What Are Skin Indentations – Why Do They Appear and How to Deal with Them?

The cutaneous lesions known as *striae distensae* represent structural disruptions within the reticular layer of the dermis, arising from the fragmentation of collagen and elastin fibers due to excessive mechanical stretching. Visually, they manifest as linear, elongated bands with irregular margins that, during the initial inflammatory phase, exhibit an intense red-purple hue—resembling fresh epidermal lacerations or microtrauma. Over time, these lesions undergo progressive depigmentation (atrophic phase), adopting a pearlescent or silvery appearance attributable to vascular regression and connective tissue atrophy. A defining characteristic of *striae* is the absence of cutaneous adnexal structures within the scarred area: sebaceous glands (*glandulae sebaceae*), sweat glands (*glandulae sudoriferae*), and hair follicles are conspicuously absent. The anatomical distribution of *striae* correlates with regions subject to dynamic volumetric changes, most commonly affecting the abdominal area (particularly in pregnant women), gluteal region, thighs, and peripheral upper arms. High-risk populations include individuals with class III obesity (BMI ≥30), bodybuilders undergoing rapid muscle hypertrophy, adolescents experiencing pubertal growth spurts, and patients with endocrinopathies—notably Cushing’s syndrome or those undergoing prolonged glucocorticoid therapy. The etiopathogenesis of *striae distensae* encompasses two primary domains: (1) *physiological alterations*, linked to natural developmental processes (e.g., pregnancy, puberty, menopause) or abrupt fluctuations in body mass; and (2) *pathological alterations*, driven by hormonal imbalances, inflammatory dermatoses, or metabolic disorders. A critical predisposing factor is genetic susceptibility—certain individuals exhibit congenital hypoplasia of elastic fibers alongside diminished fibroblast activity, resulting in deficient synthesis of elastin, type I/III collagen, and reticulin. Furthermore, elevated risk is observed in young women with Fitzpatrick skin phototypes I–II (fair complexion), whose inherently thinner epidermis and reduced density of supportive fibers render them more susceptible to microtears even under moderate tensile stress.