title: Decompression of keratocystic odontogenic tumors leading to increased fibrosis, but without any change in epithelial proliferation.
abstract: OBJECTIVE
  The aim of this study was to investigate whether decompression treatment induces changes in the histology or biologic behavior of keratocystic odontogenic tumor (KCOT).
  
  
  METHODS
  Seventeen patients with KCOT underwent decompression treatment with or without enucleation. Histologic evaluation and immunohistochemical expression of p53, Ki-67, and Bcl-2 were analyzed by using conventional microscopy.
  
  
  RESULTS
  KCOT showed significantly increased fibrosis (P = .01) and a subjective reduction in mitotic activity (P = .03) after decompression. There were no statistically significant changes in the expression of proliferation markers. An increase in daughter-cysts or epithelial rests was seen after decompression (P = .04). Recurrence was noted in four of 16 cases, and expression of p53 was strongly correlated with prolonged duration of treatment (P = .01) and intense inflammatory changes (P = .02).
  
  
  CONCLUSIONS
  Structural changes in the KCOT epithelium or capsule following decompression facilitate surgical removal of the tumor. There was no statistical evidence that decompression influences expression of proliferation markers in the lining, indicating that the potential for recurrence may not be restricted to the cellular level. The statistically significant increase of p53 expression with increased duration of treatment and increase of inflammation may also indicate the possibility of higher rates of recurrence with prolonged treatment and significant inflammatory changes.
authors.affiliation: MClinDent Oral Surgery Edinburgh Dental Institute, Oral Maxillofacial Speciality Doctor at Queen Margaret and Victoria Hospitals, NHS, Fife, Scotland, UK. Electronic address: S.awni@nhs.net.
authors.forename: Sarah
authors.initials: S
authors.lastname: Awni
authors.affiliation: Consultant Oral Pathologist, Royal Infirmary of Edinburgh Hospital and Edinburgh Dental Institute, Edinburgh, Scotland, UK.
authors.forename: Brendan
authors.initials: B
authors.lastname: Conn
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D049109:Cell Proliferation; D002648:Child; D019299:Decompression, Surgical; D004848:Epithelium / Q000473:pathology; D005260:Female; D005355:Fibrosis / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009808:Odontogenic Tumors / Q000378:metabolism / Q000473:pathology* / Q000601:surgery*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012189:Retrospective Studies; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: C000595707:BCL2 protein, human; D015415:Biomarkers; D019394:Ki-67 Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53