title: Two-phase appearance of oral epithelial dysplasia resulting from focal proliferation of parabasal cells and apoptosis of prickle cells.
abstract: BACKGROUND
  One of the histologic characteristics of epithelial dysplasias of the oral mucosa is droplet-shaped rete processes resulting from a solid proliferation of basaloid cells. These basaloid cells are suddenly changed into an overlay of parakeratotic cells. However, it is unknown how this characteristic two-phase appearance is generated.
  
  
  METHODS
  Formalin-fixed paraffin sections of the oral mucosal specimens with normal, hyperplastic, dysplastic epithelia and squamous cell carcinomas were examined for apoptosis by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) method and for lymphoid cells by immunohistochemistry.
  
  
  RESULTS
  Apoptotic cells were only located in the keratinized layer of normal/hyperplastic epithelia. However, in epithelial dysplasias, apoptotic cells were scattered in the middle or even in the lower parts of the epithelial layer with frequent vacuolation changes of epithelial cells. Within the epithelial layer of dysplasias, there were increased number of lymphocytes, which were immunopositive for CD45RO, CD8, and CD57- and CD68-immunopositive (+), S-100 protein-positive and major histocompatibility complex (MHC) class II-positive monocytic lineages. They increased in number with the severity of dysplastic degrees, and they were often located in the vicinity of apoptotic epithelial cells, but decreased in carcinomas in situ and invasive carcinomas, which contained fewer numbers of apoptotic figures.
  
  
  CONCLUSIONS
  The findings indicate that intraepithelial infiltrations of both cytotoxic T cells and natural killer cells are closely related to the apoptotic phenomena of prickle cells, which may result in the characteristic 'two-phase appearance' of epithelial dysplasia.
authors.affiliation: Division of Oral Pathology, Department of Tissue Regeneration and Reconstruction, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Mei
authors.initials: M
authors.lastname: Syafriadi
authors.forename: Jun
authors.initials: J
authors.lastname: Cheng
authors.forename: Kai Yu
authors.initials: KY
authors.lastname: Jen
authors.forename: Hiroko
authors.initials: H
authors.lastname: Ida-Yonemochi
authors.forename: Makoto
authors.initials: M
authors.lastname: Suzuki
authors.forename: Takashi
authors.initials: T
authors.lastname: Saku
mesh_terms: D017209:Apoptosis; D018414:CD8-Positive T-Lymphocytes / Q000473:pathology; D002278:Carcinoma in Situ / Q000473:pathology; D002294:Carcinoma, Squamous Cell / Q000473:pathology; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000473:pathology; D004847:Epithelial Cells / Q000145:classification / Q000473:pathology; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D006801:Humans; D006965:Hyperplasia; D007694:Killer Cells, Natural / Q000473:pathology; D016131:Lymphocyte Subsets / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D009000:Monocytes / Q000473:pathology; D009061:Mouth Mucosa / Q000473:pathology*; D009062:Mouth Neoplasms / Q000473:pathology*; D009361:Neoplasm Invasiveness; D010241:Parakeratosis / Q000473:pathology; D011230:Precancerous Conditions / Q000473:pathology*; D009418:S100 Proteins / Q000032:analysis; D013602:T-Lymphocytes, Cytotoxic / Q000473:pathology; D014617:Vacuoles / Q000648:ultrastructure
chemical_list: D000949:Histocompatibility Antigens Class II; D009418:S100 Proteins