There is no significant variation in the stratum corneum thickness, although black people have a greater number of layers which are more compact and cohesive.5,6 In lightly pigmented skin, 6 to 15 strips of tape are needed to remove the stratum corneum; in black skin, from 8 to 25. Due to greater cohesion, vesicles and bullae remain intact longer than in lightly pigmented skin.7

Black skin presents lower levels of ceramides and greater transepidermal water loss,5,7 in addition to a 2.5-fold higher rate of spontaneous desquamation than white skin, justifying greater xerosis in this population.8

There is no difference in the number of melanocytes in black skin, but rather in the characteristics of the melanosomes, which are larger, non-aggregated and degrade more slowly compared to those in white skin. Its distribution also differs, present throughout the epidermis. Additionally, melanosomes have a more neutral pH and greater tyrosinase activity in black skin.5,7,9,10

There is greater melanogenesis in black people and the melanin content naturally confers a Sun Protection Factor (SPF) of 13.4 compared to 3.4 for white individuals.11 Dark skin transmits 7.4% of ultraviolet rays (UVR) B compared to 29.4% in lightly pigmented skin,7,12,13 that is, approximately four times less UV reaches the upper dermis, minimizing photoaging and the propensity for skin tumors.7,12 However, as UVR deteriorates the defense system, black skin also requires photoprotection.7,12

The relative composition of eumelanin and pheomelanin is independent of the degree of pigmentation, but there is a low level of photoprotective eumelanin in lightly pigmented skin, explaining the greater sensitivity to UVR. 14

The scalp presents macules that resemble asterisks, scales and cosmetic residues, with erythema being common. The color, seen in trichoscopy, varies between light brown and black and does not correlate with the skin color, with a perifollicular pigmented network, or honeycomb pattern, consisting of pigmented lines (corresponding to the melanocytes of the crest of the network) surrounding hypochromic areas (fewer melanocytes in the suprapapillary epidermis). A unique and normal characteristic is the presence of white dots between the follicular units, similar to the fibrosis sign of cicatricial alopecia.15

The density and number of hair follicles are lower and there are differences in their shape: they are curved, spiral-shaped, elliptical on cross-section. There is an asymmetry in the shape and cellular distribution of the hair bulb and the internal and external root sheaths.16,17 The melanosomes are present in the external root sheath and in the bulb of vellus hairs, which is why they are more heavily pigmented. The sebaceous glands are fewer and less active, secreting less sebum, leading to the dryness.16–18 Blood flow is reduced, increasing susceptibility to cicatricial alopecia. The elastic tissue anchorage to the hair follicle is reduced, favoring traction alopecia.7

Negroid hair is the most distinct phenotypic characteristic of black people. They are difficult to comb, requiring different care and less frequent washing. Hairs present knots, cracks, and longitudinal fissures along the shaft.7,19,20 There are varying degrees of curl, with mechanical fragility increasing with higher degrees of curvature. The shaft has a smaller diameter, thinner cuticle, and is drier (lower water and sebum content), with lower tensile strength, which favors breakage.1 Several extracellular matrix proteins and adherens junctions are decreased,16,17 leading to differences in hair texture, strength, and manageability. The follicular units commonly have hair shafts emerging together and the wavy fibers emerge at an angle to the scalp. The chemical composition of keratin and amino acids is similar to that of hair of other ethnic groups. Small differences have been reported in the number of low- and high-sulfur proteins (disulfide bonds).17,18 When placed in water, African-American hair has a lower percentage of radial absorption than Asian and Caucasian hair, perhaps due to differences in lipid content.16,19,20

The main differences between black skin and lightly pigmrnted skin are shown in Table 1.

Black individuals are less susceptible to irritants. This is attributed to the greater cohesion of the stratum corneum cells in dark skin. This difference is undetectable if the stratum corneum is removed.7 The clinical characteristics in patients with dark skin include lichenification, hyperpigmentation, and early papular or follicular eruption with minimal erythema.

In patch tests, there is a similarity in the general frequency of allergies between black and white individuals, but there are differences regarding sensitization to allergens, with positivity for nickel, fragrance mix, bacitracin, balsam of Peru and paraphenylenediamine (PPD). PPD, found in hair dyes, and imidazolidinyl urea, a formaldehyde-releasing preservative, were more frequently allergenic in black men compared to white men.32 The use of darker hair dyes in the black community may explain the greater sensitization to PPD and differences in sensitization patterns are likely due to cultural practices.33

Among pigmentation disorders in black skin, PIH is the most common. It occurs after skin inflammation or injury,30,40,41 resulting from excessive production or irregular dispersion of melanin.2 There are several etiologies, including infections, inflammatory diseases and skin injury caused by physical or chemical agents, including cosmetic procedures. PIH manifests as macules in the same distribution as the initial inflammatory process, the intensity of which may have a direct correlation with phototypes (Fig. 2).41

Figure 2.

Post-inflammatory hyperpigmentation: hyperchromic macules on the lumbosacral and gluteal regions.

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Post-inflammatory hypopigmentation is more common and more evident in people with dark skin. It results from inflammatory (AD, SD, contact dermatitis, psoriasis, etc.), neoplastic (mycosis fungoides), infectious (syphilis), traumatic (wounds, burns) or iatrogenic conditions (post laser, cryotherapy or chemical peelings). It appears as single or multiple hypochromic macules, without desquamation.7

PMH is a common and poorly diagnosed dermatosis. It is distributed worldwide, being more common in tropical countries in black people, preferentially affecting young women. C. acnes is believed to produce a depigmenting factor, as this bacteria can be grown from follicles in hypopigmented areas, but not from neighboring normal-appearing skin. It is characterized by confluent, ill-defined, non-desquamative hypopigmented patches located on the trunk, around the midline and, rarely, extending to the proximal extremities and head and neck regions.31 There is no pruritus, pain or previous inflammation; it is stable or progresses slowly for years, with spontaneous disappearance later in life.31 Wood's lamp examination may show red follicular fluorescence in hypopigmented areas. Dermoscopy reveals whitish, poorly defined areas without desquamation.42 Histopathology shows a decrease in melanin in the epidermis, while the dermis appears normal.43,44

PA begins around three to 16 years of age, without sex predilection, occurring more commonly in darker skin.31 Its etiopathogenesis remains unknown; however, it is believed to represent nonspecific dermatitis with residual post-inflammatory hypopigmentation. Associated findings include atrophic sebaceous glands, iron-deficiency anemia, and low serum copper levels.44 Black children may be genetically predisposed to xerosis, which can lead to PA.31 Environmental factors such as sun exposure, long and frequent baths and mechanical exfoliation seem to be predisposing factors on susceptible skin.31 It is important to inquire about personal or family history of atopy, as it is one of the minor criteria for AD.31,44 In dark skin, early lesions present as subclinical dermatitis and erythema is barely evident.31 The initial lesions are desquamative papules that evolve into clearly visible hypochromic areas, different from lightly pigmented skin, due to the contrast with healthy skin. It generally affects the face, neck and arms; histopathological findings are nonspecific.31,44

Melasma is a common acquired hyperpigmentation, typically occurring on the face, with a high prevalence in women and darker skin types. Family history, especially in darker skin, is an important risk factor.45,46 Clinically, the pigmentation is more intense and persistent. On histopathology, melanophages have been detected in the superficial dermis, with a very heterogeneous distribution, varying from one lesion to another in the same patient and even within the same area of melasma.46

Breakage is a common problem in black hair, leading to deficient growth and alopecia, due to the intrinsic characteristics of fragility and reduced tensile strength. Fragility results from the elliptical shape of the shafts originating from the curved follicle, different hair diameters and dry scalp. Transverse asymmetry, with points of weakness, reduces tensile strength.57,58 Damage to the hair shaft resulting from the removal of proteins or 18-methyl eicosanoic acid (18-MEA), the main lipid of the hair cuticle, contributes to breakage. of hair, secondary to excessive use of heat or chemical agents, in addition to hairstyles that exert traction.17,59,60

Dermoscopy (trichoscopy) shows trichorrhexis nodosa, where the shaft is nodularly dilated and lighter, and distal trichoptilosis (cracking of the ends) or central trichoptilosis (longitudinal division in the central part of the hair shaft).17,61–63

Caused by repetitive tension in hair from braids, ponytails, turbans, buns, dreadlocks, weaves, extensions, among others,64 traction alopecia generally begins in childhood.64,65 The pattern is characteristic, reflecting the distribution of traction, affecting the temporal, pre-auricular and above-the-ears regions, and may involve other parts of the scalp. Folliculitis, reduced hair density and broken hairs are seen in these areas, in addition to the fringe sign (long terminal hairs anterior to the alopecia area, which consist of fine or miniaturized residual hairs). It may be associated with headache, relieved by loosening the hair.65,66 Early diagnosis is important, when it is still reversible. Trichoscopy in the early stage shows the honeycomb pattern of the preserved scalp, perifollicular erythema, reduced hair density and vellus hairs. The advanced stage is characterized by loss of follicular openings.17,65,66 Histopathology in the initial stage shows a normal number of hair follicles, but a greater number of telogen and catagen follicles, in addition to trichomalacia (remnants of hair shafts in the ostia). In advanced stages, there is a decrease in the number of terminal follicles, replaced by fibrous tracts. There is no inflammatory infiltrate during the course of this disease.66

It results from ingrown hairs, extrafollicular or transfollicular penetration of the skin, generally secondary to the cutting of black hair.67,68 It presents as papules, pustules, plaques and nodules on the posterior region of the scalp, commonly associated with alopecia and keloids. Trichoscopy shows broken hairs with tufts, ingrown hairs and peripilar casts (Fig. 4).67,68

Figure 4.

Keloid folliculitis of the neck: sessile nodule on the back of the neck.

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Also called folliculitis and perifolliculitis capitis abscedens et suffodiens, it is a chronic scalp disorder, observed mainly in young men. The lesions, initially papulopustular, develop into painful, multifocal inflammatory nodules, connected by intercommunicating sinuses, resulting in cicatricial alopecia.7,69 On trichoscopy, characteristics of non-scarring alopecia are initially observed, with regularly distributed pinpoint white dots, enlarged follicular openings, “3D” yellow spots (accumulation of sebum and keratin), black spots and fractured hair shafts. In the terminal stage, cicatricial lesions appear, characterized by ivory-white confluent areas, without follicular ostia.68–70

Formerly known as hot comb alopecia (a method of straightening hair), pseudopelade, and follicular degeneration syndrome, CCCA is most common in young to middle-aged women of African descent. The etiology is unknown but with an apparent influence of genetic factors, traction, heat and chemicals. It is characterized by a chronic and progressive lesion on the vertex of the scalp, which progresses in a centrifugal and symmetrical manner, with activity in the peripheral zone, surrounding the central zone of cicatricial alopecia.7,71–73 Signs of inflammation are absent, although erythema, follicular pustules and desquamation may appear. It is usually asymptomatic, but pain, pruritus or burning sensation in the scalp may occur.73,74 There is a spontaneous reduction in inflammation after years or decades.75 Trichoscopy reveals a preserved pigmented honeycomb network and irregularly distributed white dots. A grayish-white peripilar halo is a specific and sensitive sign, corresponding on histopathology to follicular ostia surrounded by fibrosis.74,75 Other characteristics include hair shaft variability, perifollicular erythema, broken hairs as black dots within the follicular openings or as short broken shafts, asterisk-like pigmented macules with sparse, vellus-like terminal hair shafts and scattered white patches.74–76 In the early stage histopathology reveals a perifollicular lymphocytic infiltrate with perifollicular fibroplasia. In later stages, there is destruction of the follicular epithelium and fragments of hair shafts sorrounded by granulomatous inflammation, followed by replacement of the follicles by connective tissue besides tufting/polytrichia of the hair follicles.76

LPP is a rare variant of LP, which begins after the age of 30, predominantly in black women.80 Although the pathogenesis is the same as in classic LP,81 sunlight is an important factor, in addition to chemical agents (contactants and drugs) and microorganisms.80,81 The initial lesions are small round or oval macules, gray or brown, with irregular ill-defined edges, which coalesce to form diffuse, reticulated, perifollicular or annular pigmented areas,80,82 distributed mainly in body regions exposed to the sun, starting on the face and neck, spreading to the upper extremities and trunk, symmetrically, rarely affecting the oral mucosa, the scalp, nails, palms and soles.80,82 There are no Wickham striae.82 Eventually, there are classic LP lesions. Pruritus is mild or absent.81 One variant is LPP inversus, which affects skin not exposed to the sun, particularly flexural and intertriginous areas, in which a transition from papules to macules can be observed (Fig. 5). Mechanical stimuli are triggers. Other variants are: localized, segmental, linear, zosteriform and oral mucosa LPP.80–82

Figure 5.

Lichen planus pigmentosus: slightly raised papules and bright hyperchromic macules in the axilla.

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Dermoscopy of LPP inversus shows homogeneous brown areas (epidermal pigmentation), as well as brown-gray or blue-gray dots and globules (pigmentary incontinence), which are initially grouped into a diffuse pattern of black pigmentation. Over time, they converge forming reticular, linear and cobblestone patterns. White dots are secondary to lack of pigmentation in the follicular openings, and the absence of pigment in the grooves may be due to lack of exposure to friction.82

Histopathologically, the lichenoid inflammatory infiltrate is similar to the one seen in classic LP,81 but it regresses quickly, without the proliferation of keratinocytes, and the melanin deposited in the dermis remains for months to years.82 Direct immunofluorescence is rarely positive, with IgM and C3 at the dermal-epidermal junction and IgG and IgA in keratinocytes.81,82 It can be associated with hepatitis C, endocrinopathies, autoimmune diseases and malignancies, as well as other variants of LP.80–82

Although the risk for skin cancer is lower in black people, exposure to UV rays is also a risk factor.30 The repair of DNA damage induced by UV radiation is more efficient in black people. 93 Black individuals are less likely to use sun protection, as they believe it is unnecessary.30Table 393–95 illustrates the main characteristics and differences between non-melanoma and melanoma cancer in black skin.

Mycosis fungoides (MF) is the most common type of lymphoma in black skin, accounting for more than 50% of CTCLs,30 with an incidence rate of 4.0 and 6.1/100,000 for white and black patients, respectively.96,97 Black individuals present with MF at an earlier age and at a higher T stage than white ones. Clinically, MF generally presents as patches, plaques or tumors located, preferably, in covered areas, but can also present with erythroderma. The lesions are hyperpigmented in darker skin, rather than erythematous, with a hypopigmented variant. Hyperpigmented lesions correlate with shorter survival, while hypopigmented ones correlate with longer survival and an indolent course.96

Sezary Syndrome (SS) is a rare leukemic variant of CTCL, defined by the triad of erythroderma, neoplastic T cells (Sezary cells) in the blood, and lymphadenopathy. Like MF, SS also has a higher prevalence in black individuals compared to white ones. As on lightly pigmented skin, it can be difficult to differentiate it from other diffuse eruptions. The biggest concern is that pruritus and changes secondary to scratching are attributed to xerosis.96,97

It is limited to sub-Saharan Africa and is typically seen in young, HIV-negative black men, aged 25 to 40. Clinical manifestations can range from indolent to aggressive and lethal. Its presentation can be locally invasive or aggressive with/or without mucocutaneous involvement. There are four subtypes: benign nodular; locally aggressive with invasion of soft tissues and bones; florid and disseminated with the involvement of skin and viscera; and lymphadenopathic, spreading rapidly to lymph nodes and viscera. The last is the most aggressive and is associated with African children aged one to five years.7,98

DFSP is a rare, slow-growing, spindle cell neoplasm located in the dermis or subcutaneous tissue. The incidence among black people is twice as high and the tumors are larger than in white individuals, one explanation being the delay in diagnosis.99 It is more common in the trunk than in the head and neck, with no difference for the extremities.100 The risk of death in black individuals is 1.7-fold greater than in whites and depends on size.99,100

There is a rare, pigmented variant, called Bednar tumor, which occurs in 5% of cases, mainly in blacks,100 observed in young and middle-aged adults, occasionally in the pediatric age group. Histogenesis is unexplained and may be related to remnants of embryonic breast tissue or local trauma, with two theories having been proposed: neuroectodermal differentiation or melanocytic colonization.99,100 It has been reported in association with dermal melanocytosis (nevus of Ito) and is believed that it originates from a neuromesenchymal cell. It is most commonly located on the trunk, especially on the shoulders and back, and can also affect the head and neck, as well as the extremities. 99,100 Clinically, it resembles a keloid. The majority appear as masses, plaques, or protruding, firm, multilobulated nodules, with a wide base and slow growth, in the dermis and subcutaneous tissue. On histopathology, it consists of spindle cells, with mild pleomorphism.99,100 Pigment-laden dendritic cells differentiate this lesion from conventional DFSP.100 Immunohistochemistry detects CD34 positivity in the cells.99 The biological behavior is that of intermediate malignancy and it must be differentiated from other pigmented, fusiform skin lesions.99,100