The association between gingival crevicular fluid TGF-beta1 levels and periodontal status in HIV-1(+) patients.
BACKGROUND
The purpose of this study was to investigate the relationship between transforming growth factor-beta 1 (TGF-beta1) in gingival crevicular fluid (GCF) and the periodontal status of subjects who were positive for the human immunodeficiency virus (HIV)-1.


METHODS
Medical and demographic variables, including age, cigarette smoking, CD4 cell count, and viral load values, were recorded. At the baseline and 6-month visits, gingival index (GI), plaque index, bleeding on probing, probing depth (PD), and attachment loss (AL) were recorded, and GCF samples were taken with paper strips from three periodontitis sites (GI >0; PD > or =5 mm; AL > or =3 mm), three gingivitis sites (GI >0; PD < or =3 mm; AL = 0), and two healthy sites (GI = 0; PD < or =3 mm; AL < or =2 mm) in 25 subjects who were HIV-1(+). GCF TGF-beta1 levels were determined by enzyme-linked immunosorbent assays. A statistical software package was used to analyze the data.


RESULTS
The mean amounts of GCF TGF-beta1 were greater in gingivitis and periodontitis sites than in healthy sites (P <0.0001). GCF levels of TGF-beta1 correlated with PD, AL, age, smoking pack-years, CD4 cell count, and viral load at the baseline and 6-month visits (0.0001 < P <0.05). An active site was defined as a site that had > or =2 mm new AL during the 6-month study period. An active patient was defined as a patient who had one or more active site(s) during the study period. Repeated-measures analysis of 18 active sites versus 182 inactive sites indicated that GCF TGF-beta1 levels were higher in active sites than in inactive sites (P <0.0001). Eleven of the 25 study subjects had active sites at the end of the 6-month study period. The mean GCF TGF-beta1 level and the mean AL and PD for these 11 active subjects were higher than for the 14 inactive subjects (P <0.0001).


CONCLUSIONS
In subjects who are HIV-1(+), sites with high GCF levels of TGF-beta1 are at significantly greater risk for the progression of established periodontitis.
Alpagot
T
T
Department of Periodontics, Arthur A Dugoni School of Dentistry, University of the Pacific, San Francisco, CA 94115, USA. talpagot@pacific.edu
Konopka
K
K
Bhattacharyya
M
M
Gebremedhin
S
S
Düzgüneş
N
N
D018791:CD4 Lymphocyte Count; D003774:Dental Plaque Index; D018450:Disease Progression; D005500:Follow-Up Studies; D005881:Gingiva / Q000276:immunology; D005883:Gingival Crevicular Fluid / Q000737:chemistry / Q000276:immunology*; D005884:Gingival Hemorrhage / Q000145:classification / Q000276:immunology; D005891:Gingivitis / Q000145:classification / Q000276:immunology; D006679:HIV Seropositivity / Q000276:immunology* / Q000821:virology; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000145:classification / Q000276:immunology; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000145:classification / Q000276:immunology; D010518:Periodontitis / Q000145:classification / Q000276:immunology; D012307:Risk Factors; D012907:Smoking / Q000276:immunology; D053773:Transforming Growth Factor beta1 / Q000032:analysis*; D019562:Viral Load
D053773:Transforming Growth Factor beta1