Striae Distensae: A Comprehensive Review and Evidence-Based Evaluation of Prophylaxis and Treatment

S. Al-Himdani; S. Ud-Din; S. Gilmore; A. Bayat


The British Journal of Dermatology. 2014;170(3):527-547. 

In This Article


Epidemiology and Quality of Life

Striae distensae can occur in adolescence, pregnancy and obesity.[2,3,6,8,22,23] The prevalence cited is equally diverse in these groups and ranges from 43% to 88% and 6% to 86%, in pregnant women and adolescents, respectively.[2,6,7,8,20,24,25,26,27] Among obese individuals of body mass index (BMI) 27-51, the prevalence is reported to be 43%.[22] Studies in other patient groups such as non-pregnant women and adult males also report varied prevalences ( Table 2 ).[4,10,27,28]

Geographically disparate studies of SD demonstrate similar micro- and macroscopic appearances.[2,24,25] However, inter-racial differences in the severity of SD have been observed in a study carried out by Elbuluk et al.[30] Of 48 women evaluated, African-American women were more severely affected than white women within the same geographical region. The authors did also note that there was a difference in BMI and smoking status between the two groups, which may indicate that other factors aside from race are involved.

Prevalence and anatomical regions affected vary depending upon sex and age ( Table 2 ). In adolescents, approximately 40% of male and 70% of female subjects are affected.[2,3] In adolescent males the lower back and knees are usually affected whilst in female subjects the thighs and calves are more often involved. During pregnancy, the abdomen and breasts are common sites for SD (Figure 1).

Figure 1.

Striae distensae. Areas typically affected by striae distensae in (a) adolescent males (n = 131), (b) adolescent females (n = 131) and (c) pregnant women (n = 110). Values represent the percentage of patients with striae in each area.[2, 8]

Yamaguchi et al. elucidated a significant difference in the 'emotion' score of a validated questionnaire (Skindex-29) in Japanese women with SD compared with those without SD.[31] Although this study is limited by its lack of racial diversity, the psychological impact of SD is evident.

Risk Factors and Aetiology

Most SD research has focused on pregnant women and adolescents. A positive family history is a risk factor in both of these groups alike.[26,32] Among adolescents, BMI and childhood obesity both influence risk of developing SD.[2] Other important risk factors and associations have been reported (Figure 2). Risk factors in pregnant women may be constitutional or pregnancy related ( Table 3 ).[28] Constitutional factors include maternal age and BMI. Younger women more commonly develop SD, implicating a constitutional difference in the stretching ability of the skin in younger women.[5,7,8,20,24,25,28] The association of pregnancy-associated factors such as birthweight, gestational age, weight gain during pregnancy and polyhydramnios with the occurrence of SD support the theory that the changes associated with pregnancy also play a role in their development.[5,20,24] Numerous clinical conditions, surgical interventions and medications have been associated with SD ( Table 4 ).[8,13,33,34,50,51,52]

Figure 2.

Risk factors and associations with striae distensae.[2, 7–9, 20, 24–26, 30] BMI, body mass index.

Striae distensae are also described in monozygotic twins,[53] in a familial form[54] and in Marfan syndrome,[33] indicating an important genetic predisposition. This is supported by biopsy findings that report slower migration and proliferation rates in fibroblasts of patients with SD.[55] Three main theories relating to SD formation are described: mechanical stretching of the skin, hormonal changes and an innate structural disturbance of the integument. Mechanical stretching of the skin is postulated due to the perpendicularity of SD to the direction of the skin.[15] However, contradictory studies dispute this theory. While a greater degree of physiological stretching would be expected with increased abdominal girth in pregnancy and on the extensor surfaces of joints, the latter shows no significant increase in the frequency of SD.[54,56]

Striae distensae are often encountered in states in which hormonal alterations occur. Adrenocorticotrophic hormone and cortisol are thought to promote fibroblast activity, leading to increased protein catabolism and thus alterations to collagen and elastin fibres.[57] Additionally, increased urinary excretion of corticosteroids (17-ketosteroid) has been reported in patients with SD.[58] Pregnancy-related hormones are also believed to influence SD formation.[8,59,60,61] Cordeiro et al.[59] described increased oestrogen and androgen receptors in skin exhibiting SD compared with normal skin. Lower serum relaxin levels were demonstrated in pregnant women with SD compared with those without SD at 36 weeks' gestation by Lurie et al.[61] The connective tissue in skin types with less relaxin would be expected to be less lax and thus at greater risk of structural disruption of the elastic fibre network during stretching than more lax skin with greater relaxin content. Salter et al. identified a positive correlation between the presence of SD and prolapse in 108 women. More than half of the women with prolapse reported SD compared with only 25% in the non-prolapse group. Both conditions have been associated with decreased collagen content.[60] Reduced expression of procollagen and fibronectin genes in SD tissue was described by Lee et al.[16] In a similar way to keloid disease and scleroderma, which are thought to develop due to disordered gene expression of the extracellular matrix,[62,63] SD may also present altered gene expression, contributing to their formation.

Histopathogenesis of Striae Distensae

Striae rubrae and striae albae are distinct, evolutionarily linked forms of SD.[8] Their distinction has therapeutic implications ( Table 5 , Fig. 3).[72] In addition to their contrasting macroscopic appearances, distinctions can be made based on their ultrastructural appearances.[68–70] Hermanns and Piérard[64] described two additional types of SD, striae nigrae and striae caerulea, which occur in those with darker skin due to increased melanization. The colour of the SD is related to the stage of evolution and to melanocyte mechanobiological influences.[65]

Figure 3.

Striae distensae. Photographs and histological comparisons of normal skin (a, b), striae rubrae (c–e) and striae albae (f–h). Haematoxylin and eosin staining. (a) Normal skin histology; (b) haphazardly arranged small collagen fibres and thin elastin fibres in the papillary dermis, surrounded by ground substance; coarse elastic fibres and thick bundles of collagen parallel to the direction on the skin in the reticular dermis. (c) Striae rubrae are tense, red and erythematous; (d, e) fine elastic fibres predominate in the dermis with thicker tortuous fibres in the periphery;17 there is a reduction and reorganization of elastin and fibrillin fibres and structural changes in collagen are seen.[16, 66, 68, 69, 71] (f) Striae albae appear pale, depressed and wrinkled; (g,h) histology demonstrates 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 in a scar.[64–66, 68–70]

Early histopathological dermal alterations may be visualized on electron microscopy, including mast cell degranulation and macrophage activation leading to elastolysis of the mid-dermis.[73] Release of enzymes by mast cells, including elastases, is proposed as a key initiatory process in SD pathogenesis.[66] As well as the inflammatory process, alterations in collagen, elastin and fibrillin content have been characterized (Fig. 3). The reorganization of fibrillin and elastin are thought to play an important role in SD pathogenesis and those predisposed to developing SD may have an underlying deficiency of fibrillin.[68]

Evaluation and Severity of Striae Distensae

A universal approach to evaluating the severity of SD does not exist. Visual scoring and imaging modalities have been reported in the literature ( Table 6 ). Approaches to evaluating SD severity visually include the Davey[9] and Atwal scores,[20] although these have not been validated specifically for SD.

For an objective evaluation of skin topography, imaging devices may be used, including three-dimensional (3D) cameras, reflectance confocal microscopy and epiluminescence colorimetry.[64,74,75] These provide a means of evaluating a response to treatment on an ultrastructural level although they have not yet been validated for use specifically in SD. Epiluminescence colorimetry and dermoscopy may be used to identify SD colour. As treatment response varies according to the colour, this may play a therapeutic role in targeting SD based on colour in order to obtain the best treatment outcomes.[64]


A treatment modality that is consistently effective with minimal adverse effects does not exist to date. Not only does therapeutic outcome depend on the type of SD but also the patients' Fitzpatrick skin type.[65] Most adverse effects, particularly with lasers, occur in patients with darker skin types (Fitzpatrick skin types III–IV).[79] Lifestyle measures such as exercise were demonstrated by one study to have no effect on SD.[35]

Topical agents. A number of topical agents have been evaluated ( Table 7 ). Tretinoin is thought to work through its affinity for fibroblasts and induction of collagen synthesis.[11,80,81] It has maximal efficacy in striae rubrae and poor, unpredictable responses in striae albae.[11,94,95] In a double-blind randomized control trial by Kang et al., 26 white subjects received either treatment (0·1% tretinoin) or vehicle cream. The cream was applied once a day for 24 weeks. Length and width measurements of SD, punch biopsies and both objective and subjective evaluations were reported outcome measures. The severity of SD was rated at each visit on a scale: mild (0-3), moderate (4–6) or severe (7-9). A statistically significant reduction in the mean length and width (14% and 8%, respectively) were reported following treatment. After 6 months, 80% (n = 8) of the tretinoin-treated patients had definite marked improvement compared with 8% (n = 1) in the vehicle-treated group. No significant differences were found on histological assessments.[80]

Creams, lotions and ointments are used by up to 78% of pregnant women, thus incurring a significant expense.[31,96] They are commonly targeted at pregnant women at risk of developing striae gravidarum during pregnancy.[97] A Cochrane review undertaken in 2012 evaluated six topical agents in over 800 women and found no statistically significant evidence to support their use in the prevention of SD.[96] The studies included were relatively small and included women at different stages in their pregnancy. Creams evaluated included Alphastria®, Trofolastin®, cocoa butter, olive oil and Verum®.

Trofolastin cream contains Centella asiatica, which is thought to stimulate fibroblasts and has an antagonistic effect against glucocorticoids.[98] Mallol et al.[73] applied Trofolastin or placebo cream to 41 and 39 women, respectively, in a double-blind randomized controlled trial (RCT). Application was to the abdomen, breasts, buttocks and hips. Checks during pregnancy evaluated the degree of striae using an arbitrary, nonvalidated score (0, no striae; 1, few and thin striae; 2, many thin striae or few thick striae; 3, many thick striae). The authors report that 22% fewer women developed SD in the prophylactically treated group compared with the placebo group, following daily application of cream to the abdomen, breasts, buttocks and hips during pregnancy. However, this study may have a degree of attrition bias, with 20% incomplete outcomes reported (100 women took part yet only 80 were in the final analysis). It is stated that this was mostly due to 'address change' (n = 19). Additionally, there are no details regarding how women were allocated to either the treatment or placebo groups.

Many cocoa butter products are marketed and are easily accessible for use in the prevention and treatment of SD. Buchanan et al.[19] evaluated the efficacy of the cream in a double-blind RCT. A total of 150 women were treated with the cocoa butter and an equal number applied placebo cream daily to all four quadrants of the abdomen. Women were enrolled before 16 weeks of pregnancy. At 26 and 36 weeks of pregnancy and at delivery the Davey method was used to evaluate the stretch mark severity by different observers using photographs. Authors report that there was no significant difference between patients developing SD in the cocoa butter and placebo groups. The exact method of allocation of pregnant women to either treatment or placebo groups in this study is unclear.

Ud-Din et al.[82] conducted a double-blind RCT evaluating the effect of topical silicone and placebo gel applied to two sides of the abdomen of 20 women. Following daily application, outcomes were evaluated using biopsies, tissue tonometry, full-field laser perfusion imaging, spectrophotometric intracutaneous analysis and subjective evaluation. Results demonstrated increased melanin and decreased haemoglobin, collagen and pliability over the 6-week period in both groups. Histology also demonstrated a reduction of rete ridges on both sides. These findings indicate a potential beneficial effect of massage on SD. Compared with placebo, increased collagen and reduced pigmentation in the silicone-treated group was reported. Although this study demonstrates positive results, it is limited by the relatively small number of patients.

Chemical/mechanical debridement techniques. Acid-peel treatments such as glycolic acid (GCA) and trichloroacetic acid (TCA) are thought to act by increasing collagen synthesis.[90,91,99] Mazzarello et al.[93] undertook a double-blind RCT of 40 women to assess the effect of 70% GCA topical therapy on SD of the thigh. Patients were divided into two groups: striae albae and striae rubrae. In each group, patients applied the treatment to the left thigh and a placebo to the right thigh with a total of six applications over 6 months. Reported outcome measures included skin texture analysis using scanning electron microscopy as well as haemoglobin and melanin levels using spectrophotometry. After treatment, the striae rubrae group demonstrated a significant decrease in furrow width and in haemoglobin. The striae albae group demonstrated a similar decrease in furrow width and an increase in melanin. No significant differences were reported in parameters of the placebo-treated areas. Although outcomes appear positive, there is no report of randomization in this study and details regarding how patients were allocated to each group are lacking. Although the authors state that this is a double-blinded study, the details of how blinding was undertaken are not clear. The correct concentration should be applied, as higher levels may result in irreversible scarring.[100,101]

Microdermabrasion is a skin resurfacing technique using aluminium oxide.[102] It has been reported to increase type-I collagen and have a greater effect on striae albae.[103]

Nonablative laser techniques. These lasers target haemoglobin or melanin and several have been utilized in studies on SD including: the 585-nm pulsed-dye laser (PDL), the 1064-nm neodymium-doped YAG (Nd-YAG),[36] the 308-nm xenon chloride (XeCl) excimer laser and the 577-nm copper bromide laser[104] ( Table 8 ). Few studies evaluating the efficacy of laser therapies in SD are of high level evidence. These studies are understandably difficult to blind, but a significant proportion of the studies also lack controls. Therefore outcomes need to be interpreted carefully.

The 585-nm PDL is a vascular laser that targets dilated blood vessels in striae rubrae and is reported to increase the collagen content of SD.[105] McDaniel et al.[106] undertook a controlled study of 39 patients with SD. Treatment sites included the abdomen, thighs and breasts. Four treatment protocols were used with different spot distances and fluences. Untreated SD acted as controls. Outcomes were measured by subjective analysis, shadow profilometry and histopathological analysis. A significant reduction in skin shadowing was reported in patients with SD in all protocols compared with controls. Additionally, elastin regained its normal appearance in SD treated with low-fluence PDL. The principal investigator who undertook the subjective analysis was not blinded to the treatment protocols.[106]

The 308-nm XeCl excimer laser is an ultraviolet (UV) laser and has been used to treat SD.[120] Alexiades-Armenakas et al. conducted an RCT of 31 patients with hypopigmented lesions, of which 9 were SD. Lesions were randomized by alternate allocation to receive treatment or not. Treatments were performed at biweekly intervals then fortnightly until either a maximum of 10 treatments were undertaken, or 75% increase in colorimetric measurements relative to baseline or 100% visual pigment correction was obtained. Outcome measures included visually assessed pigment correction relative to control (assessed by three blinded observers) and skin pigmentation levels measured on a colorimeter. A statistically significant improvement in pigmentation on the colorimetric assessment was identified in treated SD vs. site-matched controls. Improved visual pigmentation level compared with controls was also reported but this declined towards baseline after 6 months. Alternate allocation in this study carries a high risk of selection bias. There was also no mention of whether the investigator or patients were blinded to treatment. Attrition bias may be another concern as there is no report of how many patients were in the final analysis.

Ablative laser treatment. This includes the short-pulsed 10 600-nm CO2 laser. These lasers trigger epidermal vaporization and coagulation of the underlying dermis.[79] They present a risk of hyperpigmentation, particularly in those with darker skin.[79,130]

Light therapy and radiofrequency devices. Intense pulsed light (IPL), radiofrequency (RF) and UV radiation therapy have been used in studies to treat SD ( Table 8 ). IPL emits visible light with a spectrum of 515–1200 nm, which helps to organize collagen fibres. Repeated sessions may be required to maintain positive effects.[100,108,109,110] RF devices increase collagen production by inducing collagen type I mRNA expression.[105,111,131] They produce heat, which converts electrical current to thermal energy that is uniformly dispersed to different tissue depths.[105,111]

Fractional resurfacing. Fractional photothermolysis is a laser resurfacing technique that acts by creating small zones of thermal damage named 'microthermal zones'.[132,133] This results in epidermal necrosis followed by collagen synthesis.[102,112,132,134]

Other techniques. Other techniques reported in the literature include percutaneous collagen induction therapy and needling therapy ( Table 8 ). There are no widely accepted surgical procedures used in the treatment of SD.