title: Downregulated gene expression of TGF-βs in diabetic oral wound healing.
abstract: BACKGROUND
  Healing of tooth extraction sockets in poorly controlled diabetic patients is often delayed and accompanied by severe infection. The exact cellular and molecular mechanisms underlying the pathogenesis of this complication are still not fully understood.
  
  
  OBJECTIVE
  The purpose of this study was to investigate molecular changes associated with delayed oral wound healing in diabetes.
  
  
  METHODS
  Six to eight weeks old male type 2 diabetes and age matched control inbred mice were used and maxillary molar tooth extractions were performed. At 4 and 7 days after tooth extraction, the edentulous mucosa of the mice were harvested, and analyzed for histology and gene expression of key wound healing factors.
  
  
  RESULTS
  In the diabetic model, histological analysis showed that epithelial tissue migration for wound closure was delayed after tooth extraction compared to the control. Quantitative real-time PCR revealed that expression of the TGF-β1, TGF-β2, TGF-β3, TGFβRII and TGFβRIII genes was significantly downregulated in the diabetic model at 4 and 7 days after tooth extraction.
  
  
  CONCLUSIONS
  These results suggest that delayed wound healing of oral mucosa in diabetes may be associated with decreased expression levels of these regulatory genes which play important roles in controlling epithelial wound closure.
authors.affiliation: Department of Prosthodontics, New York University College of Dentistry, 345 East 24th Street, 4W, New York, NY 10010, USA. sy23@nyu.edu
authors.forename: Seiichi
authors.initials: S
authors.lastname: Yamano
authors.forename: Winston P
authors.initials: WP
authors.lastname: Kuo
authors.forename: Cortino
authors.initials: C
authors.lastname: Sukotjo
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000276:immunology*; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000235:genetics / Q000276:immunology; D004847:Epithelial Cells / Q000473:pathology; D005786:Gene Expression Regulation / Q000235:genetics; D005881:Gingiva / Q000473:pathology; D053583:Interleukin-1beta / Q000032:analysis / Q000235:genetics; D008214:Lymphocytes / Q000473:pathology; D008297:Male; D020784:Matrix Metalloproteinase 8 / Q000032:analysis / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008963:Molar / Q000601:surgery; D009061:Mouth Mucosa / Q000473:pathology / Q000601:surgery; D017346:Protein Serine-Threonine Kinases / Q000032:analysis / Q000235:genetics; D011509:Proteoglycans / Q000032:analysis / Q000235:genetics; D062326:Re-Epithelialization / Q000502:physiology; D000077294:Receptor, Transforming Growth Factor-beta Type II; D018125:Receptors, Transforming Growth Factor beta / Q000032:analysis / Q000235:genetics; D013997:Time Factors; D014081:Tooth Extraction; D016212:Transforming Growth Factor beta / Q000032:analysis* / Q000235:genetics; D053773:Transforming Growth Factor beta1 / Q000032:analysis / Q000235:genetics; D053781:Transforming Growth Factor beta2 / Q000032:analysis / Q000235:genetics; D053782:Transforming Growth Factor beta3 / Q000032:analysis / Q000235:genetics; D014945:Wound Healing / Q000235:genetics / Q000276:immunology
chemical_list: D001786:Blood Glucose; D053583:Interleukin-1beta; D011509:Proteoglycans; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D053781:Transforming Growth Factor beta2; D053782:Transforming Growth Factor beta3; C071736:betaglycan; D017346:Protein Serine-Threonine Kinases; D000077294:Receptor, Transforming Growth Factor-beta Type II; C576328:MMP8 protein, mouse; D020784:Matrix Metalloproteinase 8