title: The role of smoking and gingival crevicular fluid markers on coronally advanced flap outcomes.
abstract: BACKGROUND
  This study evaluates possible effects of smoking on the following: 1) biochemical content in gingival crevicular fluid (GCF) samples from sites of gingival recession and saliva; and 2) clinical outcomes of coronally advanced flap (CAF) for root coverage.
  
  
  METHODS
  Eighteen defects in 15 patients were included in each of the smoker and non-smoker groups. Baseline cotinine, basic fibroblast growth factor, vascular endothelial growth factor, platelet-derived growth factor, interleukin (IL)-8, IL-10, IL-12, tumor necrosis factor-α, matrix metalloproteinase (MMP)-8, MMP-9, and plasminogen activator inhibitor-1 levels were determined in GCF and saliva samples. CAF with microsurgery technique was applied. Plaque index, papilla bleeding index, recession depth (RD), recession width (RW), and root surface area were evaluated at baseline and postoperative months 1, 3, and 6. Probing depth, clinical attachment level (CAL), and keratinized gingival width (KGW) was recorded at baseline and month 6. Percentage of root coverage and complete root coverage were calculated at postoperative months 1, 3, and 6.
  
  
  RESULTS
  All biochemical parameters were similar in the two groups apart from the definite difference in salivary cotinine concentrations (P = 0.000). Compared with the baseline values, RD, RW, CAL, and root surface area decreased, and KGW increased, with no significant difference between the study groups. CAL gain, percentage of root coverage, and complete root-coverage rates were similar in the study groups.
  
  
  CONCLUSIONS
  Similar baseline biochemical data and comparably high success rates of root coverage with CAF in systemically and periodontally healthy smokers versus non-smokers suggest lack of adverse effects of smoking on clinical outcomes.
authors.affiliation: Department of Periodontology, School of Dentistry, Ege University, İzmir, Turkey.
authors.forename: Başak
authors.initials: B
authors.lastname: Kaval
authors.forename: Diane E
authors.initials: DE
authors.lastname: Renaud
authors.forename: David A
authors.initials: DA
authors.lastname: Scott
authors.forename: Nurcan
authors.initials: N
authors.lastname: Buduneli
mesh_terms: D000293:Adolescent; D000328:Adult; D003367:Cotinine / Q000032:analysis; D003774:Dental Plaque Index; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000032:analysis; D005500:Follow-Up Studies; D005883:Gingival Crevicular Fluid / Q000737:chemistry*; D005889:Gingival Recession / Q000145:classification / Q000601:surgery*; D006801:Humans; D016753:Interleukin-10 / Q000032:analysis; D018664:Interleukin-12 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis; D008297:Male; D020784:Matrix Metalloproteinase 8 / Q000032:analysis; D020780:Matrix Metalloproteinase 9 / Q000032:analysis; D008875:Middle Aged; D010512:Periodontal Index; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D010982:Platelet-Derived Growth Factor / Q000032:analysis; D011446:Prospective Studies; D012463:Saliva / Q000737:chemistry; D012907:Smoking; D013524:Surgical Flaps / Q000601:surgery*; D014092:Tooth Root / Q000473:pathology / Q000601:surgery; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis; D055815:Young Adult
chemical_list: C508606:CXCL8 protein, human; C508609:IL10 protein, human; D016209:Interleukin-8; D017395:Plasminogen Activator Inhibitor 1; D010982:Platelet-Derived Growth Factor; C051321:SERPINE1 protein, human; D014409:Tumor Necrosis Factor-alpha; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D016222:Fibroblast Growth Factor 2; D016753:Interleukin-10; D018664:Interleukin-12; C488762:MMP8 protein, human; D020784:Matrix Metalloproteinase 8; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9; D003367:Cotinine