Facial dyschromias: A review of clinical and dermoscopic features

Clinical profile

Melasma is a commonly encountered condition characterized by symmetrical hyperpigmented macules with irregular borders commonly seen over the cheeks, forehead, and mandibular region [Figure 1].^[18] Although this condition is commonly encountered among females with the skin of color, men have been reported to constitute around one-quarter of the total number of cases, as reported in a study conducted by Sarkar et al.^[19]. The risk factors for developing this condition include the presence of a family history of melasma, use of oral contraceptives, hypothyroidism, exposure to ultra-violet light, and certain drugs, including antiepileptics like phenytoin.^[20]

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Figure 1:

Clinical image of melasma.

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Melasma has been classified as centrofacial, malar and mandibular types based on the distribution of the skin lesions, with centrofacial type being reported as the most common variant. Further, melasma has been classified based on the depth of pigmentation into epidermal, dermal, and mixed types. Epidermal lesions show enhancement when examined under Wood’s lamp, which is not seen in the dermal subtype. Focal areas of enhancement are seen in the mixed subtype.^[18]

The differential diagnosis for melasma includes Hori’s nevus, LPP, exogenous ochronosis, and pigmented contact dermatitis, to name a few. Dermoscopic examination is useful in confirming the diagnosis, especially since skin biopsy is not commonly done from the face due to cosmetic concerns.^[21]

Dermoscopic profile

Dermoscopic examination of melasma showed an increase in the pseudoreticular pigment network, with sparing of follicular and eccrine openings, arcuate and annular structures, brown globules, and occasional telangiectasias [Figure 2].^[21] Nearly 98% of the patients in this study showed sparing of follicular and eccrine openings.^[22] Reticuloglobular pigmentation, patchy pigmentation, granular pattern, and telangiectasias were found to show statistically significant association with melasma.^[23] The telangiectasias reported in melasma may be due to prior topical steroid abuse, extensive photodamage or due to increased vascular endothelial growth factor, which supposedly plays an important role in melanogenesis.^[24]

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Figure 2:

Dermoscopy of melasma (DermLite DL4, ×10, non-polarized) showing increased pseudoreticular pigment network with sparing of follicular and eccrine openings.

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Histopathological profile

Classical histopathology of melasma shows an increase in epidermal melanin content across all layers without any increase in the number of melanocytes. There may also be the presence of dermal melanophages and melanin in the dermal subtype.^[25] However, recent studies have reported other dermal changes in melasma, including solar elastosis, basement membrane disruption, an increase in number of mast cells, and increased vascularity of lesions, which may have therapeutic implications.^[24]

Further, the melanocytes in melasma are found to be more biologically active, which is evidenced by the increased number of dendritic processes, rough endoplasmic reticulum, and mitochondria. Increased fragmentation of dermal elastic fibers may also be found.^[18] Thus, melasma, which was hitherto considered to be a pure pigmentary disorder, is now considered to be a disorder of skin photoaging.^[26]

Clinical profile

Exogenous ochronosis is a condition characterized by bluish-black hyperpigmentation, usually occurring following the application of hydroquinone-containing creams. This condition may present as speckled pigmentation, papules or nodules over the zygomatic region of the face and can sometimes closely resemble melasma.^[27]

Dermoscopic profile

Dermoscopy in exogenous ochronosis shows dark brown globules.^[27] Curvilinear and worm-like structures have also been described, which may be arranged in a reticular pattern. These findings help in differentiating this condition from melasma, which usually shows an accentuated pseudoreticular pigment network.^[28]

Histopathological profile

Histopathology remains the gold standard in the diagnosis of exogenous ochronosis. Characteristic ochre-colored banana-shaped bodies may be seen in the dermis, along with swelling of collagen bundles. These “banana bodies” may be highlighted using methylene blue stain.^[27]

Clinical profile

Pigmentary demarcation lines are physiological lines characterized by abrupt transition from dark pigmented areas to lighter pigmented skin, which is commonly encountered in females. These lines are present over the face, trunk, and limbs (Groups A–H), out of which groups F, G, and H have been described on the face. Group F presents as a “V”-shaped region of pigmentation over the lateral part of the face, Group G presents as a “W”-shaped region of pigmentation over the lateral face, and Group H presents as a band of pigmentation from the angle of mouth extending to the lateral chin. This condition is often mistaken for melasma and post-inflammatory hyperpigmentation.^[29]

Dermoscopic profile

Dermoscopy in pigmentary demarcation lines shows an abrupt transition between the lighter and darker areas of skin in the form of an increased pseudoreticular pigment network. White clods have also been found in the area of increased pigment network.^[29]

Clinical profile

LPP is a condition characterized by asymptomatic slate-gray pigmentation, usually seen over the face- and sun-exposed areas. This condition was first described in India by Bhutani et al.^[30] in 1974 – who described the clinical and histopathological features in 40 patients. Subsequently, several studies have been conducted describing this condition in various parts of the world.^[31]

LPP usually presents during middle age, with a female preponderance. The photo-distributed variant is usually seen in darker Fitzpatrick skin types. LPP is thought to be a delayed hypersensitivity reaction to an unknown antigen, which subsequently leads to basal cell degeneration and melanin incontinence.^[31] In India, this condition is thought to be associated with the use of mustard oil, hair dye, gooseberry oil, and cosmetics. Some other associations include co-existing lichen planus, hepatitis C, autoimmune thyroid disease, alopecia areata, and vitiligo.^[32]

LPP has an insidious onset, presenting as slate-gray to brown macules, usually over the face and photo-exposed areas [Figure 3]. There is usually no history of preceding erythema or inflammation. The various patterns of pigmentation include diffuse, reticular blotchy, perifollicular, gyrate, and annular. Rare patterns such as linear and segmental pigmentation have also been described.^[31]

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Figure 3:

Clinical image of lichen planus pigmentosus showing diffuse slate-gray pigmentation.

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Acquired dermal macular hyperpigmentation is a recently coined umbrella term used to describe conditions with dermal pigment incontinence, with or without active interface dermatitis. This umbrella term includes LPP, ashy dermatosis, and Riehl’s melanosis (pigmented contact dermatitis). The above-mentioned conditions show considerable clinical and histological overlaps with very subtle differentiating features [Table 5].^[32]

Patients with pigmented contact dermatitis usually complain of mild itching, and the pigmentation may be accompanied by fine whitish scaling. In patients with contact dermatitis to paraphenylene diamine (PPD)-containing hair dyes, the pigmentation may involve the helix, lobule of the ear and upper back. Patients with contact dermatitis to textile materials may show pigmentation over the axilla, which characteristically spares the vault. A detailed cosmetic history is, therefore, essential to differentiate this condition from LPP.^[32]

Patch testing for common allergens may be positive even in the general population. Therefore, some dermatologists consider LPP to have spectral overlap with pigmented contact dermatitis rather than being a separate condition.^[33]

Ashy dermatosis was first described in El Salvador^[34] Subsequently, it was also termed “Erythema dyschromicum perstans” in view of the characteristic erythematous, raised border seen in early lesions. In a global consensus statement on acquired dermal pigmentary disorders,^[35] it was decided that the presence of an erythematous border (current or past) surrounding the areas of pigmentation was essential to making a diagnosis of erythema dyschromicum perstans.^[35]

Dermoscopic profile

Sharma et al.^[36] performed dermoscopy and patch testing in 50 patients with LPP. The most common dermoscopic finding described included brown to gray dots and globules with varied patterns of arrangement [Table 6 and Figure 4].

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Figure 4:

Dermoscopy of lichen planus pigmentosus (DermLite DL4, ×10, polarized) showing blue dots, gray dots.

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Additional dermoscopic findings include dots and globules arranged in a “Chinese letter pattern,” as described by Devanda et al.^[37] in a cross-sectional study on 27 patients with LPP.^[37] Although Riehl’s melanosis shows significant overlap with LPP in terms of clinical and dermoscopic features, Wang and Xu^[38] described the presence of “flour-like” scales in the former, which may be a differentiating feature. Follicular plugging and perifollicular halo have also been described in Riehl’s melanosis.^[38]

However, some authors do not consider any dermoscopic feature to be specific enough to differentiate between the various acquired dermal macular hyperpigmentary disorders. A dermoscopic grading system has been devised for these disorders based on the number and arrangement of dots and globules [Table 7].^[32]

Histopathological profile

The histopathological profile of LPP varies with disease duration. Early lesions show extensive interface dermatitis, which later results in pigment incontinence [Figure 5]. Older lesions show dermal melanophages without active inflammation at the dermoepidermal junction. Immune deposits have been reported in around 15% of patients with this condition, which may include immunoglobulin M C3, deposits in a linear pattern or the colloid bodies.^[31]

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Figure 5:

Histopathology in lichen planus pigmentosus (H&E, ×200) showing basal vacuolar degeneration and pigment incontinence in the dermis. H&E: Hematoxylin and eosin.

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Although Riehl’s melanosis occurs due to contact dermatitis to various agents, spongiosis is not a commonly described finding in this condition.^[38] Patch testing is therefore considered essential to arrive at a diagnosis of pigmented contact dermatitis.^[31]

Ashy dermatosis obtains its characteristic color from melanophages in the upper dermis. Interface dermatitis is a less frequently encountered finding and is therefore not essential to diagnose this condition.^[35]

Since there is considerable overlap between the various acquired dermal macular hyperpigmentary conditions, a detailed drug history needs to be elicited, and patch testing may be considered in select cases to arrive at a possible diagnosis.^[32]

Clinical profile

Chronic cutaneous LE is of varied clinical types, with s being the most commonly encountered variant.^[39] This condition presents as well-defined erythematous scaly plaques, usually over the head and neck region, but may also be disseminated in other areas [Figure 6]. Well-established lesions may show atrophy, scarring, telangiectasia, and pigmentary alterations.^[40]

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Figure 6:

Clinical image of discoid lupus erythematosus.

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A newer variant of chronic cutaneous LE presenting as hyperpigmented macules over the head and neck region has been described. Atrophy and scarring were conspicuously absent in these lesions, making the diagnosis challenging. However, histopathology and direct immunofluorescence were consistent with the diagnosis of chronic cutaneous LE.^[41]

Another variant of chronic cutaneous LE presenting as reticulate pigmentation over the face has been reported. The pigmentation had a slate-grey to lichenoid hue, with few areas of depigmentation interspersed in between. Histopathology, direct immunofluorescence and antinuclear antibodies (ANA) titers were employed to clinch the final diagnosis of cutaneous LE.^[39]

Dermoscopic profile

DLE has been described to have various dermoscopic findings based on the site of the lesion and the duration of the disease.^[42]

The dermoscopic features in classical DLE include follicular plugging, patchy scaling, perifollicular halo, structureless white areas, rosettes, starburst pattern, and speckled pigmentation. Vascular patterns include red dots, linear blood vessels, arborizing vessels, and perifollicular erythema [Figure 7].^[43]

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Figure 7:

Dermoscopy of discoid lupus erythematosus (DermLite DL4, ×10, polarized) showing peripheral hyperpigmentation (yellow star), telangiectasia (black arrow), and scaling (blue arrow).

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The dermoscopic features of a pigmented macular variant of chronic cutaneous LE have not been extensively described in the previous literature as it is an under-recognized entity.

Histopathological profile

Classical DLE shows ortho/hyperkeratosis, epidermal atrophy, basal vacuolar degeneration, periadnexal lymphocytic infiltration, basement membrane thickening, and dermal deposition of mucin.^[44] Histopathology from the pigmented macular variant shows epidermal atrophy, basal vacuolar degeneration, and melanin incontinence. Direct immunofluorescence shows linear deposition of immunoreactants along the basement membrane zone.^[39]

Clinical profile

Facial acanthosis nigricans has an appearance similar to that of acanthosis nigricans at other sites and commonly involves the temporal regions, cheeks, chin, periorbital, and perioral regions.^[45,46] The patient may show evidence of acanthosis nigricans at other characteristic sites, and there may be overlying acrochordons.^[47] Accurately diagnosing this condition is important as it is a clue to underlying insulin resistance and metabolic complications.^[48]

Dermoscopic profile

In a clinico-investigative study conducted on 40 patients diagnosed with facial acanthosis nigricans, it was found that all cases showed cristae cutis, sulci cutis, and hyperpigmented dots within the cristae. Other patterns commonly observed include brown dots, globules, and papillary projections.^[48] It has been observed that non-polarized dermoscopy images highlight the cristae and sulci clearly, while polarized dermoscopy highlights pigmented dots.^[49] Further, the increase in severity of acanthosis nigricans corresponds to increased cristae and sulci on dermoscopy.^[50]

Dermoscopy may also be used to assess the severity of facial acanthosis nigricans – with mild cases showing only sulci, which can progressively become interconnected with folding of cristae and hyperpigmentation in moderate-to-severe facial acanthosis nigricans. Chronic cases may show additional findings such as perifollicular hyperpigmentation and large pigmented globules.^[48]

Histopathological profile

Histology of facial acanthosis nigricans shows hyperkeratosis, increased basal melanization, acanthosis, and papillomatosis. The cristae cutis on dermoscopy represents the epidermis, which is elevated by the underlying papillomatosis in the dermis. The sulci correspond to the surrounding epidermis, with the white color being due to the basket-weave cornified layer in the downwardly depressed epidermis. The papillary projections seen on dermoscopy are thought to be due to extreme papillomatosis.^[48]

Clinical profile

Maturational hyperpigmentation is a newly described facial melanosis – which is thought to be a cutaneous marker of metabolic syndrome, similar to acanthosis nigricans. It clinically presents as asymptomatic hyperpigmentation over the cheek or zygomatic region with a soft, granular surface without well-defined margins [Figure 8]. Dermoscopy and histopathology are distinct from other causes of facial melanosis.^[51]

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Figure 8:

Clinical image of maturational dyschromia.

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Dermoscopic and histopathological profile

Dermoscopy may show an brown exaggerated pseudoreticular pigment network, brown dots and globules, and characteristic “ring-like structures” which are brown oval or round rings showing perifollicular accentuation [Figure 9]. Histopathology shows increased epidermal and basal cell melanization with minimal papillomatosis.^[52]

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Figure 9:

Dermoscopy in maturational dyschromia (DermLite DL4, ×10, non-polarized) showing characteristic perifollicular ring structures

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Maturational hyperpigmentation is an under-recognized facial melanosis which has been described in African and Indian populations. Studies conducted on Indian patients have shown fasting hyperglycemia and hyperinsulinemia in patients with maturational hyperpigmentation.^[51]

Clinical profile

Post-inflammatory hyperpigmentation is a condition commonly encountered in individuals with skin of color, which may last for months to years and can be a cause of significant distress to patients. This condition may arise following several dermatological conditions, including acne vulgaris, atopic dermatitis, lichen planus, contact dermatitis, cutaneous infections, vesicobullous disorders, and chronic cutaneous LE. This condition may also arise following mechanical injury to the skin or following dermatological procedures such as lasers and chemical peels.^[53]

Post-inflammatory hyperpigmentation presents as macules over the region of initial inflammation. The color of the lesion may vary depending on the depth of the melanin pigment.^[54] The pigmentation is more intense in higher Fitzpatrick skin types and may also worsen with ultraviolet ray exposure or recurrent inflammation.^[53]

Dermoscopic profile

Jurairattanaporn et al. ^[54] found that the common dermoscopic patterns of post-inflammatory hyperpigmentation over the face include increased pseudoreticular pigment network, clustered aggregated lobules, homogenous pigmentation, and arcuate-annular structures. Vascular patterns were also commonly observed, including ill-defined erythema, red dots, straight lines, glomerular vessels, and arborizing vessels.^[54]

Histopathological profile

Epidermal post-inflammatory hyperpigmentation has been found to have increased basal layer pigmentation. Dermal post-inflammatory hyperpigmentation has been described as melanophages in the upper dermis, which may be accompanied by lymphoplasmacytic infiltrate and basal layer vacuolation.^[55]

Clinical profile

Seborrheic melanosis is a hitherto ill-defined clinical entity, largely described by dermatologists in India. The condition is said to affect the alar grooves, angles of the mouth, and labiomental crease – which are considered to be seborrheic areas of the face. Individuals with Fitzpatrick skin types IV and above are thought to be primarily affected by this condition.^[56]

Some dermatologists hypothesize that seborrheic melanosis is a form of post-inflammatory hyperpigmentation to seborrheic dermatitis of the face.^[57] Some patients may give a history of preceding flakiness or redness of skin before developing hyperpigmentation. Clinical diagnosis may be aided by some supportive findings such as oily skin, plugging of follicles with inspissated sebum, or concomitant seborrheic capitis.^[56]

Dermoscopic profile

Verma et al.^[56] described the dermoscopic features of seborrheic melanosis in 12 patients with skin of Fitzpatrick types III, IV, and V. The dermoscopic findings were divided into – vascular, pigmented, and mixed patterns. The vascular pattern showed a light pink background and arborizing vessels which were out of focus. The pigmented type of presentation was found in darker skin types – with prominent brown pigmented pseudonetwork and annular granular structures not occluding the orifices. Grey dots and clods were conspicuously found to be absent. The finding seen most commonly among patients with seborrheic melanosis include white excrescences of sebum coating the vellus hair shafts and prominence of follicular openings.^[56] Dermoscopy from alar grooves of healthy individuals may occasionally show erythema, brown globules, and vessels.^[58]

Clinical profile

Periorbital pigmentation, commonly known as “dark circles,” is a commonly encountered yet clinically ill-defined condition arising due to various causes. Genetic causes, post-inflammatory pigmentation, atopic diathesis, increased vasculature, tear trough deformity, and shadowing due to skin laxity have all been hypothesized to be some of the causative factors.^[59] Further, habits such as lack of sleep, frequent rubbing of eyes, cosmetic use, and refractive errors have also been implicated.^[60]

Periorbital pigmentation is described as bilateral homogenous hyperpigmentation predominantly involving the lower eyelid but may also extend to the upper eyelid, eyebrow region, temporal region, malar region, and the root of the nose.^[60] Periorbital pigmentation has been graded from 0 to 4 based on the extent of pigmentation^[61] [Table 8]. Periorbital pigmentation has been classified into pigmented, vascular, structural, and mixed types based on the color and pattern of pigmentation [Table 9].^[62]

Dermoscopic profile

Dermoscopic patterns described in periorbital pigmentation include scattered brown dots, blotches, and increased pigment network, predominantly in the pigmented type. Vascular type of periorbital pigmentation was found to have dilated veins, telangiectasia, along with brown dots. An additional feature seen in the structural type of periorbital pigmentation is an increase in skin markings.^[63]

Histopathological profile

Nayak et al.^[64] in their study on 50 patients with periorbital pigmentation, it was found that 90% of the patients had increased melanin in the basal and spinous layers. Dermal melanin incontinence, melanophages in the upper dermis, and lymphoplasmacytic perivascular infiltrate were uniformly found in all the patients studied. Increased pigmentation of the basal layer of vellus hair follicles in the infraorbital region has also been reported. Perl’s stain did not demonstrate hemosiderin in any of the cases.^[64]

Clinical profile

Nevus of Ota or oculodermal melanocytosis is a condition characterized by pigmentation of the skin and mucus membranes along the distribution of the first two branches of the trigeminal nerve. The onset is usually at birth or in early childhood, presenting as a bluish-gray macule which is usually unilateral, with irregular borders. The ipsilateral sclera and palate may also be involved. The diagnosis is usually made clinically, with histopathology being reserved for doubtful cases.^[65]

This condition is thought to be due to the defective migration of melanocytes from the neural crest to the epidermis, resulting in melanocytes being trapped within the dermis. Production of melanin within the dermis produces a bluish hue due to the Tyndall effect.^[66]

Dermoscopic profile

Commonly encountered dermoscopic findings include gray-brown structureless areas, brown-gray dots, and white clods in a “four-clod dots” arrangement. Characteristically, the reticular pigment network is usually not seen over the nevus.^[67] The presence of terminal hair with perifollicular hypopigmentation has also been described.^[65]

Histopathological profile

Histology reveals pigmented dendritic melanocytes within the reticular dermis, with dissection of dermal collagen bundles by melanophages.^[67]

A close clinical and histological differential for nevus of Ota is Hori’s nevus, which is a dermal melanocytosis usually encountered among Asian patients.^[22] However, this condition commonly presents in the third or fourth decade as symmetrical slate gray macules over the face without mucosal involvement.^[65]

Differentiating dermal melanocytosis from melasma is important to formulate an appropriate treatment approach, with depigmenting agents and chemical peels being used for the former and pigment-specific lasers being preferred for the latter.^[22] Dermoscopy may aid in accurate diagnosis, thereby obviating the need for skin biopsy in patients who have cosmetic concerns.^[65]

Clinical profile

Transverse nasal line is an embryological defect first described by Cornbleet in 1951, who also coined the synonyms transverse nasal groove, stria nasi transversa, and transverse nasal strip. This entity is thought to be due to an embryological defect during the fusion of the triangular and alar cartilages of the nose.^[68]

A pigmented transverse nasal band is a band-like eruption measuring about 2 mm in width, spanning the entire nasal bridge.^[69] It is an asymptomatic condition with an incidence of about 0.3% in the Indian population. Due to the faulty embryological line, retention cysts may occasionally arise over the transverse nasal band in the form of milia or pseudocomedones.^[70]

Differential diagnoses for this condition include allergic salute and wrinkles due to aging, which may be distinguished by certain clinical clues [Table 10].

Dermoscopic profile

Dermoscopic features of this condition include microcomedones appearing as brown dots and milia overlying white transverse streaks. These transverse streaks are thought to arise from adhesions and fibrosis in the nasal cartilage. Histopathology and surgical modalities are avoided in this condition due to the potential damage that can be produced to the nasal cartilage and the transverse nasal vein.^[70]

Clinical profile

Congenital melanocytic nevi (CMN) are neural crest-derived hamartomas that present at birth or shortly thereafter. This condition is prevalent in about 1–6% of newborns. These nevi are classified based on their size into small, medium, and large – measuring <1.5 cm, 1.5–20 cm, and >20 cm, respectively.^[71] Larger lesions are associated with an increased risk of developing melanoma. The risk of melanoma varies greatly based on the clinical characteristics of the lesion.^[72]

Dermoscopic profile

Dermoscopy is a useful tool for the diagnosis, follow-up, and management of benign melanocytic lesions, including CMN.^[72] It is also useful for differentiating benign and malignant melanocytic lesions.^[73]

Various dermoscopic patterns may be seen in CMN including reticular pattern, globular pattern, homogenous pattern, and cobblestone pattern. A combination of patterns may also be seen, including a reticuloglobular pattern, peripheral reticular pattern with central homogenous pigmentation, and patchy reticular pattern. Some lesions may also show additional features such as radial streaks, hypertrichosis, focal areas of hypopigmentation, milia-like cysts, and regression structures.^[71]

Histopathological profile

On histopathological examination, CMN may show nevus cells in both the epidermis and dermis. They may form orderly clusters, sheets, cords, or nests of cells. Nevus cells are found to aggregate around appendages such as hair follicles sebaceous glands, and also around neurovascular structures. Deeper extension of nevomelanocytes and periappendigeal distribution of cells are some of the features that help in differentiating this condition from acquired melanocytic nevi.^[74]

Clinical profile

Becker’s nevus was first described in 1949 by Becker as a localized hyperpigmented macule with overlying hypertrichosis, classically occurring over the shoulder region during adolescence.^[75]

Follicular Becker’s nevus is a newly described variant, presenting as hyperpigmented follicle-based macules. These lesions present unilaterally over the chest or scapular region, but may also occur over other sites.^[76] There may or may not be hypertrichosis/thick hair within the center of each follicular macule.^[77] The presence of folliculocentric macules might suggest a role of follicular epithelium in the pathogenesis of this condition.^[78]

Dermoscopic profile

The dermoscopy from folliculocentric macules shows perifollicular hypopigmentation surrounded by a network of increased pigmentation.^[78] There are areas of normal pigment network interspersed in between. In another study, the presence of thick hair has been described in the center of these hyperpigmented macules.^[77]

Histopathological profile

Hyperkeratosis, acanthosis, increased basal cell pigmentation, and, occasionally, the presence of melanophages in the papillary dermis have been reported. There is an increase in melanin content but no increased melanocyte count.^[79]

Clinical profile

Dowling–Degos disease is an autosomal dominant genodermatosis, with onset usually during early adulthood. This condition is characterized by reticulate pigmentation over the flexures. Additional features, such as perioral pits and follicular lesions, may be seen.^[80] Variants of this condition include generalized type, follicular variant, and acantholytic variant (Galli-Galli disease), to name a few. Overlap with other reticulate pigmentary disorders has also been described.^[81]

Dermoscopic profile

Follicular Dowling–Degos presents with reticulate pigmentation, follicle-based papules, pitted acneiform scars, and comedones predominantly over the face, upper trunk, and flexures. Dermoscopy shows a characteristic “Chinese-letter pattern” of linear pigmentation, which may occur over a background of normal or hyperpigmented skin. Follicular inclusion cysts may also be seen.^[82]

Histopathological profile

The histopathology of Dowling–Degos disease shows elongated hyperpigmented rete ridges, forming an “antler-like pattern.” Suprapapillary thinning and increased melanin at the tips of rete ridges are also seen.^[83] In the follicular variant, these changes are observed to be confined to the follicular infundibulum.^[82]

Clinical profile

Vitiligo is a commonly encountered acquired pigmentary skin disease associated with significant social stigma in some communities.^[84] This condition may sometimes mimic other disorders of hypopigmentation, like idiopathic guttate hypomelanosis. This condition presents as depigmented macules and may also affect the hair and mucosa.^[85]

Based on the distribution of lesions, vitiligo may be divided into segmental and non-segmental types. Non-segmental vitiligo may be further divided into acrofacial, generalized, mucosal, mixed, and other rare types.^[85] The clinical markers of the active disease include a trichrome sign, Koebnerization, inflammatory margins, and confetti-like depigmentation.^[86]

Decisions regarding the management of this condition are made based on the stability of the lesions. The stability of vitiligo lesions may be assessed by both clinical examination and dermoscopy.^[87]

Dermoscopic profile

Nirmal et al.^[87] performed dermoscopy on 85 patients clinically diagnosed with vitiligo. Dermoscopy was found to be a reliable tool for assessing the stability of vitiligo lesions, thereby obviating the need for skin biopsy [Table 11].^[87]

Other dermoscopic findings in progressive vitiligo include starburst appearance, comet-tail appearance, and sago grain appearance. Intralesional and perilesional erythema have been found to be indicators of stable and re-pigmenting lesions. Most of the dermoscopic clues regarding disease activity are located in the perifollicular region.^[84]

Histopathological profile

Vitiligo is characterized by basal hypopigmentation – which is due to an absent or significantly decreased number of melanocytes. Mild dermal inflammation may also accompany the epidermal findings. Immunohistochemistry for melanin may be performed to confirm the above-mentioned findings.^[88]

Clinical profile

Nevus depigmentosus is a relatively common condition, presenting as a hypopigmented macule with no significant change in size or distribution throughout life. Although most cases are thought to be congenital, there have been reports of cases presenting later in life.^[89]

The original diagnostic criteria suggested by Coupe in 1976 include the presence of leukoderma at birth, without alteration of distribution, texture or sensations over the lesion, and an absence of hyperpigmented border around the achromic area.^[90]

This condition presents as a well-defined hypopigmented macule, usually having serrated borders.^[91] Different clinical variants, such as isolated, segmental, and whorled, have been described based on the distribution of the lesion. Wood’s lamp usually shows an off-white accentuation of the macule.^[89]

Although the diagnosis of this condition is usually clinical, dermoscopy may aid in differentiating it from vitiligo and ash leaf macules.^[92]

Dermoscopic profile

Dermoscopy reveals the presence of structureless white areas, with few areas showing a faint pigment network. There may be peripheral projections known as pseudopods, which correspond to the serrated borders of the lesion. Total loss of pigment network is usually not a feature of nevus depigmentosus, which aids in differentiating these lesions from vitiligo.^[91] Further, the hair within these lesions is of normal color, as opposed to leukotrichia, which may be found in vitiligo.^[92]

Nevus anemics is a close differential, presenting as a hypopigmented macule since birth. Diascopy of the lesion classically shows the blending of the borders of the lesion with the surrounding skin. The same test can be replicated using contact dermoscopy. Further, non-contact dermoscopy reveals decreased vasculature in the lesional skin, with a compensatory increase in blood vessels in the surrounding skin.^[93]

Histopathological profile

Nevus depigmentosus is thought to be caused by defective melanosome synthesis and transfer, as can be demonstrated by decreased staining compared to normal skin using the Fontana–Masson stain. Ultrastructural studies have demonstrated a normal number of melanocytes with a reduction in melanosomes.^[89] These findings co-relate with the dermoscopic features of a faint pigment network, as opposed to the complete absence or reversal of pigment network, which is seen in some lesions of vitiligo.^[92]

Clinical profile

An indeterminate leprosy is an early form of leprosy presenting as an ill-defined hypopigmented patch, which usually has a minimal sensory impairment and a negative slit skin smear examination. This form of leprosy may progress to tuberculoid and then lepromatous forms if left untreated. The common sites affected by this condition include the face, outer thighs, and extensor aspect of limbs.^[94]

Dermoscopic profile

Dermoscopic findings in indeterminate Hansen include patchy areas of decreased pigment network with decreased appendageal structures in comparison to normal skin. These findings are more pronounced in borderline tuberculous leprosy but when present in indeterminate leprosy, may be a useful tool to arrive at an early diagnosis.^[95]

Histopathological profile

Histology shows predominantly perineural infiltrate, with very scant or absent bacilli. Small numbers of epithelioid histiocytes may also be found in the perineural region.^[96]

Clinical profile

Pityriasis alba is a commonly-encountered benign skin condition characterized by hypopigmented scaly macules, usually in atopic children with darker skin types. This condition may often be mistaken for leprosy or vitiligo – both of which are associated with significant social stigma. The lesions may begin as mildly erythematous macules, which may progressively become hypopigmented and scaly. This may be followed by a chronic stage not associated with scaling.^[97]

Dermoscopic profile

Pityriasis alba shows ill-defined areas of decreased pigment network with fine scaling and pigmented overlying hair.^[97] The scaling in pityriasis alba is uniformly distributed throughout the lesion, which helps in differentiating this condition from pityriasis versicolor, where the scaling may accumulate within the skin creases.^[5]

Histopathological profile

Histopathology in pityriasis alba is usually non-specific, showing a mild chronic inflammatory infiltrate and decreased basal melanin pigmentation. Non-specific features such as acanthosis, hyperkeratosis, spongiosis, and perivascular infiltrates may also be found.^[97]

Clinical profile

Tinea versicolor is a condition caused by lipophilic yeasts belonging to the genus Malassezia. It is characterized by macules with fine branny scales usually distributed over the trunk and upper back but may also be seen in other seborrheic regions, including the face [Figure 10].^[98]These scaly macules may show varied pigmentation (both hypopigmentation and hyperpigmentation) and can coalesce to form larger macules.^[99]

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Figure 10:

Clinical image of hypopigmented tinea versicolor.

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This condition is usually diagnosed based on clinical examination and KOH mount, but dermoscopy has been found to be a useful ancillary diagnostic tool.^[100]

Dermoscopic profile

Non-uniform pigmentation within the lesion was found to be a common dermoscopic finding in both hypopigmented and hyperpigmented variants. Other patterns of pigmentation include-perilesional hyperpigmentation, clear demarcation of lesional border, and inconspicuous ridges and furrows.^[101] Increased and decreased reticular pigment network have been described in the hyperpigmented and hypopigmented variants of tinea versicolor, respectively.^[99]

Scaling is a hallmark feature of tinea versicolor, which has been shown to occur in various patterns on dermoscopy. Patchy scaling was commonly found in hypopigmented lesions, and scaling within the furrows was commonly found in hyperpigmented lesions [Figure 11].^[101] Fine scaling along the natural skin creases has also been reported as a common finding.^[102] Other patterns of scaling include diffuse, peripheral, and perifollicular scaling.^[101]

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Figure 11:

Dermoscopy in tinea versicolor (DermLite DL4, ×10, polarized) showing areas of decreased pigment network with overlying patchy scales.

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Vascular patterns within the lesion were found uncommonly in a hypopigmented variant of tinea versicolor. This has been postulated to be due to ongoing inflammatory activity within the lesion.^[101] Hypopigmentation of hair follicles within the lesion has also been reported, which may possibly be due to the invasion of hair follicles by the yeast.

A unique dermoscopic feature reported in tinea versicolor is the “contrast halo sign” - characterized by a rim of increased pigment network around hypopigmented lesions and vice versa.^[99]

Clinical profile

Seborrheic dermatitis is a commonly encountered inflammatory condition, usually affecting the scalp, eyebrows, nasolabial folds, retroauricular region, and upper trunk. This condition affects around 1–3% of adults, with a male preponderance and is often more severe during winter.

Seborrheic dermatitis over the face may present as mildly hypopigmented to erythematous macules or plaques with varying degrees of scaling. The scales are typically described as yellowish and greasy.^[103] This condition may often resemble rosacea – but the presence of a darker erythematous background, fine whitish scales, and association with demodicosis is more characteristic of the latter.^[104]

Dermoscopic profile

The dermoscopic findings of seborrheic dermatitis over the scalp have been well-described, and dermoscopy is a useful tool in differentiating the former from scalp psoriasis.^[105] The dermoscopic features of seborrheic dermatitis over the face include dotted vessels, curved vessels, and polymorphous vessels, which may be superimposed on a normal or light pink background. The distribution of these vessels may be patchy or in a network. Yellowish scaling may also be found on dermoscopy.^[104]

Histopathological profile

Early lesions of seborrheic dermatitis may show spongiosis and the formation of a scale-crust. There is mild papillary dermal edema and dilated dermal blood vessels, which may correspond to the dermoscopic finding of red dots.^[104] In subacute and chronic stages, there is psoriasiform hyperplasia with scale crusts in a folliculocentric distribution.^[106]

Clinical profile

Systemic sclerosis is a multisystem disorder characterized by skin thickening and induration with internal organ involvement.^[107] This disorder may be accompanied by various forms of dyspigmentation, including salt and pepper pigmentation, Addisonian pigmentation, and pigmentary changes in the areas of sclerosis.^[108]

Salt and pepper pigmentation clinically appears as well-defined depigmented lesions, with perifollicular sparing of pigmentation. Perifollicular sparing possibly occurs due to the rich vascular supply to this region, which preserves melanogenesis.^[109]

Dermoscopic profile

Dermoscopy of salt and pepper pigmentation shows white homogenous areas, with preservation of pigmentation in the perifollicular areas. Regularly arranged brown dots at the periphery of new lesions have also been described, and this finding is thought to be a marker of disease progression.^[110]

The presence of an off-white perifollicular halo has also been demonstrated, which may be useful in differentiating perifollicular pigment sparing in systemic sclerosis from repigmenting lesions in vitiligo.^[111]

Histopathological profile

Histopathology shows areas of absent pigment in the basal keratinocytes, alternating with areas of normal pigmentation. Dermal melanophages may also be seen underlying the region of normal pigmentation.^[110]