Histopathology of Striae Distensae, with Special Reference to Striae and Wound Healing in the Marfan Syndrome*

Pinkus, Hermann; Keech, M. K.; Mehregan, Amir H.

doi:10.1038/jid.1966.43

Cited by 61 publications

(24 citation statements)

References 7 publications

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“…Pregnancy’s distinct hormonal milieu is thought to influence connective tissue that is susceptible to SG when stretched. Ultimately, abnormalities in elastic fibers (Pinkus et al, 1966, Sheu et al, 1991, Tsuji and Sawabe, 1988), collagen fibrils (Pinkus et al, 1966, Shuster, 1979), and other extracellular membrane components (Watson et al, 1998) are believed to underlie the pathogenesis of SG (Wang et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

Striae gravidarum: Risk factors, prevention, and management

Farahnik

Park

Kroumpouzos

et al. 2017

International Journal of Women's Dermatology

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BackgroundStriae gravidarum (SG) are atrophic linear scars that represent one of the most common connective tissue changes during pregnancy. SG can cause emotional and psychological distress for many women. Research on risk factors, prevention, and management of SG has been often inconclusive.MethodsWe conducted a literature search using textbooks, PubMed, and Medline databases to assess research performed on the risk factors, prevention, and management of SG. The search included the following key words: striae gravidarum, pregnancy stretch marks, and pregnancy stretch. We also reviewed citations within articles to identify relevant sources.ResultsYounger age, maternal and family history of SG, increased pre-pregnancy and pre-delivery weight, and increased birth weight were the most significant risk factors identified for SG. Although few studies have confirmed effective prevention methods, Centella asiatica extract, hyaluronic acid, and daily massages showed some promise. Treatment for general striae has greatly improved over the last few years. Topical tretinoin ≥ 0.05% has demonstrated up to 47% improvement of SG and non-ablative fractional lasers have consistently demonstrated 50 to 75% improvement in treated lesions of striae distensae.ConclusionOverall, SG has seen a resurgence in research over the last few years with promising data being released. Results of recent studies provide dermatologists with new options for the many women who are affected by these disfiguring marks of pregnancy.

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Section: Introductionmentioning

confidence: 99%

Striae gravidarum: Risk factors, prevention, and management

Farahnik

Park

Kroumpouzos

et al. 2017

International Journal of Women's Dermatology

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“…2 Vascular disease in MFS is characterized by elastic matrix abnormalities in the medial layer of the aortic wall, including fragmentation and disorganization of elastic fibers, a generalized loss of elastin content, and the accumulation of amorphous matrix components. [3][4][5][6][7][8] The elastin gene was excluded as the site of primary defect, and in 1991, a positional candidate approach demonstrated that mutations that cause MFS occur in the FBN1 gene that encodes fibrillin-1. 9 -12 This 350-kDa glycoprotein is the major structural constituent of 10-nm extracellular microfibrils.…”

mentioning

confidence: 99%

Phenotypic Alteration of Vascular Smooth Muscle Cells Precedes Elastolysis in a Mouse Model of Marfan Syndrome

Bunton

Biery

Myers

et al. 2001

Circulation Research

316

243

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Abstract-Marfan syndrome is associated with early death due to aortic aneurysm. The condition is caused by mutations in the gene (FBN1) encoding fibrillin-1, a major constituent of extracellular microfibrils. Prior observations suggested that a deficiency of microfibrils causes failure of elastic fiber assembly during late fetal development. Mice homozygous for a targeted hypomorphic allele (mgR) of Fbn1 revealed a predictable sequence of abnormalities in the vessel wall including elastic fiber calcification, excessive deposition of matrix elements, elastolysis, and intimal hyperplasia. Here we describe previously unrecognized concordant findings in elastic vessels from patients with Marfan syndrome. Furthermore, ultrastructural analysis of mgR mice revealed cellular events that initiate destructive changes. The first detectable abnormality was an unusually smooth surface of elastic laminae, manifesting the loss of cell attachments that are normally mediated by fibrillin-1. Adjacent cells adopted alteration in their expression profile accompanied by morphological changes but retained expression of vascular smooth muscle cell markers. The abnormal synthetic repertoire of these morphologically abnormal smooth muscle cells in early vascular lesions included elastin, among other matrix elements, and matrix metalloproteinase 9, a known mediator of elastolysis. Ultimately, cell processes associated with zones of elastic fiber thinning and fragmentation. These data suggest that the loss of cell attachments signals a nonproductive program to synthesize and remodel an elastic matrix. This refined understanding of the pathogenesis of vascular disease in Marfan syndrome will facilitate the development of therapeutic strategies. (Circ Res. 2001;88:37-43.)

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“…Striae are believed to be dermal scars resulting from intrinsic stretching forces on soft tissues. Pinkus et al 4 were the first to describe the increase in elastic fibers in striae and compare it with scar tissue. Bhangoo et al 5 also observed elastogenesis in scar tissue.…”

Section: Discussionmentioning

confidence: 99%

Breast Striae After Cosmetic Augmentation

Tsai

Castillo

Moliver

2014

Aesthetic Surgery Journal

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Breast SurgeryBreast augmentation is the most popular cosmetic surgical procedure in the United States; 330 631 procedures were performed in 2012.1 Any complication can be a significant disappointment for the patient and the surgeon. A known but incompletely understood complication of breast augmentation is striae distensae, also called stretch marks.Striae are linear dermal scars that form in areas of dermal damage. The histology is similar to that of scar tissue formation, but the exact origin is still unknown. Investigators have hypothesized that these scars are precipitated by an inflammatory reaction that destroys collagen and elastic fibers, with ensuing regeneration in the direction of the mechanical forces. This results in flattening and atrophy of the epidermis. Many theories have been suggested to explain the etiology of striae formation, including infection, effects of mechanical stretching, hormonal influences, genetic factors, immunosuppressed states, and chronic liver disease. Objectives: The authors investigated their own patient population to discern risk factors for new-onset striae after cosmetic breast augmentation. Methods: A retrospective chart review was performed for patients who underwent primary breast augmentation from 2005 to 2012 in a single-surgeon practice. Initial chart review revealed that only patients aged ≤25 years exhibited new striae; therefore, only patients from this age group were included. Potential risk factors examined included age, body mass index (BMI), oral contraceptive use, time of last menstrual period (LMP), parity, smoking and alcohol status, diabetes mellitus, and personal history of striae. Implant and surgical factors examined included implant material (silicone vs saline), volume, and location (submuscular vs subglandular placement) and the site of incision. Results: Of the 549 patients included in the study, 17 (3.10%) had new-onset striae, observed at a mean of 58 days postoperatively. The risk of striae was statistically significantly higher (P < .05) among patients who were younger (3.3 times), were nulliparous (14.38 times), began their LMP >14 days before surgery (9.24 times), and had a history of striae (6.11 times). There was a strong correlation between new-onset breast striae and implant size, as well as BMI (P = .07). Conclusions: There is a strong correlation between new-onset striae and hormone levels, genetic factors, and tissue stretch components in patients who undergo cosmetic breast augmentation. This information can be utilized to better educate patients about this potential complication. Level of Evidence: 4

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Histopathology of Striae Distensae, with Special Reference to Striae and Wound Healing in the Marfan Syndrome*

Cited by 61 publications

References 7 publications

Striae gravidarum: Risk factors, prevention, and management

Striae gravidarum: Risk factors, prevention, and management

Phenotypic Alteration of Vascular Smooth Muscle Cells Precedes Elastolysis in a Mouse Model of Marfan Syndrome

Breast Striae After Cosmetic Augmentation

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