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العنوان
Immunohistochemical expression of SOX 9 and CD 34 in alopecia areata /
المؤلف
Farag, Basant Elsayed Hussein.
هيئة الاعداد
باحث / بسنت السيد حسين فرج
مشرف / علاء حسن مرعي
مشرف / رانيا عبد الله عبد الله حسنين
مناقش / علاء حسن مرعي
الموضوع
Dermatology. Alopecia areata.
تاريخ النشر
2023.
عدد الصفحات
128 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الأمراض الجلدية
تاريخ الإجازة
2/10/2023
مكان الإجازة
جامعة المنوفية - كلية الطب - الامراض الجلدية والتناسلية
الفهرس
Only 14 pages are availabe for public view

from 137

from 137

Abstract

Alopecia areata (AA) is an autoimmune disorder characterized by transient, non-scarring hair loss with preservation of the hair follicle. Typically presents as smooth, sharply demarcated, round patches of hair loss without atrophy, with exclamation point hairs observed on the periphery of the patches. Special designations of the disease include alopecia universalis (AU) (total body hair loss), alopecia totalis (AT) (total scalp hair loss) or alopecia in an ophiasis pattern (band-like hair loss on the temporal and occipital scalp). The perevelance of AA is approximately 2% worldwide, which is more common in children and young adults. Often these AA patients go through frequent relapsing and remitting phases, however, the disease could be permanent in some people.
The pathogenesis of AA is not understood yet, due to the multifactorial etiology, whereas increasing data points to a complex immunopathogenesis of AA at which hair follicle immune privilege (IP) breakdown plays a crucial role. And several genes and environmental factors play a role in triggering its pathology and affect disease severity.
The hair follicle (HF) undergoing continuous programmed cycling process called the hair growth cycle which is maintained during life by hair follicle stem cells (HFSCs). HFs consist of a permanent portion, which includes sebaceous glands (SG) and the bulge area and a dynamic portion that undergoes cycles of apoptosis and active regrowth of hair cycle, the bulge area contains a specific environment called niche in where HFSCs located. Which reside in a quiescent inactive state in its niche at the bulge area. The new hair cycle started by early anagen phase, retracted dermal papilla (DP) send signals to activate HFSCs to divided into secondary germ cell (progenitor cell), Progenitor cells migrate downward to the bottom of the hair bulb near to the DP to regenerate a new hair cycle. Progenitor cells have a high proliferative activity with have a shorter lifespan than bulge cells. Thus, both HFSCs and progenitor cells play essential roles in hair regeneration.
Sex-determining region Y (SRY)-box 9 (SOX9) belongs to Sox family proteins which are a group of transcriptional regulators containing a high mobility group (HMG) domain that is highly conserved. This group of transcriptional regulators have critical functions in a number of developmental processes. In human hair follicles, SOX9 is expressed in sweat glands, sebaceous glands, the outer root sheath (ORS) in addition to bulge area. Moreover, SOX9 guides the differentiation of the exterior root sheath of adult human hair follicle in addition to regulation of HFSCs homeostasis as well as progenitor cell pools.
As a transmembrane glycoprotein, cluster of differentiation 34 (CD34) is a glycosylated cell surface transmembrane protein with prominent role in cell-cell adhesion. Was primarily thought to be a marker of hematopoietic stem cells, progenitor cells as well as endothelial cells. It was noted that human bulge cells do not express CD34, a great bulge cell marker in mice. Instead, just below the bulge of anagen human hair follicle, CD34 is found in slightly more differentiated outer root sheath cells.
We aimed in the present study to evaluate the immunohistochemical expression of SOX9 and CD34 in alopecia areata patients and to discover their role in the disease pathogenesis.
This case control study was conducted on a total number of 40 subjects; 20 cases with alopecia areata as patient group with range of age between18 – 48 years, 14 males and 6 females with a M:F ratio of (2.3:1), beside 20 ages and gender matched healthy subjects as a control group.