APOPTOSIS IN ORAL ERYTHEMA MULTIFORME

Objective. Cell death was evaluated in oral erythema multiforme to tes t the hypothesis that apoptosis may be a mechanism by which keratinocy tes die in this condition. Study design. Ten erythema multiforme and f ive control oral mucosa biopsy specimens were evaluated in immunohisto chemically stained sections for apoptosis-regulating proteins Bcl-2, B cl-x, Bar, p53, Fas, and Fas-ligand. Apoptotic keratinocytes, determin ed by a detection method for DNA fragmentation (TUNEL) and by conventi onal morphologic criteria were counted per high power field. Results, Keratinocyte staining for Bcl-2 protein was comparable in erythema mul tiforme and controls. Bcl-x expression was reduced in five erythema mu ltiforme cases. Staining for Bar protein differed in six erythema mult iforme cases and showed variable intensity in layers under the paraker atin. Only slight differences in staining patterns of Fas and Fas-liga nd proteins were noted between erythema multiforme and controls. The n umber of apoptotic keratinocytes evaluated by morphologic examination was significantly higher in erythema multiforme (mean per high power f ield, 0.90 +/- 0.2; controls, 0.06 +/- 0.04; p < 0.05, Mann-Whitney te st) and was limited in significance by the TUNEL method (erythema mult iforme, 0.43 +/- 0.1; controls, 0.02 +/- 0.02). Overexpression of p53 protein was seen in basal keratinocytes in five erythema multiforme sp ecimens (mean, 17.5 +/- 4.03 per high power field; controls 1.2 +/- 0. 3). Conclusions. There is evidence that cell death in erythema multifo rme 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 an d Fas-ligand proteins were not apparent, activation of Fas/Fas-ligand system could still be involved in the induction of apoptosis in erythe ma multiforme.