TY - JOUR
TI - Apoptosis in oral erythema multiforme
AU - Chrysomali, E.
AU - Lozada-Nur, F.
AU - Dekker, N.P.
AU - Papanicolaou, S.I.
AU - Regezi, J.A.
JO - ORAL SURGERY, ORAL MEDICINE, ORAL PATHOLOGY, ORAL RADIOLOGY AND ENDODONTICS
PY - 1997
VL - 83
TODO - 2
SP - 272-280
PB - Mosby Year Book Inc
SN - 1079-2104
TODO - 10.1016/S1079-2104(97)90016-0
TODO - BAX protein, human;  BCL2L1 protein, human;  DNA fragment;  Fas antigen;  FAS ligand;  FASLG protein, human;  membrane protein;  oncoprotein;  protein Bax;  protein bcl 2;  protein bcl x;  protein p53, adult;  aged;  apoptosis;  article;  case control study;  chemistry;  erythema multiforme;  female;  gene expression;  human;  immunohistochemistry;  keratinocyte;  male;  middle aged;  mouth disease;  mouth mucosa;  nonparametric test;  pathology, Adult;  Aged;  Aged, 80 and over;  Antigens, CD95;  Apoptosis;  bcl-2-Associated X Protein;  bcl-X Protein;  Case-Control Studies;  DNA Fragmentation;  Erythema Multiforme;  Fas Ligand Protein;  Female;  Gene Expression;  Humans;  Immunohistochemistry;  Keratinocytes;  Male;  Membrane Glycoproteins;  Middle Aged;  Mouth Diseases;  Mouth Mucosa;  Proto-Oncogene Proteins;  Proto-Oncogene Proteins c-bcl-2;  Statistics, Nonparametric;  Tumor Suppressor Protein p53
TODO - Objective. Cell death was evaluated in oral erythema multiforme to test the hypothesis that apoptosis may be a mechanism by which keratinocytes die in this condition. Study design. Ten erythema multiforme and five control oral mucosa biopsy specimens were evaluated in immunohistochemically stained sections for apoptosis-regulating proteins Bcl-2, Bcl-x, Bax, p53, Fas, and Fas-ligand. Apoptotic keratinocytes, determined by a detection method for DNA fragmentation (TUNEL) and by conventional morphologic criteria were counted per high power field. Results. Keratinocyte staining for Bcl-2 protein was comparable in erythema multiforme and controls. Bcl-x expression was reduced in five erythema multiforme cases. Staining for Bax protein differed in six erythema multiforme cases and showed variable intensity in layers under the parakeratin. Only slight differences in staining patterns of Fas and Fas-ligand proteins were noted between erythema multiforme and controls. The number of apoptotic keratinocytes evaluated by morphologic examination was significantly higher in erythema multiforme (mean per high power field, 0.90 ± 0.2; controls, 0.06 ± 0.04; p < 0.05, Mann-Whitney test) and was limited in significance by the TUNEL method (erythema multiforme, 0.43 ± 0.1; controls, 0.02 ± 0.02). Overexpression of p53 protein was seen in basal keratinocytes in five erythema multiforme specimens (mean, 17.5 ± 4.03 per high power field; controls 1.2 ± 0.3). Conclusions. There is evidence that cell death in erythema multiforme is at least in part due to apoptosis. The apoptotic mechanism may be related to an altered expression of apoptosis-regulating proteins. Although measurable alterations in the phenotypic expression of Fas and Fas-ligand proteins were not apparent, activation of Fas/Fas-ligand system could still be involved in the induction of apoptosis in erythema multiforme.
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