Striae distensae (SD; striae, stretch marks, striae atrophicans, striae gravidarum) are common skin lesions, which can pose a significant psychological burden for patients. Since the first histological description in 1889,[1] SD have presented a considerable challenge in terms of both their evaluation and treatment. Although frequently encountered by both patients and clinicians, the prevalence of SD cited in the literature varies tremendously, ranging from 11% to 88%.[2-10] Additionally, anatomical sites affected vary, with areas commonly affected including the abdomen, breasts, thighs and buttocks.[2, 3]
Two clinically and histopathologically recognizable forms of SD have been described: striae rubrae and striae albae.[11] The initial erythematous and violaceous-appearing lesions are referred to as striae rubrae. These fade into wrinkled, hypopigmented, atrophic scar-like marks named striae albae, which have been described as a permanent form of SD.[12] When occurring following pregnancy, the term striae gravidarum refers to the same entity, usually developing after the 24th week of gestation.[8, 13] Although the vast majority of SD have been reported in pregnant women and adolescents,[6, 13] they have also been described in association with Cushing syndrome and following the administration of both short- and long-term oral and topical corticosteroids.[13-15] Further to this, a number of key aetiological theories have been postulated. These include inadequate development of the skin (particularly elastic fibres and collagen),[16, 17] mechanical stretching of the skin and endocrine imbalance.[18, 19]
Several methods of assessing SD, visually or instrumentally, have been utilized in previous studies.[9, 20] Here we present a comprehensive review of the literature, incorporating articles from multiple search engines and languages. We focus on the epidemiology, aetiology, clinical evaluation, prevention and treatment of SD.
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Methods
We conducted searches of Medline, Embase and Google Scholar in order to identify relevant studies relating to SD published from 1950 to 2013. Articles in French, Spanish, Turkish and Portuguese were translated into English for inclusion. ‘Stretch marks’, ‘striae distensae’, ‘striae gravidarum’, ‘striae rubrae’, ‘striae albae’ and ‘striae atrophicans’ were the search terms used. Information was obtained from review articles and primary research papers. Articles were grouped by primary treatment strategy. Articles were assessed and assigned a level of evidence (LOE) adapted from the Oxford Centre for Evidence-Based Medicine.[21] These levels, ranging from LOE-1 to LOE-5, are based on study methodology and design (Table 1).
Table 1. Levels of evidence (LOE)
LOE-2Systematic review with homogeneity of cohort studies
RCT
Cohort study
‘Outcomes’ research; ecological studies
LOE-3Systematic review with homogeneity of case–control studies
Nonrandomized controlled trial
Individual case–control study
LOE-4Case series
Comparative study
LOE-5Case reports
Expert opinion without critical appraisal/based on physiology/bench research or ‘first principles’
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Results
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, 6-8, 20, 24-27] 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]
Table 2. Comparison of striae distensae among different patient population groups[2-8, 10, 15, 20, 24-29]
Patient groupLocation (most common to least common)Proposed mechanism of formationAverage age (years)Approximate prevalence (%)
Adult nonpregnant womenBreasts and thighsPostpregnancy2935
Adolescent femalesThighs, buttocks, breastsStretching of the skin during growth spurt, adrenocortical hyperactivity13–1472–77
Adolescent malesButtocks, thighs, calves, backStretching of the skin during growth spurt, adrenocortical hyperactivity146–86
Adult malesButtocksSudden weight gain/loss, muscular exerciseND11
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 (Fig. 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]
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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 (Fig. 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, 50-52]
Table 3. Constitutional and pregnancy-related factors associated with striae distensae
FactorDavey (1972)[9]Murphy et al. (1992)[28]Chang et al. (2004)[6]Thomas and Liston (2004)[5]Atwal et al. (2006)[20]Osman et al. (2007)[8]Ghasemi et al. (2007)[7]Maia et al. (2009)[25]Canpolat et al. (2010)[24]
Maternal age+++++
Maternal BMI+++++
Maternal weight+
Thickness of abdominal skin fold+
Positive family history++
Smoker+
Use of cream+
Pregnancy related
Birthweight++++++
Gestational age+
Weight gained during pregnancy+++
Polyhydramnios+
Table 4. Medical conditions, surgery, medications and other factors linked with striae distensae[2, 9, 13, 14, 33-52]
Associations with striae distensae
Marfan syndrome, Cushing syndrome, anorexia nervosa, typhoid fever, rheumatic fever, chronic liver disease, obesity
Surgery
Augmentation mammoplasty, tissue expanded skin, tension-requiring skin sutures, organ transplantation, cardiac surgery
Medications
Systemic and topical corticosteroids, HIV therapy, chemotherapy, tuberculosis therapy, contraceptives, neuroleptics
Other
Pregnancy, puberty, stretch and weight training, idiopathic
Figure 2. Risk factors and associations with striae distensae.[2, 7-9, 20, 24-26, 30] BMI, body mass index.
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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, 59-61] 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]
Table 5. Histological comparisons of striae rubrae and striae albae[17, 18, 64-67]
Striae rubraeStriae albae
Clinical appearanceRaised pink linear lesionsPale, depressed and finely wrinkled lesions; appear similar to scars
EpidermisOedema between melanocytes and keratinocytes; increased melanogenesisEpidermal atrophy, loss of rete ridges and absent hair follicles; reduction in melanocytes leading to leucoderma
Papillary dermisVascular ectasia and possible angiogenesisLack of vascular stimulation
Reticular dermisCollagen fibres structurally altered; elastic fibres reduced and reorganized; fine elastic fibres predominate throughout dermis with thick, tortuous fibres toward the periphery; reduced fibrillin microfibrils at the dermal–epidermal junctionDensely packed collagen parallel to skin surface; predominantly thick elastic fibres in dermis with normal appearance in periphery
Inflammatory cellsDermal oedema, cuffing of the small vessels by lymphocytes, absent mast cells and prominent fibroblasts; increased glycosaminoglycan contentEosinophils predominate among collagen fibres
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]
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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.
Table 6. Visual and imaging techniques used to assess type, severity and efficacy of treatments of striae distensae (SD)[7, 9, 20, 64, 65, 74-78]
MethodType of striaeExplanation of method
Davey methodStriae rubrae and albaeAbdominal SD. Abdomen divided into quadrants using midline vertical and horizontal lines through umbilicus as divisions. Each quadrant given a score (0, no SD; 1, moderate number of SD; 2, many SD). Score is given out of 8
Atwal scoreStriae rubrae and albaeMaximum score of six for each site (abdomen, hips, breasts, thigh/buttocks). Score 0–3 for presence of striae (0, no SD; 1, < 5 SD; 2, 5–10 SD; 3, > 10 SD); score 0–3 for presence of erythema (0, no erythema; 1, light red/pink; 2, dark red; 3, purple). Score out of 24
DermoscopyStriae rubrae, caerulae, nigrae and albaeVisualization of melanin networks and distinction of different types of striae due to the differences in melanin pigmentation: striae rubrae demonstrate a hypermelanosis while striae albae demonstrate leucoderma secondary to reduced melanocytes
Epiluminenscence colorimetryStriae rubrae, caerulae, nigrae and albaeComputer device that measures colour from observer-defined small areas in photographs
Reflectance confocal microscopyStriae rubrae and albaeUsed in vivo. Low-power infrared laser reflects light from a single in-focus plane at different levels of depth in the skin. Readily visualizes the collagen and elastic fibre architecture and may be used to monitor treatment efficacy. SD appear more anisotropic and have greater skin roughness than adjacent skin. Not useful in evaluating inflammatory changes in striae formation
Primos 3D cameraStriae rubrae and albaeReflected light absorbed by a high-resolution camera that records height differences from which a 3D image is produced. 3D image demonstrates the skin-surface topography including the depth, distribution and variation of skin furrows
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]
Treatment
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]
Table 7. Summary and levels of evidence for topical treatments used in the treatment of striae distensae (SD)
AuthorTreatment evaluatedForm of treatmentStriae typeDosageNo. of subjects (T/C)OutcomeAdverse effectsStudy designLevel of evidence
80% (n =8) of tretinoin-treated patients had definite marked improvement, compared with 8% (n =1) in control group.
Reduced length and width of striae by 14% and 8%, respectively, compared with increased length and width in control by 10% and 24%, respectively.
No significant difference in dermal collagen and elastic fibres in treatment compared with placebo
Erythema or scaling first 2 months (55%)RCT2
Rangel et al.[81]TretinoinTherapeuticNot stated0·1% daily, 3 months20
Reduction in length of stretch marks by up to 20%. Significant global improvement from baseline noted in all stretch marks.
Half of the abdomen was treated and the other half acted as the control. No randomization in this study
Erythema or scaling in first month (55%)Nonrandomized controlled trial3
Mallol et al.[73]Trofolastin (Centella asiatica) vs. placeboProphylaxisNot statedDaily, 12th week pregnancy until labour80 (41/39)
Results demonstrated that 56% in placebo and 34% in treated group developed striae.
The arbitrary score (from 0–3) for intensity was 1·42 for the treated group and 2·13 for the placebo group.
In women with a history of SD during puberty, the treatment cream gave a significant absolute prevention of SD of 89%
None statedRCT2
Ud-Din et al.[82]Silicone vs. placebo either side of abdomenTherapeuticNot statedDaily for 6 weeks20
Results demonstrated increased melanin, with decreased haemoglobin, collagen and pliability on both sides.
Collagen levels were significantly higher and melanin lower with silicone gel compared with controls
None statedRCT2
Draelos et al.[83]Centella asiatica/hyaluronic acidTherapeuticRubraeTwice daily, 12 weeks52
Statistically significant difference in participant and investigator evaluations of overall appearance, colour, softness and texture between treatment and control groups.
Patient's untreated thigh acted as control.
No placebo used
None statedRCT2
Wierrani et al.[84]Verum® (hyaluronic acid)ProphylaxisNot statedUnknown50 (24/26)
One-third of women with prophylactic treatment developed SD compared with two-thirds in the control group.
Better results in those women that were not overweight.
Unclear risk of attrition and performance bias
None statedRCT2
de Buman et al.[85]Alphastria® vs. placeboProphylaxisNot statedUnknown90 (30/30/30)Three groups: A = Alphastria cream, B = cream with excipients and vitamins, C = placebo with just excipient. 10% in prophylactically treated compared with 70% in placebo treated developed striaeNone statedRCT2
Osman et al.[86]Cocoa butter vs. placeboProphylaxisNot statedDaily, 12–18 weeks' gestation until delivery175 (91/84)No significant difference in development of SD between treatment and placebo groupsNone statedRCT2
Buchanan et al.[19]Cocoa butter vs. placeboProphylaxisNot statedDaily, 12–15 weeks' gestation until delivery300 (150/150)No significant difference in development of striae between treatment and placebo groupsNone statedRCT2
Taavoni et al.[87]Olive oilProphylaxisNot statedTwice daily, 18–20 weeks' gestation, for 8 weeks70 (35/35)
Subjects randomized into control or intervention group.
Intervention group applied olive oil and control group underwent no intervention.
No significant difference in development of SD between treatment and control groups. No placebo used for control group
None statedRCT2
Timur and Kafkasli[88]Almond oil with massage vs. almond oil alone vs. controlProphylaxisNot statedCream every other day, 19th–32nd week gestation141 (47/48/46)Significant difference in frequency of SD between groups: almond oil and massage 20%, almond oil alone 38·8%, control 41·2%None statedNonrandomized controlled trial3
Mendez et al.[89]Hydrant cream wet skin vs. hydrant cream dry skinProphylaxisNot statedDaily, 16–18 weeks' gestation until delivery50
Percentage of women without SD was 57% when cream applied on wet skin compared with 44% when applied to dry skin.
Skin on the patients forearm acted as a control.
None statedRCT2
Ash et al.[90]20% glycolic acid/10% ascorbic acid/2% zinc sulfate/0·5% tyrosine vs. 20% glycolic acid/0·05% tretinoin. Applied onto SD on abdomen or thighs with area split into halvesTherapeuticAlbaeDaily, 12 weeks10
Both regimens improved appearance of SD.
They both increased epidermal thickness and decreased papillary dermal thickness.
Increased elastin content with topical 20% glycolic acid and 0·05% tretinoin.
No control group
HyperpigmentationComparative study4
Adatto and Deprez[91]Sand abrasion and 15% TCA then post-peel creamTherapeuticAll types1–8 treatments (mean 4·2)69
Average improvement of 70% on all types of striae and locations.
Results better in striae rubrae.
PIH at 4 weeks especially in darker skinCase series4
Deprez[92]TCA then post-peel creamTherapeuticNot stated50% TCA, up to eight treatments50
Striae reduced in depth.
Almost all patients had 60–75% improvement at end of treatment
No control and no randomization in this study
Erythema and hyperpigmentationCase series4
Mazzarello et al.[93]Group A (striae rubrae) = 70% glycolic acid vs. placebo. Group B (striae albae) = 70% glycolic acid vs. placeboTherapeuticAll typesSix treatments over 6 months40
Decrease in furrow width of striae in both groups.
Striae rubrae showed decrease in haemoglobin and striae albae an increase in melanin.
Patient's other thigh acted as control
None statedNonrandomized controlled trial3
Total studies: 16LOE-1: 0; LOE-2: 10; LOE-3: 3; LOE-4: 3
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.
Table 8. Summary and levels of evidence for laser, light and miscellaneous therapies used to treat striae distensae (SD)[129]
AuthorDevice evaluatedStriae typeFitzpatrick skin typeWavelength and regimenNo. of subjects (T/C)OutcomeAdverse effectsStudy designLevel of evidence
585-nm.
Four protocols (spot diameter, fluence): 1 = 10 mm, 2·5 J cm−2; 2 = 10 mm, 3·0 J cm−2; 3 = 7 mm, 2·0 J cm−2; 4 = 7 mm, 4·0 J cm−2
39
The 10-mm spot size with 3·0 J cm−2 improved the SD better than other treatment protocols.
Significant reduction in skin shadowing in SD with all protocols (shadow profilometry). Normal-appearing elastin in SD treated with low-fluence PDL
Mild transient purpura or slight erythemaNonrandomized controlled trial3
Jimenez et al.[113]PDLAlbae 11, rubrae 9II–IV585-nm, two treatments at baseline and at week 620
No significant difference between control and treated SD after 12 weeks.13/20 and 9/20 subjects had decreased area of striae in treated and nontreated areas, respectively.
None of the striae albae had a change in colour.
Four of nine striae rubrae showed improvement
PIH in one patientNonrandomized controlled trial3
Nehal et al.[114]PDLAlbaeNot stated585-nm, 10 mm spot size and fluence of 4·25 J cm−2. Treated at 2-month intervals for 1–2 years5
Subjectively reported slightly improved appearance of SD.
No pre- or post-treatment photographic improvement.
Histologically no significant changes reported following treatment
PIH in darker skin typesCase series4
Suh et al.[105]PDL/RFAlbae 36, rubrae 1III–IV585-nm, three treatments at baseline, Thermage RF device used with fluences 53–97 J cm−2 (dial setting 10·5–13·5) with 2–3 passes. (PDL/RF), week 4 (PDL), week 8 (PDL)37
Subjective assessment showed 89% of patients had ‘good and very good’ overall improvement in SD while 59% in were graded ‘good and very good’ in elasticity.
No control and no randomization in this study
Transient purpura (16%) and PIH (3%)Case series4
Goldman et al.[36]Nd:YAG laserRubraeII–IV1064-nm, average number of treatment sessions was 3·45 with an interval of 3–6 weeks20
Results considered as excellent by 55% and 40% of patients and doctors, respectively.
No control and no randomization in this study
Minimal oedema and erythemaCase series4
Tay et al.[107]Nonablative diode laserAlbae 9, rubrae 2IV–VI1450-nm, three treatments at 6-week intervals11No patients showed any noticeable improvement compared with control areas (one side of the body was treated with other side acting as control). Not all outcomes are reported in the resultsTransient erythema, PIH (64%, n =7)RCT2
de Angelis et al.[32]Er:glass fractional nonablative laserAll typesII–IV1540-nm, 2–3 passes, 2–4 total treatments at 6-week intervals5150% or greater overall improvement at 6 months (unblinded assessment), 51–75% improvement (blinded assessment). No control in this studyTransient oedema, erythema, PIHCase series4
Stotland et al.[115]Er:glass fractional nonablative laserAlbae 13, rubrae 1I–IV1550-nm, 8–12 passes with fluences of 12–18 J cm−2, six treatments in total14Overall improvement of 26–50% in 63% of patients (n =5), < 25% improvement in dyschromia in 50% of patients (n =4), improved texture of 26–50% in 50% of patients (n =4). Untreated striae acted as controls.Post-treatment oedema, erythema and papulesRCT2
Guimarães et al.[116]Er:glass fractional nonablative laserRubraeNot stated1540-nm, eight sessions in total10
Post-breast augmentation SD.
Three patients completed eight treatments.
One month after the last treatment, all patients showed a marked improvement in the striae.
No controls or randomization
Post-laser erythema, PIH in 10% (n =1)Case series4
Yang and Lee[117]Er:glass fractional nonablative laser vs. ablative fractional CO2 laserAlbaeIVEr:glass 1550-nm at a pulse of 50 mJ and spot density 100 spots cm−2. CO2 pulse energy 40–50 mJ and spot density 75–100 spots cm−2. Three treatments at 4-week intervals22
Abdomen split into two halves and each half randomized to one of the two treatments.
No statistical difference between the two lasers but significant clinical and histological improvement comparing pre- and post-treatment.
No control used
PIH (36%)Comparative study4
Goldberg et al.[110]XeCl excimer UVB laser vs. UVB light deviceAlbaeII–IVUp to 10 treatments, XeCl 308-nm, UVB 290–320-nm10
Increased melanin, hypertrophy and increased number of melanocytes in all treated SD.
Maintained at 6 months.
No control and no randomization in this study
Not statedComparative study4
Goldberg et al.[118]XeCl excimer laserAlbaeII–IV308-nm, treatments continued until 15 completed or > 75% increase in pigmentation75
Clinically evident improvement in striae reported in 80% of subjects.
Average of 8·4 treatments.
For the first 10 patients, half the area of trunk/extremity acted as a control. In the remaining 65, both sides were treated
Erythema (100%)Case series4
Ostovari et al.[119]XeCl excimer laserAlbaeI–IV308-nm, weekly until 10 treatments completed or until 100% repigmentation1080% of patients had a poor or moderate result based on photographs and 70% based on patients' self-assessment.PIHNonrandomized controlled trial3
Alexiades-Armenakas et al.[120]XeCl excimer laserAlbaeNot stated308-nm, every 2 weeks until maximum of 10 treatments, 75% or 100% increase in colorimetric or visual pigment correction, respectively9
68% improvement in mean pigmentation relative to normal skin control.
Mean percentage pigmentation 102% compared with control.
Overall excellent pigment correction maintained to 2 months follow-up
Transient erythemaRCT2
Longo et al.[104]Copper bromide laserNot statedII–III577-nm, 1–5 sessions 1 month apart15
Five out of 15 subjects experienced complete disappearance of striae, other subjects: 50–90% improvement of dimensions.
In 13/15 results were maintained after 1 year.
No control and no randomization in this study
ErythemaCase Series4
Al-Dhalimi and Abo Nasyria[121]IPL 650-nm vs. 590-nmRubraeIII–IV
Two cut-off filters used 590-nm on left and 650-nm on right, starting fluence 13 J cm−2 increased to 15·5 J cm−2.
Five sessions at 2-week intervals
20
Significant reduction in total number of SD on right from 256 to 240. Significant reduction in SD on left from 251 to 228. Also decreased sum of lengths and maximum widths.
No control and no randomization in this study
Severe erythema (60%, n =6)Comparative study4
Hernández-Pérez et al.[100]IPLAlbae80% IV, 20% III515–1200-nm, five sessions once every 2 weeks15
Sum of the total length of striae reduced from 375to 239 cm.
Reduced number of striae from a total of 117 to 94. Significant difference in post-treatment dermal thickness.
No control and no randomization in this study
PIH (40%)Case Series4
Sadick et al.[108]UVA/UVB light therapy (MulticlearTM)AlbaeII–IVUVB 296–315-nm, UVA1 360–370-nm, twice weekly for maximum of 10 treatments9
Five subjects had completely repigmented striae, three had 76–100% improvement and one had 51–75% improvement.
Improvement only short term.
No randomization in this study
PIH (> 50%)Nonrandomized controlled trial3
Trelles et al.[109]Infrared light system (NovaPlus)AlbaeII–IVThree passes per session over four sessions, 15 days apart10
Four patients reported results as ‘fair’, two as ‘better’ and four as ‘same’. 3D optical skin imaging showed improvement of 25–50% in depth corresponding to SD.
Histology showed improvements compared with specimens at baseline.
No control and no randomization in this study
Minimal erythema for 24 hCase series4
Manuskiatti et al.[111]RF deviceAlbae 16, rubrae 1IV–V
Six, weekly treatments.
TriPollar RF device (3 electrodes) used at range of 40–50 W and frequency range 1 MHz
17
38% and 12% of subjects had 25–50% and 51–75% improvement in striae, respectively, on assessment. 12%, 23% and 65% of subjects rated their contentment as slightly satisfied, satisfied and very satisfied, respectively.
No control and no randomization in this study
None reportedCase series4
Suh et al.[122]Plasma fractional RF and platelet-rich plasma and ultrasoundNot statedIII–VFortnightly for total of four sessions18Two blinded reviewers rated ‘excellent’ results (75–100% improvement) in 33% (n =6) of subjects, ‘very good’ (50–74% improvement) in 38·9% (n =7), ‘good’ (25–49% improvement) in 22·4% (n =4) and ‘mild’ (1–24% improvement) in 5·6% (n =1). No control and no randomization in this studyPIH (11%)Case series4
Kim et al.[123]Intradermal RF and autologous platelet-rich plasmaNot statedIVThree sessions once every 4 weeks, RF device frequency of 1134 kHz19Objective assessment demonstrated 5% of patients with excellent improvement (n =1), 37% with marked improvement (n =7), 32% with moderate improvement (n =6) and 26% with mild improvement (n =5). No control and no randomization in this studyTransient bruising lasting 3–7 days (100%)Case series4
Ryu et al.[124]Fractionated microneedle RF vs. fractional CO2 laserNot statedIVThree treatment groups: fractional CO2 laser (n =10), microneedle RF (n =10), and both (n =10)30
Improvement evaluated on a visual analogue scale 1–4 (1 = minimal improvement or steady state, 4 = near total improvement), was 2·2 in the fractional CO2 laser-treated group, 1·8 in the microneedle RF-treated group and 3·4 in the combination group.
A thickened epidermis and increase in collagen fibres observed in the combination-treated sites.
No control and no randomization in this study
Transient PIH, pain and pruritusComparative study4
Lee et al.[79]Short-pulsed CO2 laserAlbaeIV10 600-nm27
Results showed that 7% (n =2) had > 75% improvement, 52% (n =14) had 51–75% improvement, 33% (n =9) had 26–50% improvement and 7% (n =2) had 0–25% improvement.
No control and no randomization in this study
Short-term erythema (100%) 4 weeks and mild PIH resolving within 4 weeksCase series4
Nouri et al.[125]Short-pulsed CO2 laser vs. control vs. PDLNot statedIV–VI
CO2 10 600-nm, two passes then saline wash.
PDL 585-nm
4
At 20-week follow-up, type IV skin showed no improvement with PDL, type VI showed hyperpigmentation.
The short pulsed CO2 showed persistent erythema and marked hyperpigmentation in types IV and VI skin respectively
Persistent erythema and PIH in skin types IV and VI with CO2 laserNonrandomized controlled trial3
Bak et al.[112]Fractional photothermolysis (Fraxel SR 1500)Rubrae 16, albae 6Not stated1500-nm, two sessions of eight passes at 4-week intervals22
27% (n =6) of patients showed marked improvement of SD while 63% (n =16) showed mild improvement.
Significant increase in average epidermal and dermal thickness from baseline.
No control and no randomization in this study
Erythema, mild pigmentation, PIH (9%)Case series4
Abdel-Latif and Albendary[103]MicrodermabrasionRubrae 12, albae 8II–IVFive treatments at weekly intervals20
Other half of body acted as control. ‘Good to excellent’ improvement in striae in 50% of subjects.
Remaining 50% had ‘mild to moderate’ improvement.
Most improvement in striae rubrae.
Significantly increased type I procollagen α1 mRNA in treatment compared with controls.
No randomization
Transient erythema (25%, n =5) and PIH (20%, n =4)Nonrandomized controlled trial3
Shin et al.[126]
Group A (3 areas) = laser/laser and collagen/collagen.
Group B (3 areas) = laser/laser and placebo/placebo
AlbaeIII–IVSuccinylated atelocollagen and ablative fractional resurfacing laser, three laser treatments at 4-week intervals12
Clinical improvement scores evaluated by two doctors found a significant difference between atelocollagen and placebo sites after laser treatment and also between atelocollagen and placebo.
No randomization
Erythema (100%) for 2–3 days, PIH (75%), one patient developed psoriasisNonrandomized controlled trial3
Aust et al.[127]Percutaneous collagen induction therapyNot statedNot statedSingle 30-min procedure22
At 6 months follow-up improved skin texture, skin tightening, dermal neovascularization and no change in pigmentation.
Increased collagen I and elastin on biopsy.
No control and no randomization in this study
None reportedCase series4
Park et al.[128]Needling therapyAlbae 11, rubrae 5III–IVThree treatments at 4-week intervals16
Results reported were that 37% (n =6) of patients were highly satisfied, 50% (n =8) were somewhat satisfied and 13% (n =2) were unsatisfied.
Increased collagen was found in the dermis post-treatment and the fragmented dermal elastin fibres normalized post-treatment.
No control and no randomization in this study
Pain, erythema, spotty bleeding and pruritusCase series4
Total studies: 30LOE-1: 0; LOE-2: 3; LOE-3: 7; LOE-4: 20
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, 108-110] 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.
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Conclusions
Striae distensae affect a substantial proportion of the worldwide population and pose a psychological burden to those affected. A multitude of companies target pregnant women and others affected by SD, with the aim of preventing or treating these cosmetically undesirable lesions.
Important associated factors have been recognized in both pregnant women and adolescents. Among pregnant women, pregnancy-related risk factors and constitutional factors associated with SD exist. Although visual scoring methods for severity are commonly used, no validated measure of assessing SD has been reported in the literature. Imaging techniques allow objective evaluation of SD in vivo. They may be potentially used for evaluation of SD maturation as well as responses to and comparisons of treatments. No high-quality, large, double-blind RCT exists in the literature that supports the use of creams and lotions in the prevention of pregnancy-related SD, and most evidence points to a lack of efficacy of topical preventative agents. Additionally, most articles that evaluate the use of lasers for treatment of SD are of evidence base levels 3–5. Significant side-effects may occur with both topical treatments and laser devices. Pre-treatment assessment of SD type and Fitzpatrick skin type is important to allow treatment regimens to be instigated with minimal adverse effects.
Double-blind, RCTs with large patient numbers are required to evaluate fully the evidence behind topical therapies and laser devices in the prevention and treatment of SD.
Two clinically and histopathologically recognizable forms of SD have been described: striae rubrae and striae albae.[11] The initial erythematous and violaceous-appearing lesions are referred to as striae rubrae. These fade into wrinkled, hypopigmented, atrophic scar-like marks named striae albae, which have been described as a permanent form of SD.[12] When occurring following pregnancy, the term striae gravidarum refers to the same entity, usually developing after the 24th week of gestation.[8, 13] Although the vast majority of SD have been reported in pregnant women and adolescents,[6, 13] they have also been described in association with Cushing syndrome and following the administration of both short- and long-term oral and topical corticosteroids.[13-15] Further to this, a number of key aetiological theories have been postulated. These include inadequate development of the skin (particularly elastic fibres and collagen),[16, 17] mechanical stretching of the skin and endocrine imbalance.[18, 19]
Several methods of assessing SD, visually or instrumentally, have been utilized in previous studies.[9, 20] Here we present a comprehensive review of the literature, incorporating articles from multiple search engines and languages. We focus on the epidemiology, aetiology, clinical evaluation, prevention and treatment of SD.
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Methods
We conducted searches of Medline, Embase and Google Scholar in order to identify relevant studies relating to SD published from 1950 to 2013. Articles in French, Spanish, Turkish and Portuguese were translated into English for inclusion. ‘Stretch marks’, ‘striae distensae’, ‘striae gravidarum’, ‘striae rubrae’, ‘striae albae’ and ‘striae atrophicans’ were the search terms used. Information was obtained from review articles and primary research papers. Articles were grouped by primary treatment strategy. Articles were assessed and assigned a level of evidence (LOE) adapted from the Oxford Centre for Evidence-Based Medicine.[21] These levels, ranging from LOE-1 to LOE-5, are based on study methodology and design (Table 1).
Table 1. Levels of evidence (LOE)
- RCT, randomized controlled trial. Adapted from Oxford Centre of Evidence-Based Medicine.[21]
LOE-2Systematic review with homogeneity of cohort studies
RCT
Cohort study
‘Outcomes’ research; ecological studies
LOE-3Systematic review with homogeneity of case–control studies
Nonrandomized controlled trial
Individual case–control study
LOE-4Case series
Comparative study
LOE-5Case reports
Expert opinion without critical appraisal/based on physiology/bench research or ‘first principles’
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Results
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, 6-8, 20, 24-27] 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]
Table 2. Comparison of striae distensae among different patient population groups[2-8, 10, 15, 20, 24-29]
Patient groupLocation (most common to least common)Proposed mechanism of formationAverage age (years)Approximate prevalence (%)
- ND, No data in the literature.
Adult nonpregnant womenBreasts and thighsPostpregnancy2935
Adolescent femalesThighs, buttocks, breastsStretching of the skin during growth spurt, adrenocortical hyperactivity13–1472–77
Adolescent malesButtocks, thighs, calves, backStretching of the skin during growth spurt, adrenocortical hyperactivity146–86
Adult malesButtocksSudden weight gain/loss, muscular exerciseND11
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 (Fig. 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]
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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 (Fig. 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, 50-52]
Table 3. Constitutional and pregnancy-related factors associated with striae distensae
FactorDavey (1972)[9]Murphy et al. (1992)[28]Chang et al. (2004)[6]Thomas and Liston (2004)[5]Atwal et al. (2006)[20]Osman et al. (2007)[8]Ghasemi et al. (2007)[7]Maia et al. (2009)[25]Canpolat et al. (2010)[24]
- BMI, body mass index; +, statistically significant.
Maternal age+++++
Maternal BMI+++++
Maternal weight+
Thickness of abdominal skin fold+
Positive family history++
Smoker+
Use of cream+
Pregnancy related
Birthweight++++++
Gestational age+
Weight gained during pregnancy+++
Polyhydramnios+
Table 4. Medical conditions, surgery, medications and other factors linked with striae distensae[2, 9, 13, 14, 33-52]
Associations with striae distensae
- HIV, human immunodeficiency virus.
Marfan syndrome, Cushing syndrome, anorexia nervosa, typhoid fever, rheumatic fever, chronic liver disease, obesity
Surgery
Augmentation mammoplasty, tissue expanded skin, tension-requiring skin sutures, organ transplantation, cardiac surgery
Medications
Systemic and topical corticosteroids, HIV therapy, chemotherapy, tuberculosis therapy, contraceptives, neuroleptics
Other
Pregnancy, puberty, stretch and weight training, idiopathic
Figure 2. Risk factors and associations with striae distensae.[2, 7-9, 20, 24-26, 30] BMI, body mass index.
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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, 59-61] 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]
Table 5. Histological comparisons of striae rubrae and striae albae[17, 18, 64-67]
Striae rubraeStriae albae
Clinical appearanceRaised pink linear lesionsPale, depressed and finely wrinkled lesions; appear similar to scars
EpidermisOedema between melanocytes and keratinocytes; increased melanogenesisEpidermal atrophy, loss of rete ridges and absent hair follicles; reduction in melanocytes leading to leucoderma
Papillary dermisVascular ectasia and possible angiogenesisLack of vascular stimulation
Reticular dermisCollagen fibres structurally altered; elastic fibres reduced and reorganized; fine elastic fibres predominate throughout dermis with thick, tortuous fibres toward the periphery; reduced fibrillin microfibrils at the dermal–epidermal junctionDensely packed collagen parallel to skin surface; predominantly thick elastic fibres in dermis with normal appearance in periphery
Inflammatory cellsDermal oedema, cuffing of the small vessels by lymphocytes, absent mast cells and prominent fibroblasts; increased glycosaminoglycan contentEosinophils predominate among collagen fibres
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]
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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.
Table 6. Visual and imaging techniques used to assess type, severity and efficacy of treatments of striae distensae (SD)[7, 9, 20, 64, 65, 74-78]
MethodType of striaeExplanation of method
Davey methodStriae rubrae and albaeAbdominal SD. Abdomen divided into quadrants using midline vertical and horizontal lines through umbilicus as divisions. Each quadrant given a score (0, no SD; 1, moderate number of SD; 2, many SD). Score is given out of 8
Atwal scoreStriae rubrae and albaeMaximum score of six for each site (abdomen, hips, breasts, thigh/buttocks). Score 0–3 for presence of striae (0, no SD; 1, < 5 SD; 2, 5–10 SD; 3, > 10 SD); score 0–3 for presence of erythema (0, no erythema; 1, light red/pink; 2, dark red; 3, purple). Score out of 24
DermoscopyStriae rubrae, caerulae, nigrae and albaeVisualization of melanin networks and distinction of different types of striae due to the differences in melanin pigmentation: striae rubrae demonstrate a hypermelanosis while striae albae demonstrate leucoderma secondary to reduced melanocytes
Epiluminenscence colorimetryStriae rubrae, caerulae, nigrae and albaeComputer device that measures colour from observer-defined small areas in photographs
Reflectance confocal microscopyStriae rubrae and albaeUsed in vivo. Low-power infrared laser reflects light from a single in-focus plane at different levels of depth in the skin. Readily visualizes the collagen and elastic fibre architecture and may be used to monitor treatment efficacy. SD appear more anisotropic and have greater skin roughness than adjacent skin. Not useful in evaluating inflammatory changes in striae formation
Primos 3D cameraStriae rubrae and albaeReflected light absorbed by a high-resolution camera that records height differences from which a 3D image is produced. 3D image demonstrates the skin-surface topography including the depth, distribution and variation of skin furrows
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]
Treatment
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]
Table 7. Summary and levels of evidence for topical treatments used in the treatment of striae distensae (SD)
AuthorTreatment evaluatedForm of treatmentStriae typeDosageNo. of subjects (T/C)OutcomeAdverse effectsStudy designLevel of evidence
- C, control; PIH, postinflammatory hyperpigmentation; RCT, randomized controlled trial; T, treatment; TCA, trichloroacetic acid.
80% (n =8) of tretinoin-treated patients had definite marked improvement, compared with 8% (n =1) in control group.
Reduced length and width of striae by 14% and 8%, respectively, compared with increased length and width in control by 10% and 24%, respectively.
No significant difference in dermal collagen and elastic fibres in treatment compared with placebo
Erythema or scaling first 2 months (55%)RCT2
Rangel et al.[81]TretinoinTherapeuticNot stated0·1% daily, 3 months20
Reduction in length of stretch marks by up to 20%. Significant global improvement from baseline noted in all stretch marks.
Half of the abdomen was treated and the other half acted as the control. No randomization in this study
Erythema or scaling in first month (55%)Nonrandomized controlled trial3
Mallol et al.[73]Trofolastin (Centella asiatica) vs. placeboProphylaxisNot statedDaily, 12th week pregnancy until labour80 (41/39)
Results demonstrated that 56% in placebo and 34% in treated group developed striae.
The arbitrary score (from 0–3) for intensity was 1·42 for the treated group and 2·13 for the placebo group.
In women with a history of SD during puberty, the treatment cream gave a significant absolute prevention of SD of 89%
None statedRCT2
Ud-Din et al.[82]Silicone vs. placebo either side of abdomenTherapeuticNot statedDaily for 6 weeks20
Results demonstrated increased melanin, with decreased haemoglobin, collagen and pliability on both sides.
Collagen levels were significantly higher and melanin lower with silicone gel compared with controls
None statedRCT2
Draelos et al.[83]Centella asiatica/hyaluronic acidTherapeuticRubraeTwice daily, 12 weeks52
Statistically significant difference in participant and investigator evaluations of overall appearance, colour, softness and texture between treatment and control groups.
Patient's untreated thigh acted as control.
No placebo used
None statedRCT2
Wierrani et al.[84]Verum® (hyaluronic acid)ProphylaxisNot statedUnknown50 (24/26)
One-third of women with prophylactic treatment developed SD compared with two-thirds in the control group.
Better results in those women that were not overweight.
Unclear risk of attrition and performance bias
None statedRCT2
de Buman et al.[85]Alphastria® vs. placeboProphylaxisNot statedUnknown90 (30/30/30)Three groups: A = Alphastria cream, B = cream with excipients and vitamins, C = placebo with just excipient. 10% in prophylactically treated compared with 70% in placebo treated developed striaeNone statedRCT2
Osman et al.[86]Cocoa butter vs. placeboProphylaxisNot statedDaily, 12–18 weeks' gestation until delivery175 (91/84)No significant difference in development of SD between treatment and placebo groupsNone statedRCT2
Buchanan et al.[19]Cocoa butter vs. placeboProphylaxisNot statedDaily, 12–15 weeks' gestation until delivery300 (150/150)No significant difference in development of striae between treatment and placebo groupsNone statedRCT2
Taavoni et al.[87]Olive oilProphylaxisNot statedTwice daily, 18–20 weeks' gestation, for 8 weeks70 (35/35)
Subjects randomized into control or intervention group.
Intervention group applied olive oil and control group underwent no intervention.
No significant difference in development of SD between treatment and control groups. No placebo used for control group
None statedRCT2
Timur and Kafkasli[88]Almond oil with massage vs. almond oil alone vs. controlProphylaxisNot statedCream every other day, 19th–32nd week gestation141 (47/48/46)Significant difference in frequency of SD between groups: almond oil and massage 20%, almond oil alone 38·8%, control 41·2%None statedNonrandomized controlled trial3
Mendez et al.[89]Hydrant cream wet skin vs. hydrant cream dry skinProphylaxisNot statedDaily, 16–18 weeks' gestation until delivery50
Percentage of women without SD was 57% when cream applied on wet skin compared with 44% when applied to dry skin.
Skin on the patients forearm acted as a control.
None statedRCT2
Ash et al.[90]20% glycolic acid/10% ascorbic acid/2% zinc sulfate/0·5% tyrosine vs. 20% glycolic acid/0·05% tretinoin. Applied onto SD on abdomen or thighs with area split into halvesTherapeuticAlbaeDaily, 12 weeks10
Both regimens improved appearance of SD.
They both increased epidermal thickness and decreased papillary dermal thickness.
Increased elastin content with topical 20% glycolic acid and 0·05% tretinoin.
No control group
HyperpigmentationComparative study4
Adatto and Deprez[91]Sand abrasion and 15% TCA then post-peel creamTherapeuticAll types1–8 treatments (mean 4·2)69
Average improvement of 70% on all types of striae and locations.
Results better in striae rubrae.
PIH at 4 weeks especially in darker skinCase series4
Deprez[92]TCA then post-peel creamTherapeuticNot stated50% TCA, up to eight treatments50
Striae reduced in depth.
Almost all patients had 60–75% improvement at end of treatment
No control and no randomization in this study
Erythema and hyperpigmentationCase series4
Mazzarello et al.[93]Group A (striae rubrae) = 70% glycolic acid vs. placebo. Group B (striae albae) = 70% glycolic acid vs. placeboTherapeuticAll typesSix treatments over 6 months40
Decrease in furrow width of striae in both groups.
Striae rubrae showed decrease in haemoglobin and striae albae an increase in melanin.
Patient's other thigh acted as control
None statedNonrandomized controlled trial3
Total studies: 16LOE-1: 0; LOE-2: 10; LOE-3: 3; LOE-4: 3
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.
Table 8. Summary and levels of evidence for laser, light and miscellaneous therapies used to treat striae distensae (SD)[129]
AuthorDevice evaluatedStriae typeFitzpatrick skin typeWavelength and regimenNo. of subjects (T/C)OutcomeAdverse effectsStudy designLevel of evidence
- Er, erbium; IPL, intense pulsed light; Nd:YAG, neodymium-doped YAG; PDL, pulsed-dye laser; PIH, postinflammatory hyperpigmentation; RCT, randomized controlled trial; RF, radiofrequency; UV, ultraviolet.
585-nm.
Four protocols (spot diameter, fluence): 1 = 10 mm, 2·5 J cm−2; 2 = 10 mm, 3·0 J cm−2; 3 = 7 mm, 2·0 J cm−2; 4 = 7 mm, 4·0 J cm−2
39
The 10-mm spot size with 3·0 J cm−2 improved the SD better than other treatment protocols.
Significant reduction in skin shadowing in SD with all protocols (shadow profilometry). Normal-appearing elastin in SD treated with low-fluence PDL
Mild transient purpura or slight erythemaNonrandomized controlled trial3
Jimenez et al.[113]PDLAlbae 11, rubrae 9II–IV585-nm, two treatments at baseline and at week 620
No significant difference between control and treated SD after 12 weeks.13/20 and 9/20 subjects had decreased area of striae in treated and nontreated areas, respectively.
None of the striae albae had a change in colour.
Four of nine striae rubrae showed improvement
PIH in one patientNonrandomized controlled trial3
Nehal et al.[114]PDLAlbaeNot stated585-nm, 10 mm spot size and fluence of 4·25 J cm−2. Treated at 2-month intervals for 1–2 years5
Subjectively reported slightly improved appearance of SD.
No pre- or post-treatment photographic improvement.
Histologically no significant changes reported following treatment
PIH in darker skin typesCase series4
Suh et al.[105]PDL/RFAlbae 36, rubrae 1III–IV585-nm, three treatments at baseline, Thermage RF device used with fluences 53–97 J cm−2 (dial setting 10·5–13·5) with 2–3 passes. (PDL/RF), week 4 (PDL), week 8 (PDL)37
Subjective assessment showed 89% of patients had ‘good and very good’ overall improvement in SD while 59% in were graded ‘good and very good’ in elasticity.
No control and no randomization in this study
Transient purpura (16%) and PIH (3%)Case series4
Goldman et al.[36]Nd:YAG laserRubraeII–IV1064-nm, average number of treatment sessions was 3·45 with an interval of 3–6 weeks20
Results considered as excellent by 55% and 40% of patients and doctors, respectively.
No control and no randomization in this study
Minimal oedema and erythemaCase series4
Tay et al.[107]Nonablative diode laserAlbae 9, rubrae 2IV–VI1450-nm, three treatments at 6-week intervals11No patients showed any noticeable improvement compared with control areas (one side of the body was treated with other side acting as control). Not all outcomes are reported in the resultsTransient erythema, PIH (64%, n =7)RCT2
de Angelis et al.[32]Er:glass fractional nonablative laserAll typesII–IV1540-nm, 2–3 passes, 2–4 total treatments at 6-week intervals5150% or greater overall improvement at 6 months (unblinded assessment), 51–75% improvement (blinded assessment). No control in this studyTransient oedema, erythema, PIHCase series4
Stotland et al.[115]Er:glass fractional nonablative laserAlbae 13, rubrae 1I–IV1550-nm, 8–12 passes with fluences of 12–18 J cm−2, six treatments in total14Overall improvement of 26–50% in 63% of patients (n =5), < 25% improvement in dyschromia in 50% of patients (n =4), improved texture of 26–50% in 50% of patients (n =4). Untreated striae acted as controls.Post-treatment oedema, erythema and papulesRCT2
Guimarães et al.[116]Er:glass fractional nonablative laserRubraeNot stated1540-nm, eight sessions in total10
Post-breast augmentation SD.
Three patients completed eight treatments.
One month after the last treatment, all patients showed a marked improvement in the striae.
No controls or randomization
Post-laser erythema, PIH in 10% (n =1)Case series4
Yang and Lee[117]Er:glass fractional nonablative laser vs. ablative fractional CO2 laserAlbaeIVEr:glass 1550-nm at a pulse of 50 mJ and spot density 100 spots cm−2. CO2 pulse energy 40–50 mJ and spot density 75–100 spots cm−2. Three treatments at 4-week intervals22
Abdomen split into two halves and each half randomized to one of the two treatments.
No statistical difference between the two lasers but significant clinical and histological improvement comparing pre- and post-treatment.
No control used
PIH (36%)Comparative study4
Goldberg et al.[110]XeCl excimer UVB laser vs. UVB light deviceAlbaeII–IVUp to 10 treatments, XeCl 308-nm, UVB 290–320-nm10
Increased melanin, hypertrophy and increased number of melanocytes in all treated SD.
Maintained at 6 months.
No control and no randomization in this study
Not statedComparative study4
Goldberg et al.[118]XeCl excimer laserAlbaeII–IV308-nm, treatments continued until 15 completed or > 75% increase in pigmentation75
Clinically evident improvement in striae reported in 80% of subjects.
Average of 8·4 treatments.
For the first 10 patients, half the area of trunk/extremity acted as a control. In the remaining 65, both sides were treated
Erythema (100%)Case series4
Ostovari et al.[119]XeCl excimer laserAlbaeI–IV308-nm, weekly until 10 treatments completed or until 100% repigmentation1080% of patients had a poor or moderate result based on photographs and 70% based on patients' self-assessment.PIHNonrandomized controlled trial3
Alexiades-Armenakas et al.[120]XeCl excimer laserAlbaeNot stated308-nm, every 2 weeks until maximum of 10 treatments, 75% or 100% increase in colorimetric or visual pigment correction, respectively9
68% improvement in mean pigmentation relative to normal skin control.
Mean percentage pigmentation 102% compared with control.
Overall excellent pigment correction maintained to 2 months follow-up
Transient erythemaRCT2
Longo et al.[104]Copper bromide laserNot statedII–III577-nm, 1–5 sessions 1 month apart15
Five out of 15 subjects experienced complete disappearance of striae, other subjects: 50–90% improvement of dimensions.
In 13/15 results were maintained after 1 year.
No control and no randomization in this study
ErythemaCase Series4
Al-Dhalimi and Abo Nasyria[121]IPL 650-nm vs. 590-nmRubraeIII–IV
Two cut-off filters used 590-nm on left and 650-nm on right, starting fluence 13 J cm−2 increased to 15·5 J cm−2.
Five sessions at 2-week intervals
20
Significant reduction in total number of SD on right from 256 to 240. Significant reduction in SD on left from 251 to 228. Also decreased sum of lengths and maximum widths.
No control and no randomization in this study
Severe erythema (60%, n =6)Comparative study4
Hernández-Pérez et al.[100]IPLAlbae80% IV, 20% III515–1200-nm, five sessions once every 2 weeks15
Sum of the total length of striae reduced from 375to 239 cm.
Reduced number of striae from a total of 117 to 94. Significant difference in post-treatment dermal thickness.
No control and no randomization in this study
PIH (40%)Case Series4
Sadick et al.[108]UVA/UVB light therapy (MulticlearTM)AlbaeII–IVUVB 296–315-nm, UVA1 360–370-nm, twice weekly for maximum of 10 treatments9
Five subjects had completely repigmented striae, three had 76–100% improvement and one had 51–75% improvement.
Improvement only short term.
No randomization in this study
PIH (> 50%)Nonrandomized controlled trial3
Trelles et al.[109]Infrared light system (NovaPlus)AlbaeII–IVThree passes per session over four sessions, 15 days apart10
Four patients reported results as ‘fair’, two as ‘better’ and four as ‘same’. 3D optical skin imaging showed improvement of 25–50% in depth corresponding to SD.
Histology showed improvements compared with specimens at baseline.
No control and no randomization in this study
Minimal erythema for 24 hCase series4
Manuskiatti et al.[111]RF deviceAlbae 16, rubrae 1IV–V
Six, weekly treatments.
TriPollar RF device (3 electrodes) used at range of 40–50 W and frequency range 1 MHz
17
38% and 12% of subjects had 25–50% and 51–75% improvement in striae, respectively, on assessment. 12%, 23% and 65% of subjects rated their contentment as slightly satisfied, satisfied and very satisfied, respectively.
No control and no randomization in this study
None reportedCase series4
Suh et al.[122]Plasma fractional RF and platelet-rich plasma and ultrasoundNot statedIII–VFortnightly for total of four sessions18Two blinded reviewers rated ‘excellent’ results (75–100% improvement) in 33% (n =6) of subjects, ‘very good’ (50–74% improvement) in 38·9% (n =7), ‘good’ (25–49% improvement) in 22·4% (n =4) and ‘mild’ (1–24% improvement) in 5·6% (n =1). No control and no randomization in this studyPIH (11%)Case series4
Kim et al.[123]Intradermal RF and autologous platelet-rich plasmaNot statedIVThree sessions once every 4 weeks, RF device frequency of 1134 kHz19Objective assessment demonstrated 5% of patients with excellent improvement (n =1), 37% with marked improvement (n =7), 32% with moderate improvement (n =6) and 26% with mild improvement (n =5). No control and no randomization in this studyTransient bruising lasting 3–7 days (100%)Case series4
Ryu et al.[124]Fractionated microneedle RF vs. fractional CO2 laserNot statedIVThree treatment groups: fractional CO2 laser (n =10), microneedle RF (n =10), and both (n =10)30
Improvement evaluated on a visual analogue scale 1–4 (1 = minimal improvement or steady state, 4 = near total improvement), was 2·2 in the fractional CO2 laser-treated group, 1·8 in the microneedle RF-treated group and 3·4 in the combination group.
A thickened epidermis and increase in collagen fibres observed in the combination-treated sites.
No control and no randomization in this study
Transient PIH, pain and pruritusComparative study4
Lee et al.[79]Short-pulsed CO2 laserAlbaeIV10 600-nm27
Results showed that 7% (n =2) had > 75% improvement, 52% (n =14) had 51–75% improvement, 33% (n =9) had 26–50% improvement and 7% (n =2) had 0–25% improvement.
No control and no randomization in this study
Short-term erythema (100%) 4 weeks and mild PIH resolving within 4 weeksCase series4
Nouri et al.[125]Short-pulsed CO2 laser vs. control vs. PDLNot statedIV–VI
CO2 10 600-nm, two passes then saline wash.
PDL 585-nm
4
At 20-week follow-up, type IV skin showed no improvement with PDL, type VI showed hyperpigmentation.
The short pulsed CO2 showed persistent erythema and marked hyperpigmentation in types IV and VI skin respectively
Persistent erythema and PIH in skin types IV and VI with CO2 laserNonrandomized controlled trial3
Bak et al.[112]Fractional photothermolysis (Fraxel SR 1500)Rubrae 16, albae 6Not stated1500-nm, two sessions of eight passes at 4-week intervals22
27% (n =6) of patients showed marked improvement of SD while 63% (n =16) showed mild improvement.
Significant increase in average epidermal and dermal thickness from baseline.
No control and no randomization in this study
Erythema, mild pigmentation, PIH (9%)Case series4
Abdel-Latif and Albendary[103]MicrodermabrasionRubrae 12, albae 8II–IVFive treatments at weekly intervals20
Other half of body acted as control. ‘Good to excellent’ improvement in striae in 50% of subjects.
Remaining 50% had ‘mild to moderate’ improvement.
Most improvement in striae rubrae.
Significantly increased type I procollagen α1 mRNA in treatment compared with controls.
No randomization
Transient erythema (25%, n =5) and PIH (20%, n =4)Nonrandomized controlled trial3
Shin et al.[126]
Group A (3 areas) = laser/laser and collagen/collagen.
Group B (3 areas) = laser/laser and placebo/placebo
AlbaeIII–IVSuccinylated atelocollagen and ablative fractional resurfacing laser, three laser treatments at 4-week intervals12
Clinical improvement scores evaluated by two doctors found a significant difference between atelocollagen and placebo sites after laser treatment and also between atelocollagen and placebo.
No randomization
Erythema (100%) for 2–3 days, PIH (75%), one patient developed psoriasisNonrandomized controlled trial3
Aust et al.[127]Percutaneous collagen induction therapyNot statedNot statedSingle 30-min procedure22
At 6 months follow-up improved skin texture, skin tightening, dermal neovascularization and no change in pigmentation.
Increased collagen I and elastin on biopsy.
No control and no randomization in this study
None reportedCase series4
Park et al.[128]Needling therapyAlbae 11, rubrae 5III–IVThree treatments at 4-week intervals16
Results reported were that 37% (n =6) of patients were highly satisfied, 50% (n =8) were somewhat satisfied and 13% (n =2) were unsatisfied.
Increased collagen was found in the dermis post-treatment and the fragmented dermal elastin fibres normalized post-treatment.
No control and no randomization in this study
Pain, erythema, spotty bleeding and pruritusCase series4
Total studies: 30LOE-1: 0; LOE-2: 3; LOE-3: 7; LOE-4: 20
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, 108-110] 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.
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Conclusions
Striae distensae affect a substantial proportion of the worldwide population and pose a psychological burden to those affected. A multitude of companies target pregnant women and others affected by SD, with the aim of preventing or treating these cosmetically undesirable lesions.
Important associated factors have been recognized in both pregnant women and adolescents. Among pregnant women, pregnancy-related risk factors and constitutional factors associated with SD exist. Although visual scoring methods for severity are commonly used, no validated measure of assessing SD has been reported in the literature. Imaging techniques allow objective evaluation of SD in vivo. They may be potentially used for evaluation of SD maturation as well as responses to and comparisons of treatments. No high-quality, large, double-blind RCT exists in the literature that supports the use of creams and lotions in the prevention of pregnancy-related SD, and most evidence points to a lack of efficacy of topical preventative agents. Additionally, most articles that evaluate the use of lasers for treatment of SD are of evidence base levels 3–5. Significant side-effects may occur with both topical treatments and laser devices. Pre-treatment assessment of SD type and Fitzpatrick skin type is important to allow treatment regimens to be instigated with minimal adverse effects.
Double-blind, RCTs with large patient numbers are required to evaluate fully the evidence behind topical therapies and laser devices in the prevention and treatment of SD.
