• Linear atrophic lesions that reflect dermal damage (‘breaks’) at sites of mechanical stress due to stretching of the skin, hence the popular term ‘stretch marks’; most commonly observed in adolescents undergoing growth spurts or weight gain and on the abdomen in up to 75% of pregnant women.

• Striae are multiple, symmetric, and arranged along the lines of cleavage, with the typical sites of involvement and characteristic patterns shown in Fig. 82.1; early lesions may be red-purple in color (striae rubra) but with time, most striae become skin-colored to white with fine wrinkling (striae alba) (Fig. 82.2).

• Additional causes include hypercortisolism (e.g. Cushing’s syndrome), application of potent topical CS (especially in areas of occlusion such as major body folds), and heredity; in weightlifters, mechanical stress and muscle enlargement can lead to striae.

• DDx: linear focal elastosis, in particular when lesions are present on the lower mid-back.

• Rx: difficult and striae often become less noticeable over a period of years; possible modest improvement with topical tretinoin 0.1% cream; lasers (e.g. pulsed dye for striae rubra, 308 nm excimer for striae alba) reportedly lead to improvement.

• Herniations of fat in the heel region where there is reduced dermal connective tissue; the skin-colored papules appear with the pressure of weight-bearing and disappear when the leg is raised (Fig. 82.3A); occasionally occur on the wrist.

• In an infantile variant, larger nodules occur on the medial aspect of the heel and their appearance does not require weight-bearing (Fig. 82.3B).

• Well-circumscribed, skin-colored, flaccid lesions that result from a marked focal decrease in elastic tissue within the dermis (Fig. 82.4).

• Often arises de novo (primary form), with lesions usually measuring 1–2 cm in diameter; there are also secondary forms of anetoderma that can follow inflammation or infection of the skin (e.g. acute cutaneous lupus, varicella, lepromatous leprosy) or are seen in association with cutaneous tumors (e.g. involuted infantile hemangiomas) or the antiphospholipid antibody syndrome.

• Anetoderma of prematurity presents as atrophic lesions resulting from minor iatrogenic trauma to immature skin in the setting of neonatal intensive care.

• Although the individual lesions of the primary form are often elevated, they can be even with the skin surface or depressed (Fig. 82.4C); however, all lesions are soft to palpation and the focal reduction in elastic tissue results in a feel similar to that of an abdominal hernia (referred to as a ‘buttonhole’ sign which is also seen in neurofibromas).

• The primary form favors the neck, upper trunk, and upper extremities of young adults, with lesions appearing over a period of years, while the distribution pattern of the secondary form reflects that of the preceding inflammatory disorder.

• DDx: post-traumatic scars, papular elastorrhexis (similar clinical appearance but firm to palpation), anetoderma-like scars (perifollicular elastolysis) due to acne vulgaris, pseudoxanthoma elasticum-like papillary dermal elastolysis (flexural areas).

• Rx: difficult; for secondary form, treatment of underlying disease may prevent new lesions; surgical excision can lead to scars.

• Minimally depressed hyperpigmented patches, primarily of the posterior trunk (Fig. 82.5); the characteristic ‘cliff-drop’ sign at the peripheral edge may be subtle; significant overlap with ‘burnt-out’ plaque-type morphea, and notably a minority of patients have both disorders.

• Onset typically during adolescence or young adulthood; the patches are often oval in shape, 2–8 cm in diameter, number from one to several, and persist for decades; rarely, lesions are present at birth or arise along the lines of Blaschko (atrophoderma of Moulin; Fig. 82.6).

• Because the reduction in the thickness of the dermis is subtle, an elliptical biopsy that includes both involved and uninvolved skin and is sectioned longitudinally is usually required for diagnosis.

• DDx: morphea, but in contrast to atrophoderma, induration and/or an inflammatory rim is observed; post-inflammatory hyperpigmentation; if a limited number of lesions, dermatofibrosarcoma protuberans (primarily in children).

• Rx: difficult; modest improvement in hyperpigmentation reported with pigment-specific laser therapy.

• Idiopathic disorder characterized by large, skin-colored patches with fine wrinkling and occasionally follicular papules with central delling; the lesions are often clinically subtle (Fig. 82.7) and histologically, there is a selective loss of elastic tissue in the mid dermis best demonstrated by special elastic stains.

• Most commonly affects the trunk, neck, and arms of middle-aged Caucasian women.

• DDx: the major entity is generalized acquired cutis laxa.

• Rx: none currently available.

• Small depressions at the sites of hair follicles.

• Clinical presentations include.

– As atrophoderma vermiculatum of the cheeks (Fig. 82.8), which can be sporadic, inherited in an autosomal dominant manner, or be a component of the keratosis pilaris atrophicans spectrum in which there is also follicular hyperkeratosis (Table 82.1; Fig. 82.9).

– As patulous follicles on the dorsal aspect of the hands and feet in the X-linked dominant Bazex–Dupré–Christol syndrome in which patients also develop BCCs and alopecia.

– As follicular pits within streaks along the lines of Blaschko in the X-linked dominant disorder Conradi–Hünermann–Happle syndrome (form of chondrodysplasia punctata).

• Acquired thin linear depressions on the face that measure 2–10 mm in length and can be admixed with small circular depressions; there is no history of preceding inflammation, acne, or trauma (Fig. 82.10).