Striae, or stretch marks, are a common complaint and can be distressing. They may affect the abdomen, buttocks, thighs, breasts, back, axillae and groin. They are classified according to appearance or epidemiology, as:
Striae are a form of dermal scarring associated with stretching of the dermis. They often result from a rapid change in weight (gain and loss) or are associated with endogenous or exogenous corticosteroids. Proposed mechanisms relate to hormones, physical stretch, and structural alterations of dermal collagen and elastic tissue. Adrenocorticotropic hormones promote fibroblast activity and increase protein catabolism. Pregnancy-related hormones may also contribute. Serum relaxin has been described to be lower in women with striae distensae.[3] Deficiency of fibrillin has also been proposed. [4] Genetic factors are unexplored, except that decreased expression of collagen and fibronectin genes is reported to be associated with striae.
Striae distensae occur in pregnancy (43% to 88%), puberty (6% to 86%) and obesity (43%). Striae atrophicans follow medical conditions, particularly Cushing syndrome/disease, and treatments, usually exogenous topical or systemic corticosteroids [5], or surgery. Other associated diseases are Marfan syndrome[6], anorexia nervosa[7], various febrile illnesses, and chronic liver disease. Medications associated with striae also include chemotherapy, prolonged antibiotic therapy, contraceptives[8], and neuroleptics.
Striae are more common in females than in males and may be more common in certain races. They can appear more prominent in dark-skinned individuals. A positive family history is a risk factor for striae. During pregnancy, striae are more common in younger women than in older women. Several studies have noted greater prevalence with large abdominal circumference and large weight gain (due to fetal size or polyhydramnios). [9] One study reported that striae were more prevalent in smokers than non-smokers.
Pathophysiology is thought to involve elastases released from mast cells and macrophage activity. [10] Elastolysis of the mid-dermis is followed by a reorganization of collagen and fibrillin.
Histopathology of striae rubrae reveals excessive fine elastic fibers in the papillary dermis with thicker tortuous fibers in the periphery, with perivascular lymphocytes, dilated dermal vessels and edema. There are reduction and reorganization of elastin and fibrillin fibers, and structural changes in collagen fibers, which are thicker and densely packed in parallel rows. Histopathology of striae albae shows epidermal atrophy, loss of rete ridges, less vascularity, and densely packed, thin and scar-like horizontal collagen bundles.[4] They appear similar to mature atrophic scars.
Electron microscopy studies have also reported mast cell degranulation, macrophage activation, and elastolysis of mid dermis.[11]
History may explain the appearance of striae by association with stretched skin, for example, in pregnancy, pubertal growth spurt, muscular exercise, or weight gain. Inquire about topical application of potent corticosteroid or prolonged systemic steroids during the recent or remote past. If striae are widespread and none of these explanations are relevant, take a full medical history and conduct a thorough clinical examination.[12]
The initial striae rubrae are slightly raised pink or violaceous linear marks (striae rubrae), which fade over months to years to hypopigmented, atrophic, wrinkled scars (striae albae). The marks are perpendicular to the direction of skin tension. They fade with time. In pregnancy, they occur on the abdomen, breasts, and thighs. In adolescents, they are common on thighs, buttocks, breasts (females) and back (males).
Striae rubrae are sometimes pruritic. Otherwise, striae are asymptomatic. Treatment is sought because of their unsightly appearance.
Authors have used various methods of assessing the type and severity of striae when discussing the efficacy of treatments. These are not standardized or validated. Dermoscopy shows increased melanization in striae rubrae and reduced melanization in striae albae. [13] A biopsy is not necessary or useful.
The aim of treatment is to reduce redness, swelling and irritation in striae rubrae, and to increase collagen and elastic fiber production, improve hydration, and reduce inflammation in striae albae.[14]
Topical management is commonly recommended to prevent and treat striae, with very little if any evidence of efficacy, according to several published comprehensive reviews. Clinical trials have been of low quality involving small numbers of subjects.
Physical treatments are also advocated but also have little evidence to support their use.
The effect of treatments is difficult to assess. For example, laser protocols use differing devices, fluence, pulse duration, spot size and treatment frequency and number. The utility of combination strategies is unknown.[14]
Platelet-rich plasma injections are also under investigation.[27]
When using any of these modalities, it is important to have standardized pre-treatment and post-treatment photographs. Furthermore, it is important to take these photographs six and twelve months out after the course of treatments. Many published reports do not have standardized photographs, nor do they have long-term follow up.
Over time, many striae improve. The best time to perform a treatment (with proper photographs as discussed) is once the striae have stabilized. Many creams for striae are promoted on the internet with little evidence of the efficacy. The public should be made aware that the efficacy is very limited Newer lasers and radiofrequency treatments hold promise as they do try to modify the vascularity and the collagen and perhaps the elastin. Again, there is no clear leader among the many lasers that are promoted. The needle radiofrequency seems to show promise as, in theory, the deeper deliver of the energy may allow "shrinkage" of the striae in all directions, thereby improving the overall appearance. (Level V).
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[10] | Sheu HM,Yu HS,Chang CH, Mast cell degranulation and elastolysis in the early stage of striae distensae. Journal of cutaneous pathology. 1991 Dec [PubMed PMID: 1774350] |
[11] | Zheng P,Lavker RM,Kligman AM, Anatomy of striae. The British journal of dermatology. 1985 Feb [PubMed PMID: 3970840] |
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