, vascular morphology, and other additional clues.[18] Dermoscopic features of melasma include the following[8],[18],[19],[20] [Figure 2]A,B and [Figure 3]:- Light brown to dark brown pigment depending upon the depth of melanin in the skin
- Reticular or pseudo reticular pigment network, annular and arcuate structures
- Perifollicular and peri-appendageal sparing
- Brown and gray dots and globules
- Vascular prominence in some cases and telangiectasia resulting from steroid abuse
 | Figure 2 (A) Dermoscopy of melasma shows pseudoreticular pattern of brown pigment (blue arrow), perifollicular sparing (blue circle) (Dermlite DL4, polarized, ×10); (B) Dermoscopy of melasma shows pseudoreticular pattern of pigment and vascular prominence (blue arrow) (Dermlite DL4, polarized, ×10).
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 | Figure 3 Dermoscopy of treated melasma shows clearing of pigment and telangiectasia (blue arrow) (Heine Delta 20, polarized, ×10).
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Exogenous ochronosis
Exogenous ochronosis (EO) is characterized by blue-black cutaneous pigmentation due to the deposition of ochre-colored pigment in the dermis, resulting from prolonged use of skin-lightening creams containing hydroquinone. Topical use of phenol, resorcinol, picric acid, and mercury have also been implicated.[21] EO can be clinically confused with other facial melanosis, resulting in prescription of topical depigmenting agents that further aggravates this condition. Dermoscopy at the outset is valuable in ruling out differentials especially in patients not responding to treatment or worsening after initial improvement, coarse texture of the skin on palpation, and presence of fine telangiectasia and hyperchromia with speckling or reticulation.[22] Histopathological examination remains the gold standard for diagnosis with characteristic yellow-brown or ochre-colored banana-shaped fibers in the papillary dermis.[21]
Dermoscopy features of EO include the following[8],[22] [Figure 4]:- Diffuse brown background with perifollicular greyish blue dark amorphous structures with some of them obliterating the follicular openings
- Irregular, grey brown, globular, annular, arciform and structures
- Curvilinear and “worm like” structures at places
- Fine telangiectasia
 | Figure 4 Dermoscopy of early ochronosis shows pseudoreticular black to brown pigment network, brown dots and globules (blue arrow) and perifollicular brown-gray amorphous structures (orange circle) (Heine Delta 20, polarized, ×10).
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Riehl’s melanosis (pigment contact dermatitis)
Riehl’s melanosis or pigment contact dermatitis (PCD) is characterized by patchy or diffuse brown hyperpigmentation over head and neck region predominantly affecting the lateral side of the face than the center. It is considered as the noneczematous variant of contact dermatitis with a possible type 4 hypersensitivity response to a low concentration of allergen that is not severe enough to cause a spongiotic dermatitis but produces basal layer vacuolar damage resulting in pigment incontinence.[23] Histopathologic features are basal cell vacuolar damage and pigment incontinence in addition to a normal to atrophic epidermis and mild spongiosis.[14]
Dermoscopic features may vary as per the location of the pigmentation.[24] Features include an accentuated diffuse brown pseudoreticular network, regularly distributed brown dots in early PCD to finer gray to blue dots (representing deeper pigment incontinence), follicular keratotic plugs, telangiectasia, and scales over an erythematous background.[14] 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 [Figure 5]A and B.[24] | Figure 5 (A) Dermoscopy of early pigmented contact dermatitis shows diffuse brown pseudoreticular pigment network, uniform distribution of brown-gray dots (red arrow) (Dermlite DL4, polarized, ×10); (B) Dermoscopy of late pigmented contact dermatitis looks almost similar to LPP. It shows pseudo-reticular gray-blue pigment network (blue arrow), gray-blue dots and globules of varying size and perifollicular pigment (blue circle) (Dermlite DL4, polarized, ×10).
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Erythema ab igne
It is a benign condition presenting as a reticulated pattern of erythema and hyperpigmentation from repeated cutaneous exposure to either direct heat or infrared radiation resulting from occupational exposures or excessive use of warm water bottle, heating pads, or laptops. Repeated excessive exposure to heat damages superficial blood vessels resulting in hemosiderin deposition and hyperpigmentation. Overlying hyperkeratosis and hyperelastosis may develop subsequently. HPE is nonspecific with features of atrophy, telangiectasia, hemosiderin deposition, and hyperkeratosis and hyperelastosis in later stages.[25]
Early lesion has features of homogenous red-brown pigmentation surrounded by erythematous areas on dermoscopy. Hyperpigmented lesions has diffuse brownish pigmentation, telangiectasia and fine whitish scaling.[25],[26]
Pigmentary demarcation lines
Pigmentary demarcation lines (PDL), also referred to as Futcher’s or Voight’s lines, are abrupt transition lines between darkly pigmented skin color and normal skin color. These are mainly of cosmetic concern, seen in darker skin types. There are eight groups of PDL with A to E present over trunk or extremities and F to H located over face. Facial PDL can be mistaken with melasma and PIH. Histopathology is nonspecific with increase in melanisation. Dermoscopy shows clear borders of abrupt transition between darkly and less pigmented skin areas with an exaggerated or prominent reticular or pseudoreticular pattern [Figure 6].[27] | Figure 6 Dermoscopy of pigmentary demarcation line shows clear demarcation between pigmented and nonpigmented area (blue arrow) and exaggerated reticular pattern of pigment (Dermlite DL4, polarized, ×10).
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Primary cutaneous amyloidosis
Primary cutaneous amyloidosis (PCA) is a benign cutaneous disorder, resulting from amyloid deposition in the papillary dermis of the previously healthy skin without any internal organ deposition. Common presentations include macular amyloidosis presenting as areas of rippled hyperpigmentation usually over upper back or extensor aspects of limbs, papular, or lichen amyloidosis as dome shaped brown papules symmetrically over legs and biphasic/mixed variant with features of both.
Dermoscopy features has been described as per the clinical variant of cutaneous amyloidosis as following [Figure 7]A and B:- “Hub and spoke pattern” with a brown or white centre surrounded by radiating hyperpigmented streaks.[28]
- Papular amyloidosis: Central hub is replaced by central scar-like white area encircled by thick brown to black pigmentation.[28]
- Nodular amyloidosis: Atypical patterns with yellow, teardrop-like areas and orange-yellow homogeneous backgrounds with elongated and serpentine vessels.[29]
- Central white area surrounded by hyperpigmented blotches and shining white streaks on polarised dermoscopy may be seen but not clearly visible in darker skin.[30]
 | Figure 7 (A) Dermoscopy of lichen amyloidosis shows hub and spoke pattern with central pigment and radiating brown lines (blue arrow), sometimes central pigment is replaced by scar like or white structure less area (red circle) (Dermlite DL4, polarized, ×10); (B) Dermoscopy of macular amyloidosis showing incomplete hub and spoke pattern (blue circle) with central hub missing in most, it appears more like cluster of pigmented dots and globules. (Heine Delta 20, polarized, ×10).
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Additionally, high dynamic range conversion is a useful tool in accentuating pigmentary patterns on dermoscopy.[31]
Frictional melanosis
Friction melanosis, as the name suggests, is an acquired hypermelanosis resulting from habit of persistent rubbing with usual presentation as areas of hyperpigmentation over bony prominences. A variety of nomenclature in literature encompasses this entity which result from friction such as Lifa disease, Daveners dermatosis, and frictional asymptomatic darkening of the extensor surfaces. Squeezing of melanosomes into the dermis due to persistent friction and their further engulfment by the macrophages has been proposed as its pathogenesis.[32] Histopathology findings include irregular acanthosis, basal layer hyperpigmentation, patchy pigment incontinence, perivascular lympho-histiocytic infiltrate in the papillary dermis, and vertical orientation of collagen fibers.
Dermoscopic features show a structureless brown area and reticular pigmentary network.[26] There may be brown to gray dots and prominent follicular openings as well [Figure 8]. | Figure 8 Dermoscopy of frictional melanosis shows pseudoreticular brown pigment network, structureless brown area (orange arrow), and prominent follicular openings (blue arrow) (Dermlite DL4, polarized, ×10).
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Terra firma-forme dermatosis and dermatosis neglecta
Terra firma-forme dermatosis (TFFD) and dermatitis neglecta (DN) are frequently confused entities. TFFD presents with asymptomatic hyperpigmented plaques resembling dirty skin that characteristically can be removed by rubbing with alcohol. Usual presentation is over face, neck, and trunk. DN results from progressive accumulation of sebum, sweat, keratin, dirt, and debris from voluntary or unconscious inadequate frictional cleansing of the skin. This presents as a localized hyperpigmented patch or a verrucous plaque in a chronically neglected case. The lesions are routinely amenable to removal by washing with soap and water differentiating it from TFFD. Histopathological features in TFFD are acanthosis, papillomatosis, lamellar hyperkeratosis, compact orthokeratosis with whorls, and increased epidermal melanin.[33] Biopsy findings in DN show epidermal atrophy, reduced rete pegs, and prominent basketweave hyperkeratosis. TFFD can easily be mistaken with DN. Although TFFD possibly occurs due to delayed maturation and retention of keratinocytes and melanin in the epidermis, DN results from inadequate cleaning of skin. Dermoscopy may aid in differentiating these two conditions. TFFD has a more regular “polygonal plate-like” brown scales arranged in a mosaic pattern vis-a-vis DN with an irregular “cornflake-like” dark brown scaling pattern [Figure 9]A–C.[34] | Figure 9 (A) Dermoscopy of TFFD shows polygonal brown scales arranged in mosaic like pattern (blue arrow) (Heine Delta 20, polarized, ×10); (B) Dermoscopy of TFFD shows clearing of scales with alcohol (Heine Delta 20, polarized, ×10); (C) Dermoscopy of dermatosis neglecta shows irregular dark brown scales (red arrow) (Dermlite DL4, polarized, ×10).
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Acanthosis nigricans and maturational hyperpigmentation
Acanthosis nigricans (AN) clinically presents as coarse velvety hyperpigmented plaques symmetrically over neck and flexural regions of the body. Variants of AN include benign, obesity associated, syndromic, malignant, acral, unilateral, medication-induced, and mixed AN. Clinically, facial AN may mimic “maturational hyperpigmentation (MH)” that is another ill-defined and poorly recognized entity. However, MH has some distinctive features such as a relatively softer surface with finer granularity and clinically indistinct margins, and distinctive dermoscopy and histopathology.[35] Histopathology of AN reveals acanthosis, papillomatosis, hyperkeratosis, and hyperpigmentation of the basal layer.[36] Histological features of MH has slight papillomatosis with significant basal layer melanisation.[35]
Dermoscopy of AN shows linear crista cutis and sulcus cutis with hyperpigmented dots (corresponding to papillomatosis) in the crista cutis [Figure 10]A and B),[8] whereas dermoscopy of MH lacks crista and sulci but shows brown rings and clods with perifollicular accentuation [Figure 11].[35] | Figure 10 (A) Dermoscopy of acanthosis nigricans of neck shows linear sulcus cutis and crista cutis (blue arrow) and hyperpigmented brown dots (blue circle) (Heine Delta 20, polarized, ×10); (B) Dermoscopy of acanthosis nigricans of face shows linear sulcus cutis and crista cutis and hyperpigmented brown dots (yellow circle). These features are less prominent as compared to AN of neck (Dinolite edge, polarized).
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 | Figure 11 Dermoscopy of maturational hyperpigmentation shows brown rings and clods with perifollicular accentuation (blue circle). It does not show linear sulcus cutis and crista cutis and reticular pigment network. (Heine Delta 20, polarized, ×10).
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Postinflammatory hyperpigmentation
Postinflammatory hyperpigmentation (PIH) is an acquired hypermelanosis developing secondary to any cutaneous trauma/injury (thermal/chemicals) or any inflammatory entity (acne, lichen planus, etc.). Individuals with skin of color are predisposed to develop PIH. Sun exposure further aggravates PIH. Pathogenesis involves an initial inciting epidermal injury or inflammation stimulating melanin synthesis and subsequent transfer of melanin to surrounding keratinocytes (epidermal melanosis). Blue-gray pigmentation results from damage to basal layer resulting in melanin incontinence into dermis. Histopathology is nonspecific with patchy epidermal pigmentation and/or dermal melanosis. Correlation of adequate history and clinical examination is required to reach an accurate diagnosis here.
Dermoscopy of PIH of an inflammatory condition may present with dermoscopic features which are characteristic of the original lesion.[26] Moreover, it hints toward epidermal, dermal, or mixed component of pigmentation based on color of pigmentation (dark brown, gray dots, and/or blotches or mixed pattern, respectively) thereby helping in planning further treatment [Figure 12].[8] | Figure 12 Dermoscopy of post inflammatory hyperpigmentation shows nonspecific brown pigment pattern (Dermlite DL4, polarized, ×10).
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Seborrheic melanosis
Seborrheic melanosis is a poorly defined entity that has been postulated as PIH secondary to seborrheic dermatitis.[37] It presents as localized darkening of seborrheic areas of the face, predominantly over the alar grooves, angles of the mouth, and labio-mental crease and is seen more commonly in Asian, African, and Hispanic population. Dermoscopic findings have been categorised into vascular, pigmented, and mixed pattern. Vascular pattern refers to arborizing and linear vessels over a light pink background. Pigmented pattern shows a prominent hyperpigmented pseudo-network with some annular granular structures with brown dots not occluding the follicular orifices. There is absence of gray dots and clods. Mixed pattern has features of both.[37] Prominent pseudo-network and brown dots corresponds to combination of epidermal melanin, acanthosis, and increased melanin-containing keratinocytes [Figure 13].[37] | Figure 13 Dermoscopy of seborrheic melanosis shows pigment pseudo-network (blue arrow), erythema and gelatinous filament like structures suggesting Demodex tails (Dermlite DL4, polarized, ×10).
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Confluent and reticulated papillomatosis (Gougerot-Carteaud syndrome)
Confluent and reticulated papillomatosis (CARP) is an acquired keratinization disorder of uncertain etiology presenting as asymptomatic, hyperpigmented, scaly, flat papules, patches, or plaques with reticular pattern at the edges, usually over anterior and posterior upper trunk. Dermoscopy shows fine whitish scaling and brownish areas in a cobblestone (closely aggregated, squarish/polygonal, flat globules) or sulci-gyri pattern.[38] This pigmentation corelates to combination of basal layer hypermelanization, acanthosis, and papillomatosis. Folliculo-centric whitish structures (hyperkeratosis and acanthosis of follicular epidermis) and “V” hair may also be seen [Figure 14].[39] | Figure 14 Dermoscopy of Confluent and reticulated papillomatosis shows fine white scaling (orange arrow) and brown pigment network in sulci and gyri pattern (blue arrow). The histopathology of CARP is similar to AN with less prominent features, so is dermoscopy (Dermlite DL4, polarized, ×10).
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Nevus of Ota and Becker’s nevus
Nevus of Ota is a dermal melanocytosis along the trigeminal nerve’s ophthalmic and maxillary branches presenting as unilateral mottled bluish gray or bluish brown macules over zygomatic and temporal areas since birth. Sclera and oral mucosa can also be involved. Rare presentation with bilateral macules or delayed onset in adolescence is seen as well. Pigmented dendritic melanocytes and melanophages dissecting the collagen bundles in reticular dermis is seen histopathologically. Dermoscopic features show gray-blue to blue brown structureless areas in a patchy distribution with scattered gray-brown dots and perifollicular hypopigmentation [Figure 15].[40] | Figure 15 Dermoscopy of Nevus of Ota shows gray- blue structureless area (blue arrow) and perifollicular hypopigmentation (Dermlite DL4, polarized, ×10).
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Becker’s nevus (BN) is a cutaneous hamartoma presenting as circumscribed hyperpigmented patch with variable degree of hypertrichosis on and around the lesion, usually near the large joints (especially shoulders and elbows). Hyperkeratosis, acanthosis, elongation, and fusion of rete ridges and with hyperplasia of dermal smooth muscle is seen on HPE.[41] The dermoscopic features in BN include terminal hairs, perifollicular hypopigmentation, and a well-defined pigment network with blotchy hyperpigmentation at the center of patch, whereas a normal pigment pattern at the periphery.[41] Focal hypopigmentation, skin furrow hypopigmentation, and vessels may be seen [Figure 16].[42] | Figure 16 Dermoscopy of Becker’s nevus shows terminal hairs (blue arrow), perifollicular hypopigmentation (blue circle) and reticular pigment network (orange arrow) (Heine delta 20, polarized, ×10).
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| Conclusion | | |
Dermoscopy is useful in diagnosis, prognosis, and follow up of disorders of hyperpigmentation. Similar to histopathology, even dermoscopy should be evaluated in light of clinical differential diagnosis and not as a stand-alone modality. With regular practice and attention to detail towards dermoscopic findings, it can be a useful tool in dermatology practice in general and for disorders of hyperpigmentation.
Financial support and sponsorship
Nil.Conflict of interest
There are no conflicts of interest.
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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], [Figure 15], [Figure 16]
[Table 1]
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