dc.creatorSaldanha, JB
dc.creatorPimentel, SP
dc.creatorCasati, MZ
dc.creatorSallum, EA
dc.creatorBarbieri, D
dc.creatorMoreno, H
dc.creatorNociti, FH
dc.date2004
dc.dateAPR
dc.date2014-11-13T13:58:28Z
dc.date2015-11-26T18:07:49Z
dc.date2014-11-13T13:58:28Z
dc.date2015-11-26T18:07:49Z
dc.date.accessioned2018-03-29T00:49:56Z
dc.date.available2018-03-29T00:49:56Z
dc.identifierJournal Of Periodontology. Amer Acad Periodontology, v. 75, n. 4, n. 565, n. 571, 2004.
dc.identifier0022-3492
dc.identifierWOS:000221157400011
dc.identifier10.1902/jop.2004.75.4.565
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/68538
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/68538
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/68538
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1293676
dc.descriptionBackground: A series of animal and in vitro data confirms that nicotine impairs bone healing, diminishes osteoblast function, and causes autogenous bone graft morbidity. Therefore, this study aimed to investigate the impact of nicotine on the healing of bone defects treated by the guided bone regeneration (GBR) principle. Methods: Sixteen mongrel dogs were used. One defect was surgically created bilaterally and randomly assigned as an expanded polytetrafluoroethylene (ePTFE) membrane site or a non-membrane control site. The animals were randomly assigned to one of the following groups: group 1, placebo (n = 8) and group 2, subcutaneous administration of nicotine (2 mg/kg) twice daily (n = 8). After 4 months, the animals were sacrificed and the specimens routinely processed for semi-serial decalcified sections. The evaluated parameters were bone height, bone width, bone density, and bone area of newly formed bone. Results: Intergroup analysis (Kruskal-Wallis) showed that membrane-protected defects in the placebo group demonstrated an increased bone area when compared to membrane-protected defects in the nicotine group and non-membrane sites, regardless of nicotine administration (P<0.05). In addition, nicotine administration significantly affected bone density in membrane- and non-membrane-protected sites (P<0.05). Conclusions: Within the limits of the present study, nicotine might affect, but not prevent, bone healing in defects treated by guided bone regeneration. The mechanisms of this effect should be investigated further.
dc.description75
dc.description4
dc.description565
dc.description571
dc.languageen
dc.publisherAmer Acad Periodontology
dc.publisherChicago
dc.publisherEUA
dc.relationJournal Of Periodontology
dc.relationJ. Periodont.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectanimal studies
dc.subjectguided bone regeneration
dc.subjectnicotine/adverse effects
dc.subjectsmoking/adverse effects
dc.subjecttobacco/adverse effects
dc.subjectwound healing
dc.subjectFibroblasts In-vitro
dc.subjectTissue Regeneration
dc.subjectAugmentation
dc.subjectInhalation
dc.subjectImplants
dc.subjectDefects
dc.subjectSmoking
dc.subjectGraft
dc.subjectCells
dc.titleGuided bone regeneration may be negatively influenced by nicotine administration: A histologic study in dogs
dc.typeArtículos de revistas


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