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Article: Plaque-induced marginal tissue reactions of osseointegrated oral implants: a review of the literature.

TitlePlaque-induced marginal tissue reactions of osseointegrated oral implants: a review of the literature.
Authors
Issue Date1992
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CLR
Citation
Clinical Oral Implants Research, 1992, v. 3 n. 4, p. 149-161 How to Cite?
AbstractAn intimate contact between bone and titanium implants was first demonstrated in 1969, and since then the bone-implant interface of osseointegrated implants has been investigated extensively. However, investigations of the marginal tissues and the microflora associated with osseointegrated implants have almost exclusively been carried out over the last decade. This review covers the clinical, radiographic, histologic, and microbiologic studies of marginal tissues of osseointegrated oral implants. In general, successfully osseointegrated implants exhibit low amounts of plaque concomitant with the absence of marginal inflammation. However, plaque accumulation may cause inflammatory reactions around the implants, sometimes giving rise to mucosal hyperplasia. Apparently, keratinized mucosa is not a requisite for the maintenance of peri-implant health if oral hygiene is adequate, but the presence of peri-implant keratinized mucosa is generally advocated. Alveolar bone loss around successful implants is minimal, but significant focal loss may occur due to plaque-induced inflammation or perhaps repeatedly extensive implant load. The progression of plaque-induced alveolar bone loss of osseointegrated implants may be different from that of teeth. It is unknown whether simultaneous marginal inflammation and excessive implant load further increase the loss of alveolar bone height. Both the light microscopic and ultrastructural characteristics of marginal tissues of implants and teeth are similar except for a lack of root cementum with inserting gingival collagen fibers of implants. Clinical inflammatory reactions are histologically characterized by an increased number of inflammatory cells infiltrating the connective tissue. The scattered subgingival microbiota associated with osseointegrated implants surrounded by healthy or slightly inflamed marginal tissues is similar to that of teeth with healthy gingiva. The microbiota associated with implants affected by marginal inflammation and bone loss is complex and consists predominantly of gram-negative anaerobic rods; this, again, is a similarity to periodontal disease.
Persistent Identifierhttp://hdl.handle.net/10722/153812
ISSN
2015 Impact Factor: 3.464
2015 SCImago Journal Rankings: 1.427

 

DC FieldValueLanguage
dc.contributor.authorSchou, Sen_US
dc.contributor.authorHolmstrup, Pen_US
dc.contributor.authorHjørtingHansen, Een_US
dc.contributor.authorLang, NPen_US
dc.date.accessioned2012-08-08T08:21:43Z-
dc.date.available2012-08-08T08:21:43Z-
dc.date.issued1992en_US
dc.identifier.citationClinical Oral Implants Research, 1992, v. 3 n. 4, p. 149-161en_US
dc.identifier.issn0905-7161en_US
dc.identifier.urihttp://hdl.handle.net/10722/153812-
dc.description.abstractAn intimate contact between bone and titanium implants was first demonstrated in 1969, and since then the bone-implant interface of osseointegrated implants has been investigated extensively. However, investigations of the marginal tissues and the microflora associated with osseointegrated implants have almost exclusively been carried out over the last decade. This review covers the clinical, radiographic, histologic, and microbiologic studies of marginal tissues of osseointegrated oral implants. In general, successfully osseointegrated implants exhibit low amounts of plaque concomitant with the absence of marginal inflammation. However, plaque accumulation may cause inflammatory reactions around the implants, sometimes giving rise to mucosal hyperplasia. Apparently, keratinized mucosa is not a requisite for the maintenance of peri-implant health if oral hygiene is adequate, but the presence of peri-implant keratinized mucosa is generally advocated. Alveolar bone loss around successful implants is minimal, but significant focal loss may occur due to plaque-induced inflammation or perhaps repeatedly extensive implant load. The progression of plaque-induced alveolar bone loss of osseointegrated implants may be different from that of teeth. It is unknown whether simultaneous marginal inflammation and excessive implant load further increase the loss of alveolar bone height. Both the light microscopic and ultrastructural characteristics of marginal tissues of implants and teeth are similar except for a lack of root cementum with inserting gingival collagen fibers of implants. Clinical inflammatory reactions are histologically characterized by an increased number of inflammatory cells infiltrating the connective tissue. The scattered subgingival microbiota associated with osseointegrated implants surrounded by healthy or slightly inflamed marginal tissues is similar to that of teeth with healthy gingiva. The microbiota associated with implants affected by marginal inflammation and bone loss is complex and consists predominantly of gram-negative anaerobic rods; this, again, is a similarity to periodontal disease.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.meshAlveolar Bone Loss - Etiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDental Implants - Adverse Effectsen_US
dc.subject.meshDental Plaque - Complications - Microbiologyen_US
dc.subject.meshGingivitis - Etiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMouth Mucosa - Pathologyen_US
dc.subject.meshPeriodontal Diseases - Etiologyen_US
dc.subject.meshPeriodontitis - Etiologyen_US
dc.subject.meshProsthesis-Related Infectionsen_US
dc.titlePlaque-induced marginal tissue reactions of osseointegrated oral implants: a review of the literature.en_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.pmid1298429-
dc.identifier.scopuseid_2-s2.0-0027035024en_US
dc.identifier.volume3en_US
dc.identifier.issue4en_US
dc.identifier.spage149en_US
dc.identifier.epage161en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSchou, S=7004351351en_US
dc.identifier.scopusauthoridHolmstrup, P=7006745411en_US
dc.identifier.scopusauthoridHjørtingHansen, E=7006669007en_US
dc.identifier.scopusauthoridLang, NP=7201577367en_US

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