title: Study of apoptosis in oral pemphigus vulgaris using immunohistochemical marker Bax and TUNEL technique.
abstract: BACKGROUND
  Pemphigus vulgaris (PV) is an autoimmune mucocutaneous disease presenting clinically with blisters or erosions of the skin and mucous membrane. The main histopathologic characteristic of this disease is suprabasal vesicles due to loss of cell-cell adhesion between keratinocytes named acantholysis. Studies have shown that apoptosis is increased in PV. The purpose of this study is to investigate the role of apoptosis in blister formation in PV.
  
  
  METHODS
  This cross-sectional study was conducted on 25 specimens of oral PV. The presence of apoptosis was evaluated using the TUNEL technique in the normal perilesional region, vesicle area, and acantholytic cells. Also, the expression of Bax pro-apoptotic marker was assessed by the biotin-streptavidin immunohistochemical method. SPSS software was used for Wilcoxon test analysis. P values <0.05 were considered significant.
  
  
  RESULTS
  The percentage and intensity staining of TUNEL-positive cells were noteworthy. There were statistically significant differences between basal and parabasal (P = 0.05), tombstone with vesicle roof (P = 0.038) and basal with tombstone (P = 0.038). However, the expression and staining intensity of pro-apoptotic marker Bax were weak, and no statistically significant differences were observed between the various areas.
  
  
  CONCLUSIONS
  The results obtained in the present study suggest that the process of apoptosis occurs early in PV because it was observed in the perilesional normal appearing tissue. Also, the process of apoptosis may cause exacerbation or speeding of the bulla formation. In other words, inhibition of apoptosis in the patients could reduce the severity of the lesions.
authors.affiliation: Torabinegad Dental Research Center and Department of Oral & Maxillofacial Pathology, School of Dentistry, Isfahan University of Medical Sciences, Isfahan, Iran. Deihimy@dnt.mui.ac.ir
authors.forename: Parviz
authors.initials: P
authors.lastname: Deyhimi
authors.forename: Payam
authors.initials: P
authors.lastname: Tavakoli
mesh_terms: D000051:Acantholysis / Q000473:pathology; D017209:Apoptosis / Q000502:physiology*; D015415:Biomarkers / Q000032:analysis; D001768:Blister / Q000473:pathology; D002448:Cell Adhesion / Q000502:physiology; D004396:Coloring Agents; D003430:Cross-Sectional Studies; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D015603:Keratinocytes / Q000473:pathology; D009059:Mouth Diseases / Q000473:pathology*; D009061:Mouth Mucosa / Q000473:pathology; D010392:Pemphigus / Q000473:pathology*; D051028:bcl-2-Associated X Protein / Q000032:analysis*
chemical_list: C494826:BAX protein, human; D015415:Biomarkers; D004396:Coloring Agents; D051028:bcl-2-Associated X Protein