Therapeutic Update on the Treatment of Striae Distensae openaccess articles

January 2015 | Volume 14 | Issue 1 | Feature | 11 | Copyright © 2015

Deborah S. Sarnoff MD FAAD FACP

Abstract

No abstract available

Purchase Original Article

Purchase a single fully formatted PDF of the original manuscript as it was published in the JDD.

Download the original manuscript as it was published in the JDD.

Contact a member of the JDD Sales Team to request a quote or purchase bulk reprints, e-prints or international translation requests.

To get access to JDD's full-text articles and archives, upgrade here.

Save an unformatted copy of this article for on-screen viewing.

Print the full-text of article as it appears on the JDD site.

→ proceed | ↑ close
table 1

The precise etiology of striae distensae (SD) remains to be elucidated. Obesity and rapid weight gain or weight loss have been shown to be associated with the formation of SD.1 While many believe that mechanical stretching of connective tissue, causing it to rupture, is the main cause, others suggest that normal growth, associated with high serum levels of steroid hormones may be the cause.2 Elevated serum levels of steroid hormones have a catabolic effect on the fibroblast activity, causing a decrease in deposits of collagen in the substance of the dermal matrix. High risk groups include adolescents and pregnant women who experience a rapid increase in size of particular regions of the body. SD are two and a half times more frequent in women, compared to men. In boys, the outer aspects of the thighs and the lumbosacral region are the most common sites; in girls, the thighs, upper arms, buttocks and breasts are the most common.3

Early SD are pinkish red, so-called striae rubra (SR), and may be slightly raised. They typically become darker purple in color, but eventually become white and slightly atrophic, so-called striae alba (SA). Histologically, SD are indistinguishable from scars. Collagen bands in the upper reticular dermis are stretched and are aligned parallel to the surface of the skin. There is overall loss of collagen and elastin, with flattening of the rete ridges.4

SD are most likely to respond to therapy in the earliest stages (SR). Once they become mature and whitened (SA), they are very difficult to eradicate. Treatment consists of various topical therapies, as well as lasers and light devices, RF devices, microdermabrasion and needling.

Topical Therapy

Tretinoin has been shown to clinically improve the appearance of early SR without much effect on mature SA. In one study, 22 patients applied 0.1% tretinoin (n=10) or a placebo (n=12) daily for 6 months. Targeted striae in the group treated with tretinoin decreased in mean length by 14%; and mean width by 8%, compared with an increase of 10% and 24% in mean length and width, respectively, in patients who received the placebo.5 In another study, Rangel et al treated pregnancyrelated striae of the abdomen in 20 women post-partum. After 0.1% tretinoin cream was applied daily for 3 months, target lesions decreased by 20%.6

Use of other retinoids, such as tazarotene or adapalene also may be useful. However, no topical retinoid should be used in pregnant or breast-feeding females due to possible absorption and teratogenic effects.7

While there are no well-controlled published studies, glycolic acid, an AHA, has been known to stimulate collagen production by fibroblasts and it has been used with varying degrees of success in treating striae.8

Trichloroacetic acid (TCA 10-35%) has also been used to treat striae. While there is a lack of published data, many anecdotal results reveal improvement in color and texture of striae when a low concentration of TCA is applied at monthly intervals.9

Microdermabrasion

Microdermabrasion has been used to treat acne scars, fine wrinkles and mottled pigmentation.10 Applied to the stratum corneum, microdermabrasion appears to induce epidermal signal transduction pathways that set in motion a cascade of molecular events, capable of causing remodeling and repair.11 In an Egyptian study, 20 patients with SD received 5 microdermabrasion treatments at weekly intervals on half the body; the SD on the other half of the body served as a control. There was an overall good-to-excellent response in over half the subjects; upregulation of type I precollagen MRNA was found in all treated SD samples.12 Improvement was greater in lesions of SR than SA.

Lasers and Light Devices

The 585nm flashlamp pulsed dye laser (PDL) at low energy densities is commonly used to target the dilated blood vessels of SR. A series of treatments at 4-to-6-week intervals has been purported to increase the amount of collagen in the extracellular matrix.13,14 The PDL has a moderate, beneficial effect in reducing the degree of erythema in SR, but no apparent benefit in SA. Because of the potential for adverse effects, PDL should be performed with extreme caution or not at all in Fitzpatrick V-VI patients.

↑ back to top


  • 1
  • 2

Related Articles