الفهرس 
STRIAE DISTENSAE: OVERVIEW
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Abstract
Striae distensae, commonly known as stretch marks, is a skin condition that is often asymptomatic but creates considerable cosmetic concerns for patients. Striae are visible linear scars which form in areas of dermal damage produced by stretching of the skin.In the early stages, striae may appear pink to red (striae rubra), which over time become atrophic and attain white color (striae alba).
Several observations within the disease express gender influence. The highest incidence of striae is between 10 and 16 years of age among girls, and between 14 and 20 years of age among boys. The commonest sites are the outer aspect of the thighs and lumbosacral region in males, while in females; the disease affects thighs, upper arms, buttocks, and breasts.
The causes of striae are not clear; some authors suggest Mechanical effect of stretching, which is proposed to lead to rupture of the connective tissue framework (e.g., pregnancy, obesity, weight lifting), others suggest Increase in the levels of body steroid hormones; Cushing’s syndrome, local or systemic steroid therapy that has a catabolic effect on fibroblasts, others suggest Genetic factors (absence of striae in pregnancy in people with Ehlers-Danlos syndrome and their presence as one of the minor diagnostic criteria for Marfan syndrome suggest an important genetic element), and other authors suggest Immunosuppression states associated with pregnancy-induced hypertension medications, human immunodeficiency virus, or diseases such as tuberculosis and typhoid.
The histological studies revealed: in the early stages, inflammatory changes may be conspicuous, but later the epidermis is thin and flattened. Recent SD shows a deep and superficial perivascular lymphocytic infiltrate around the venules. Collagen bands on the upper third of the reticular dermis are stretched and aligned parallel to the surface of the skin. In the latter stages, there is thinning of the epidermis due to flattening of the rete ridges and loss of collagen and elastin.
Our study was conducted on 15 males and 15 females aiming at studying the influence of gender on expression of estrogen, androgen, and glucocorticoid receptors in SD. We included three groups of subjects Group I included 5 healthy females & 5 healthy males serving as controls, group II included 10 females having SD, and group III included 10 males having SD. Control group were subjected to one punch biopsy, while females and males having striae were subjected to two punch biopsies from lesional and non lesional skin.
In mallory stained slides of normal male and female the collagen fibers were condensed below the epidermis at the dermo-epidermal junction, collagen fibers in papillary dermis were arranged as branching fine bundles. The papillary dermis run relatively thicker in males than females. In slides obtained from non-lesional skin in female and male with striae there were thin collagen bundles in the papillary dermis running in different directions. There was occasional absence of the collagen condensation in the grenz zone. However, in the lesional skin of both male and female with striae there were thick collagen bundles in the papillary dermis running parallel to dermo-epidermal junction indicating increased fibrosis.
Statistical analysis of immunohistochemical results revealed that there were increased estrogen expressions in the nuclei of epidermal cells in male cases than female cases in lesional area. When we compared estrogen expressions in control male and males with SD we found that estrogen expressions were higher in control than male with SD.
When we compared estrogen expressions in epidermis and dermis between control female and females with SD we found it higher in control female than female with SD.
On studying the expressions of AR we found that AR expressions in lesional area and non-lesional area in both epidermis and dermis were higher in male cases than female cases with SD. When we compared control males with male with SD we found androgen expressions higher in male with SD than control male.
On studying the expression of GR we found that GR expressions were higher in male with striae than control, and when we compared female control with female with striae we also, found GR expression higher in female with striae than control female.
To conclude we assume that there may be an influence of gender on the cutaneous expression of hormonal receptors such as ER, AR, and GR, which may be one of the mechanisms underlying the pathogenesis of SD. Our assumption is supported by many significant findings. ER was higher in male patients with striae than female patients with striae, but it was higher in control than patients with striae. AR was higher in male patients with striae than female patients with striae, it was higher in males with striae than normal male, but was higher in normal female than female with striae. GR was higher in control groups than cases with striae with no significant difference between male and female with striae.