Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/5646
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dc.contributor.authorHaynes, D.en
dc.contributor.authorCrotti, T.en
dc.date.issued2003en
dc.identifier.citationInflammopharmacology, 2003; 11(4-6):323-331en
dc.identifier.issn0925-4692en
dc.identifier.issn1568-5608en
dc.identifier.urihttp://hdl.handle.net/2440/5646-
dc.description© 2007 Ingenta.en
dc.description.abstractFocal bone erosion is a major pathological feature of several common inflammatory diseases. Over the past decade there have been major advances in our understanding of the factors that regulate osteoclast formation and activity. It is now apparent that receptor activator for NFB (RANK), its ligand RANKL (also known as TRANCE, osteoclast differentiation factor and osteoprotegerin (OPG) ligand) and the RANKL inhibitor OPG, are the major factors regulating osteoclast formation. These molecules influence normal bone physiology and now there is growing evidence that RANK-RANKL interactions also regulate osteoclast formation in disease. This paper reviews recent findings showing expression of RANK, RANKL and OPG in inflammatory diseases including rheumatoid arthritis, periodontal disease and peri-implant loosening. It is emerging that OPG and RANKL are key molecules regulating bone loss in disease and therapeutic intervention that targets these molecules may be helpful in treating a wide range of diseasesen
dc.language.isoenen
dc.publisherV S Pen
dc.subjectosteoclast; rankl; opg; inflammation; bone lysisen
dc.titleRegulation of bone lysis in inflammatory diseasesen
dc.typeJournal articleen
dc.identifier.rmid0020031644en
dc.identifier.doi10.1163/156856003322699500en
dc.identifier.pubid58059-
pubs.library.collectionPathology publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidCrotti, T. [0000-0002-5422-3758]en
Appears in Collections:Pathology publications

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