Associations between peri-implant crevicular fluid volume, concentrations of crevicular inflammatory mediators, and composite IL-1A -889 and IL-1B +3954 genotype. A cross-sectional study on implant recall patients with and without clinical signs of peri-implantitis.
OBJECTIVE
To assess possible relationships between peri-implant crevicular fluid (PICF) volumes, biochemical markers of the peri-implant immune response, and periodontitis-associated genotype.


METHODS
PICF samples from 29 implant maintenance patients, 24 wearing overdentures, five having single crowns and bridgework (11 patients with peri-implantitis and 18 individuals with healthy peri-implant conditions), were analyzed for per site and per crevicular-fluid-volume concentrations of interleukin-1beta, plasminogen activator inhibitor type 2, and prostaglandin E2 by ELISA. Associations between the three substance concentrations and to crevicular fluid flow rate were analyzed by linear regression analysis. The possible differentiating influence of the composite interleukin-1A and -1B genotype on the patients' peri-implant health and biochemical inflammatory status was checked formally with t-test statistics and the Wilcoxon' test. One implant per patient was chosen for analysis.


RESULTS
In patients with healthy peri-implant conditions, genotype-positive individuals showed elevated crevicular fluid flow rates and at the same time reduced mediator concentrations. In patients with an implant affected from peri-implantitis, no statistically significant influence of the periodontitis-associated genotype around the fixture can be stated. There was no statistical difference between per site and per crevicular-fluid-volume concentration analyses. All three mediator concentrations were positively related to each other, while there was a strong negative correlation between crevicular fluid volume and plasminogen activator inhibitor 2 or prostaglandin E2.


CONCLUSIONS
The Interleukin-1 polymorphism investigated exerted only little influence on the peri-implant crevicular immune response, and this influence appeared to be of limited impact in sites with established peri-implantitis lesions.
Lachmann
Stefan
S
Department of Prosthodontics, University of Tübingen, Tübingen, Germany. stefan.lachmann@med.uni-tuebingen.de
Kimmerle-Müller
Evi
E
Axmann
Detlef
D
Scheideler
Lutz
L
Weber
Heiner
H
Haas
Robert
R
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000032:analysis; D003430:Cross-Sectional Studies; D015921:Dental Implants; D015232:Dinoprostone / Q000032:analysis; D005260:Female; D005838:Genotype; D005883:Gingival Crevicular Fluid / Q000737:chemistry* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D053582:Interleukin-1alpha / Q000032:analysis* / Q000235:genetics; D053583:Interleukin-1beta / Q000032:analysis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000276:immunology*; D017396:Plasminogen Activator Inhibitor 2 / Q000032:analysis; D012636:Secretory Rate / Q000502:physiology
D015415:Biomarkers; D015921:Dental Implants; D018836:Inflammation Mediators; D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D017396:Plasminogen Activator Inhibitor 2; D015232:Dinoprostone