Striae distensae (SD; striae, stretch marks, striae atrophicans, striae gravidarum) are an extremely common and well-recognized dermatologic condition entity which can cause significant distress to those affected . SD arise from progressive or rapid stretching of the dermis  and appear along cleavage lines perpendicular to the direction of greatest tension in areas with the most adipose tissue [3, 4] [Fig. 27.1]. There are two forms of SD: striae rubrae and striae albae. The acute stage (striae rubrae) is characterized by the initial erythematous, red, and stretched flat (in some cases appear slightly raised) lesions which are aligned perpendicular to the direction of skin tension and can be symptomatic, while the chronic stage (striae albae) is classified when SD have faded and appear atrophic, wrinkled, and hypopigmented [5–7]. Clinically, immature acute SD are flattened or slightly raised pink or red lesions (striae rubrae). Histopathologically, they appear as inflammatory alterations with elastolysis of the mid-dermis  and mast cell degranulation . Over time and with atrophic changes, the lesions become white (striae albae). Histopathological findings of this latter phase demonstrate epidermal atrophy and loss of the rete ridges; densely packed, thin eosinophilic collagen bundles are arranged horizontally, parallel to the surface of the skin in a similar way to a scar [9, 10] [Table 27.1]. Striae nigrae and striae caerulea are two additional types of SD, which can occur in dark-skinned patient due to the increased melanization . These atrophic dermal scars with overlying epidermal atrophy are found in all ethnic groups and are usually located on the buttocks, thighs, knees, breasts, calves, and lumbosacral areas [4, 8, 12] [Fig. 27.2]. The reported prevalence of SD has been variable in the literature with figures ranging from 11 to 88% [13–15]. SD severity has been noted to be worse in Black African women compared to Caucasians, within the same geographical region [16, 17]. The clear majority of SD has been reported in pregnant women and adolescents. They are sometimes associated with Crushing’s syndrome and chronic steroid use . The exact cause of SD remains unclear, even though a combination of hormonal factors associated with mechanical stretching and rupture of connective tissue framework, tissue damage by striatoxin, pregnancy, normal growth especially in adolescents, rapid weight change, and high serum levels of steroids has been suggested [4, 8, 18]. Genetic predisposition is also presumed, since striae distensae have been reported in monozygotic twins [19, 20]. There is decreased expression of collagen and fibronectin genes in affected tissue . The role of genetic factors is further emphasized by the fact that they are common in inherited defects of connective tissue, as in Marfan’s syndrome [18, 22]. Obesity and rapid increase or decrease in weight have been shown to be associated with the development of SD . Young male weight lifters or bodybuilders develop striae on their shoulders . Striae distensae also occurs in cachetic states, such as tuberculosis, typhoid, and after intense slimming diets . Rare etiologies include human immunodeficiency virus-positive patients receiving the protease inhibitor indinavir and chronic liver disease [18, 24]. A case of idiopathic striae was also reported . The theory of Rosenthal  proposed in 1937 is still actual. He suggested four potential etiological mechanisms of striae formation: insufficient development of tegument, including elastic properties deficiency; rapid stretching of the skin; endocrinal changes; and other causes, possibly toxic.