4īlaschko lines track distinct patterns ( Figure 3). The extent of skin involvement depends on the proportion and distribution of cells with the genetic abnormalityand on the developmental stage when the mutation took place.4 The skin involvement and patterning are more widespread with mutations that occur earlier in embryogenesis but may be confined to a single anatomical region with later mutations. Other causes of mosaicism (such as postzygotic somatic mutations occurring early in embryogenesis) can also result in linear skin disorders following Blaschko lines. 3 Cells expressing a normal X chromosome make up normal skin, whereas cells expressing an abnormal X chromosome constitute contrasting, abnormal skin in the distribution of Blaschko lines. 2,3Ĭurrent thinking suggests that Blaschko lines depict the directed route of embryonic ectodermal cell migration, which illustrates how epidermal cells originate in the neural crest and move toward the periphery in embryos by directional proliferation in keratinocytes and migration in melanocytes. About 15 years later, Jackson and Happle proposed that functional X-chromosomal mosaicism by means of random X inactivation was the mechanism underlying cutaneous diseases that follow Blaschko lines. 1 This theory was extended to the coloration of tortoiseshell and calico cats, and Lyon suggested that X-linked human skin diseases showed similar patterns. In 1901, the German dermatologist Alfred Blaschko described a system of cutaneous lines that represented the typical pattern that linear nevi appeared to follow.1 Because many skin disorders that followed these lines were present at birth, Blaschko suspected that they had an embryonic origin.Ībout 60 years later, British cytogeneticist Mary Lyon proposed that the mottled appearance of female mice heterozygous for coat color genes might be explained by the random inactivation of 1 female X chromosome, leading to functional mosaicism. Could Blaschko lines explain the linearity of these disorders? Still other skin disorders are linear but not explainable in any of these ways. For instance, the distribution of poison ivy dermatitis is often linear, reflecting a linear deposition of Rhus antigen (or urushiol) on the person’s skin. Other disorders follow a linear distribution that does not correspond with dermatomes or skin cleavage lines. Langer lines are thought to represent the principal axis of orientation of collagen fibers in the dermis incisions along these lines have been thought to result in the least amount of scarring. The lesions of pityriasis rosea follow the distribution of skin cleavage lines (or Langer lines) ( Figure 2). Generally predictable pattern of dermatomal lines ( Figure 1). Some skin disorders follow known anatomic linear patterns. Oval patches in a “Christmas tree” distribution over the back seen in pityriasis rosea.Pigmentary demarcation (known as Futcher or Voigt lines) often seen along the lateral edge of the biceps in persons with dark skin.Painful, vesicular lesions of herpes zoster.Linear vesicular dermatitis caused by exposure to poison ivy.Linearity of the lesions may also suggest the diagnosis. These include the color, morphology, and location of the lesions associated symptoms, such as itching and fever and exposure to drugs or to other children who have a rash. Many factors can be considered in attempting to establish the cause of a skin disorder.
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