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Article: Antimicrobial therapy using a local drug delivery system (Arestin®) in the treatment of peri-implantitis. I: Microbiological outcomes

TitleAntimicrobial therapy using a local drug delivery system (Arestin®) in the treatment of peri-implantitis. I: Microbiological outcomes
Authors
Issue Date2006
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CLR
Citation
Clinical Oral Implants Research, 2006, v. 17 n. 4, p. 386-393 How to Cite?
AbstractObjectives: To assess the microbiological outcome of local administration of minocycline hydrochloride microspheres 1 mg (Arestin®) in cases with peri-implantitis and with a follow-up period of 12 months. Material and methods: After debridement, and local administration of chlorhexidine gel, peri-implantitis cases were treated with local administration of minocycline microspheres (Arestin®). The DNA-DNA checkerboard hybridization method was used to detect bacterial presence during the first 360 days of therapy. Results: At Day 10, lower bacterial loads for 6/40 individual bacteria including Actinomyces gerensceriae (P<0.1), Actinomyces israelii (P<0.01), Actinomyces naeslundi type 1 (P<0.01) and type 2 (P<0.03), Actinomyces odontolyticus (P<0.01), Porphyromonas gingivalis (P<0.01) and Treponema socranskii (P<0.01) were found. At Day 360 only the levels of Actinobacillus actinomycetemcomitans were lower than at baseline (mean difference: 1 × 10 5; SE difference: 0.34 × 10 5, 95% CI: 0.2 × 10 5 to 1.2 × 10 5; P<0.03). Six implants were lost between Days 90 and 270. The microbiota was successfully controlled in 48%, and with definitive failures (implant loss and major increase in bacterial levels) in 32% of subjects. Conclusions: At study endpoint, the impact of Arestin® on A. actinomycetemcomitans was greater than the impact on other pathogens. Up to Day 180 reductions in levels of Tannerella forsythia, P. gingivalis, and Treponema denticola were also found. Failures in treatment could not be associated with the presence of specific pathogens or by the total bacterial load at baseline. Statistical power analysis suggested that a case control study would require approximately 200 subjects. Copyright © Blackwell Munksgaard 2006.
Persistent Identifierhttp://hdl.handle.net/10722/154415
ISSN
2015 Impact Factor: 3.464
2015 SCImago Journal Rankings: 1.427
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPersson, GRen_US
dc.contributor.authorSalvi, GEen_US
dc.contributor.authorHeitzMayfield, LJAen_US
dc.contributor.authorLang, NPen_US
dc.date.accessioned2012-08-08T08:25:11Z-
dc.date.available2012-08-08T08:25:11Z-
dc.date.issued2006en_US
dc.identifier.citationClinical Oral Implants Research, 2006, v. 17 n. 4, p. 386-393en_US
dc.identifier.issn0905-7161en_US
dc.identifier.urihttp://hdl.handle.net/10722/154415-
dc.description.abstractObjectives: To assess the microbiological outcome of local administration of minocycline hydrochloride microspheres 1 mg (Arestin®) in cases with peri-implantitis and with a follow-up period of 12 months. Material and methods: After debridement, and local administration of chlorhexidine gel, peri-implantitis cases were treated with local administration of minocycline microspheres (Arestin®). The DNA-DNA checkerboard hybridization method was used to detect bacterial presence during the first 360 days of therapy. Results: At Day 10, lower bacterial loads for 6/40 individual bacteria including Actinomyces gerensceriae (P<0.1), Actinomyces israelii (P<0.01), Actinomyces naeslundi type 1 (P<0.01) and type 2 (P<0.03), Actinomyces odontolyticus (P<0.01), Porphyromonas gingivalis (P<0.01) and Treponema socranskii (P<0.01) were found. At Day 360 only the levels of Actinobacillus actinomycetemcomitans were lower than at baseline (mean difference: 1 × 10 5; SE difference: 0.34 × 10 5, 95% CI: 0.2 × 10 5 to 1.2 × 10 5; P<0.03). Six implants were lost between Days 90 and 270. The microbiota was successfully controlled in 48%, and with definitive failures (implant loss and major increase in bacterial levels) in 32% of subjects. Conclusions: At study endpoint, the impact of Arestin® on A. actinomycetemcomitans was greater than the impact on other pathogens. Up to Day 180 reductions in levels of Tannerella forsythia, P. gingivalis, and Treponema denticola were also found. Failures in treatment could not be associated with the presence of specific pathogens or by the total bacterial load at baseline. Statistical power analysis suggested that a case control study would require approximately 200 subjects. Copyright © Blackwell Munksgaard 2006.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CLRen_US
dc.relation.ispartofClinical Oral Implants Researchen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAnti-Bacterial Agents - Chemistryen_US
dc.subject.meshDna Probes - Analysisen_US
dc.subject.meshDna, Bacterial - Analysis - Drug Effectsen_US
dc.subject.meshDental Implantsen_US
dc.subject.meshDental Restoration Failureen_US
dc.subject.meshDrug Delivery Systems - Methodsen_US
dc.subject.meshEpidemiologic Methodsen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMinocycline - Chemistryen_US
dc.subject.meshPeriodontitis - Drug Therapy - Microbiologyen_US
dc.subject.meshTreatment Outcomeen_US
dc.titleAntimicrobial therapy using a local drug delivery system (Arestin®) in the treatment of peri-implantitis. I: Microbiological outcomesen_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.1600-0501.2006.01269.xen_US
dc.identifier.pmid16907769-
dc.identifier.scopuseid_2-s2.0-33746362551en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33746362551&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume17en_US
dc.identifier.issue4en_US
dc.identifier.spage386en_US
dc.identifier.epage393en_US
dc.identifier.isiWOS:000239187900006-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPersson, GR=7101853867en_US
dc.identifier.scopusauthoridSalvi, GE=35600695300en_US
dc.identifier.scopusauthoridHeitzMayfield, LJA=6602309146en_US
dc.identifier.scopusauthoridLang, NP=7201577367en_US
dc.identifier.citeulike774026-

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