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Article: The significance of bone in periodontal disease.

TitleThe significance of bone in periodontal disease.
Authors
Issue Date1996
PublisherWB Saunders Co. The Journal's web site is located at http://www.journals.elsevierhealth.com/periodicals/ysodo
Citation
Seminars In Orthodontics, 1996, v. 2 n. 1, p. 31-38 How to Cite?
AbstractAlthough the connective tissue attachment represents the key issue in periodontal health or disease and in periodontal therapy, the assessment of alveolar bone changes renders valuable indirect evidence for periodontal stability, progression of disease, or repair mechanisms. In periodontal disease bacterial products trigger host cells to release mediators, which may imbalance the steady state between resorption of bone and apposition of osteoid. Modulation of the hosts prostaglandin or interleukin-I synthesis by drug therapy could support the antimicrobial concept of periodontal therapy. Cross-sectional and long-term assessments of alveolar bone have been used to estimate the progression rate of periodontal disease. Inherent limitations of bone assessments in radiographs have to be considered when drawing conclusions from measurements that represent remodeling in periodontal lesions after therapy. Both bone quantity and quality seem to be of secondary importance with respect to the progression of disease, as well as response to therapy. Other risk factors that affect the microbial ecology and/or the hosts immune system seem to be the primary determinants for the periodontal health status.
Persistent Identifierhttp://hdl.handle.net/10722/153963
ISSN
2015 Impact Factor: 0.346
2015 SCImago Journal Rankings: 0.252

 

DC FieldValueLanguage
dc.contributor.authorBrägger, Uen_US
dc.contributor.authorLang, NPen_US
dc.date.accessioned2012-08-08T08:22:31Z-
dc.date.available2012-08-08T08:22:31Z-
dc.date.issued1996en_US
dc.identifier.citationSeminars In Orthodontics, 1996, v. 2 n. 1, p. 31-38en_US
dc.identifier.issn1073-8746en_US
dc.identifier.urihttp://hdl.handle.net/10722/153963-
dc.description.abstractAlthough the connective tissue attachment represents the key issue in periodontal health or disease and in periodontal therapy, the assessment of alveolar bone changes renders valuable indirect evidence for periodontal stability, progression of disease, or repair mechanisms. In periodontal disease bacterial products trigger host cells to release mediators, which may imbalance the steady state between resorption of bone and apposition of osteoid. Modulation of the hosts prostaglandin or interleukin-I synthesis by drug therapy could support the antimicrobial concept of periodontal therapy. Cross-sectional and long-term assessments of alveolar bone have been used to estimate the progression rate of periodontal disease. Inherent limitations of bone assessments in radiographs have to be considered when drawing conclusions from measurements that represent remodeling in periodontal lesions after therapy. Both bone quantity and quality seem to be of secondary importance with respect to the progression of disease, as well as response to therapy. Other risk factors that affect the microbial ecology and/or the hosts immune system seem to be the primary determinants for the periodontal health status.en_US
dc.languageengen_US
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.journals.elsevierhealth.com/periodicals/ysodoen_US
dc.relation.ispartofSeminars in orthodonticsen_US
dc.subject.meshAlveolar Bone Loss - Etiology - Physiopathologyen_US
dc.subject.meshBone Remodelingen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshMaleen_US
dc.subject.meshPeriodontitis - Complications - Immunology - Microbiologyen_US
dc.subject.meshRisk Factorsen_US
dc.titleThe significance of bone in periodontal disease.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.pmid9161281-
dc.identifier.scopuseid_2-s2.0-0030089831en_US
dc.identifier.volume2en_US
dc.identifier.issue1en_US
dc.identifier.spage31en_US
dc.identifier.epage38en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBrägger, U=7005538598en_US
dc.identifier.scopusauthoridLang, NP=7201577367en_US

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