title: The role of phosphatase and tensin homolog in drug-induced gingival overgrowth.
abstract: OBJECTIVE
  We proposed that phosphatase and tensin homolog (PTEN) might be one of the signaling proteins that alter the balance between cell growth and cell death in drug-induced gingival overgrowth. The aim of this study was to investigate the expression of PTEN in subjects using cyclosporine A and to analyze the relationship between PTEN and cell proliferation marker, proliferating cell nuclear antigen (PCNA), in cyclosporine A-induced gingival overgrowth.
  
  
  METHODS
  In total, samples from 36 subjects, i.e. 24 cyclosporine A-mediated renal transplant patients with gingival overgrowth (n = 12) or without gingival overgrowth (n = 12) and 12 matched periodontally healthy subjects, were included in the study. PTEN and PCNA expressions in gingival tissues were analyzed using immunohistochemistry, PTEN expression was also analyzed by western blot. PTEN immunoreactivity was calculated with a histologic score (HSCORE) value and PCNA immunoreactivity was calculated with the PCNA-proliferative index.
  
  
  RESULTS
  Phosphatase and tensin homolog HSCORE for the group with gingival overgrowth was found to be significantly lowest compared to the group without gingival overgrowth and the control group (p < 0.001) while the highest PTEN HSCORE was found in the control group. In addition, the PTEN HSCORE for the group without gingival overgrowth was significantly lower compared to controls (p < 0.001). The highest PCNA-proliferative index score was observed in the group with gingival overgrowth while the lowest score was observed in the control group (p < 0.001). The immunoblot signal for PTEN was significantly decreased in the group with gingival overgrowth compared to the group without gingival overgrowth and the control group (p < 0.001). Western blot results were different from immunohistochemistry and revealed there was no significant difference between the without gingival overgrowth and the control group (p > 0.05).
  
  
  CONCLUSIONS
  Our results showing decreased PTEN levels in patients with gingival overgrowth supported with increased PCNA expression suggested that PTEN might take part in the imbalance between cell proliferation and death in drug-induced gingival overgrowth.
authors.affiliation: Department of Periodontology, Faculty of Dentistry, Ondokuzmayis University, Samsun, Turkey.
authors.forename: B O
authors.initials: BO
authors.lastname: Cetinkaya
authors.forename: F
authors.initials: F
authors.lastname: Pamuk
authors.forename: G C
authors.initials: GC
authors.lastname: Keles
authors.forename: B
authors.initials: B
authors.lastname: Ayas
authors.forename: G K
authors.initials: GK
authors.lastname: Ozfidan
authors.forename: U
authors.initials: U
authors.lastname: Kayisli
authors.forename: N
authors.initials: N
authors.lastname: Arik
authors.forename: H
authors.initials: H
authors.lastname: Horton
mesh_terms: D000199:Actins / Q000032:analysis; D015153:Blotting, Western; D016022:Case-Control Studies; D016923:Cell Death / Q000502:physiology; D049109:Cell Proliferation; D016572:Cyclosporine / Q000009:adverse effects; D005260:Female; D019214:Gingival Overgrowth / Q000139:chemically induced* / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007166:Immunosuppressive Agents / Q000009:adverse effects; D047908:Intracellular Signaling Peptides and Proteins / Q000032:analysis; D008297:Male; D051059:PTEN Phosphohydrolase / Q000032:analysis* / Q000502:physiology; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis; D025521:Tumor Suppressor Proteins / Q000032:analysis* / Q000502:physiology; D055815:Young Adult
chemical_list: D000199:Actins; D007166:Immunosuppressive Agents; D047908:Intracellular Signaling Peptides and Proteins; D018809:Proliferating Cell Nuclear Antigen; D025521:Tumor Suppressor Proteins; D016572:Cyclosporine; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human
keywords: cyclosporine A; gingival overgrowth; phosphatase and tensin homolog; proliferating cell nuclear antigen