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Article: Experimental gingivitis in type 1 diabetics: A controlled clinical and microbiological study

TitleExperimental gingivitis in type 1 diabetics: A controlled clinical and microbiological study
Authors
Issue Date2005
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CPE
Citation
Journal Of Clinical Periodontology, 2005, v. 32 n. 3, p. 310-316 How to Cite?
AbstractObjective: To monitor clinical and microbiological changes during experimental gingivitis in type 1 diabetics and non-diabetics. Materials and Methods: Nine type 1 diabetics with good/moderate metabolic control and nine age-gender matched non-diabetics were recruited. Probing pocket depths in all subjects did not exceed 4 mm and none were affected by attachment loss. According to the original model, an experimental 3-week plaque accumulation resulting in experimental gingivitis development and a subsequent 2-week period of optimal plaque control were staged. Subgingival plaque samples were collected at days 0, 21 and 35 from one site per quadrant, pooled and analysed using checkerboard DNA-DNA hybridization. Results: Diabetics (mean age 25.6 ± 5.8 standard deviation (SD), range 16-35 years) had a mean HbA1c level of 8.1 ± 0.7% (SD), while non-diabetics (mean age 24.8 ± 5.7 (SD), range 15-36 years) were metabolically controlled (HbA1c ≤6.5%). Between Days 0, 21 and 35, no statistically significant differences in mean plaque and gingival index scores were observed between diabetics and non-diabetics. At days 7 and 21, however, diabetics showed statistically significantly higher percentages of sites with gingival index scores ≥2 compared with non-diabetics. Mean DNA probe counts of the red and orange complex species increased significantly (p < 0.05) between days 0 and 21 and decreased significantly (p < 0.05) between days 21 and 35 in both groups. Conclusion: Both diabetics and non-diabetics react to experimental plaque accumulation with gingival inflammation. Type 1 diabetics, however, develop an earlier and higher inflammatory response to a comparable bacterial challenge. Copyright © Blackwell Munksgaard 2005.
Persistent Identifierhttp://hdl.handle.net/10722/154305
ISSN
2015 Impact Factor: 3.915
2015 SCImago Journal Rankings: 1.848
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSalvi, GEen_US
dc.contributor.authorKandylaki, Men_US
dc.contributor.authorTroendle, Aen_US
dc.contributor.authorPersson, GRen_US
dc.contributor.authorLang, NPen_US
dc.date.accessioned2012-08-08T08:24:31Z-
dc.date.available2012-08-08T08:24:31Z-
dc.date.issued2005en_US
dc.identifier.citationJournal Of Clinical Periodontology, 2005, v. 32 n. 3, p. 310-316en_US
dc.identifier.issn0303-6979en_US
dc.identifier.urihttp://hdl.handle.net/10722/154305-
dc.description.abstractObjective: To monitor clinical and microbiological changes during experimental gingivitis in type 1 diabetics and non-diabetics. Materials and Methods: Nine type 1 diabetics with good/moderate metabolic control and nine age-gender matched non-diabetics were recruited. Probing pocket depths in all subjects did not exceed 4 mm and none were affected by attachment loss. According to the original model, an experimental 3-week plaque accumulation resulting in experimental gingivitis development and a subsequent 2-week period of optimal plaque control were staged. Subgingival plaque samples were collected at days 0, 21 and 35 from one site per quadrant, pooled and analysed using checkerboard DNA-DNA hybridization. Results: Diabetics (mean age 25.6 ± 5.8 standard deviation (SD), range 16-35 years) had a mean HbA1c level of 8.1 ± 0.7% (SD), while non-diabetics (mean age 24.8 ± 5.7 (SD), range 15-36 years) were metabolically controlled (HbA1c ≤6.5%). Between Days 0, 21 and 35, no statistically significant differences in mean plaque and gingival index scores were observed between diabetics and non-diabetics. At days 7 and 21, however, diabetics showed statistically significantly higher percentages of sites with gingival index scores ≥2 compared with non-diabetics. Mean DNA probe counts of the red and orange complex species increased significantly (p < 0.05) between days 0 and 21 and decreased significantly (p < 0.05) between days 21 and 35 in both groups. Conclusion: Both diabetics and non-diabetics react to experimental plaque accumulation with gingival inflammation. Type 1 diabetics, however, develop an earlier and higher inflammatory response to a comparable bacterial challenge. Copyright © Blackwell Munksgaard 2005.en_US
dc.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CPEen_US
dc.relation.ispartofJournal of Clinical Periodontologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshBacteria - Classification - Growth & Developmenten_US
dc.subject.meshCase-Control Studiesen_US
dc.subject.meshColony Count, Microbialen_US
dc.subject.meshDental Plaque - Complications - Microbiologyen_US
dc.subject.meshDiabetes Mellitus, Type 1 - Blood - Complicationsen_US
dc.subject.meshFemaleen_US
dc.subject.meshFollow-Up Studiesen_US
dc.subject.meshGingival Pocket - Complicationsen_US
dc.subject.meshGingivitis - Etiologyen_US
dc.subject.meshHemoglobin A, Glycosylated - Analysisen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshNucleic Acid Hybridizationen_US
dc.subject.meshPeriodontal Indexen_US
dc.titleExperimental gingivitis in type 1 diabetics: A controlled clinical and microbiological studyen_US
dc.typeArticleen_US
dc.identifier.emailLang, NP:nplang@hkucc.hku.hken_US
dc.identifier.authorityLang, NP=rp00031en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1600-051X.2005.00682.xen_US
dc.identifier.pmid15766376-
dc.identifier.scopuseid_2-s2.0-16244382322en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-16244382322&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume32en_US
dc.identifier.issue3en_US
dc.identifier.spage310en_US
dc.identifier.epage316en_US
dc.identifier.isiWOS:000227534000015-
dc.publisher.placeDenmarken_US
dc.identifier.scopusauthoridSalvi, GE=35600695300en_US
dc.identifier.scopusauthoridKandylaki, M=8262053200en_US
dc.identifier.scopusauthoridTroendle, A=8262053300en_US
dc.identifier.scopusauthoridPersson, GR=7101853867en_US
dc.identifier.scopusauthoridLang, NP=7201577367en_US
dc.identifier.citeulike120875-

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