Description

• Striae distensae (SD) Striae distensae is a common form of dermal scarring that appear on the skin and is seen in all skin types, consisting of usually multiple, symmetric, well-defined atrophic lesions following the lines of tension (Langer lines).
• Initially appear as erythematous or violaceous elevated lines (striae rubra) and then fade to a wrinkled, hypopigmented, atrophic scar overtime (striae alba) in lighter skinned individuals. These are termed striae nigrae and striae cerulean respectively in darker skin due to increased melanization (1).
• System(s) affected: skin
• Synonym(s): stretch marks

Pediatric Considerations
During puberty, SD appear in areas that rapidly increase in size.

Pregnancy Considerations
Common finding on the abdomen, breast, and thighs of pregnant women, especially during the 3rd trimester—called striae gravidarum

Epidemiology

Incidence
Incidence range of 43–88% for women during pregnancy (1)

Prevalence

• Adult nonpregnant female: 35%
• Adult males: 11%
• Adolescent females: 72–77%
• Adolescent males: 6–86%

Etiology and Pathophysiology

• Specific etiology of SD is unknown.
• Three main theories are proposed as likely contributing to SD formation: mechanical stretching, hormonal changes, and innate structural disturbance of the skin (1,2).
• Mechanical stretching theorized to cause rupture of connective tissue framework
• Hormonal alterations in levels of adrenocorticotropic hormones, cortisol, and relaxin are most related to development of SD (1).
• Adrenocorticotropic hormones and cortisol are thought to promote fibroblast activity causing destruction and alterations of collagen and elastin fibers (1).
• Women who develop SD during pregnancy were found to have increased estrogen and androgen receptors in their skin and had lower measured serum relaxin levels than control groups who did not develop SD (1).
• Innate structural defects whether genetic or transient cause disruptions in the elastic fiber integrity of the skin. Generally, conditions with decreased relaxin and collagen content as well as reduced expression of procollagen and fibronectin genes are associated with higher prevalence of SD (1).
• In striae rubra, inflammatory changes predominate; dermal alterations visible on transmission electron microscopy include mast cell degranulation and macrophage activation leading to elastolysis in the mid-dermis (1).
• In striae alba, histologic findings include epidermal atrophy; thin, eosinophilic collagen bundles arranged horizontally, which is parallel to surface of the skin as is seen in other scar formation (1).
• Skin samples from SD can have marked reduction in visible elastin content compared to adjacent normal dermis as well as decrease in fibrillin content (1).
• This reorganization of fibrillin and elastin after a possible insult to the skin is thought to play a critical role in pathogenesis of SD (1).

Genetics
Genetic predisposition is noted with positive monozygotic twin studies and multiple genetic connective tissue disorders.

Risk Factors

• Pregnancy, specifically young maternal age, large birth weight, later gestational age, increased weight gain during pregnancy, and polyhydramnios
• Positive family history
• BMI >27

Commonly Associated Conditions

• Connective tissue disorders: Marfan syndrome, Ehlers-Danlos syndrome, mitral valve prolapse, and pelvic prolapse (2)
• Immunosuppression states: HIV, TB, and typhoid
• Other medical conditions: Cushing syndrome, rheumatic fever, anorexia nervosa, chronic liver disease, obesity
• Surgery: breast augmentation, tissue-expanded skin, organ transplantation (immunosuppressed state), and cardiac surgery
• Medications: systemic and topical corticosteroids, HIV therapy, chemotherapy, TB therapy, contraceptives, and neuroleptics
• Other: pregnancy, puberty, and weight training