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Article: Immunohistochemical localization of RANK, RANKL and OPG in healthy and arthritic canine elbow joints

TitleImmunohistochemical localization of RANK, RANKL and OPG in healthy and arthritic canine elbow joints
Authors
Issue Date2009
PublisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journals/VSU
Citation
Veterinary Surgery, 2009, v. 38 n. 6, p. 780-786 How to Cite?
AbstractObjective To determine if the receptor activator of nuclear factor-κB-receptor activator of nuclear factor-κB ligand-osteoprotegerin (RANK-RANKL-OPG) system is active in bone remodeling in dogs and, if so, whether differences in expression of these mediators occur in healthy and arthritic joints. Study Design Experimental study. Sample Population Fragmented processus coronoidei (n=20) were surgically removed from dogs with elbow arthritis and 5 corresponding healthy samples from dogs euthanatized for reasons other than elbow joint disease. Methods Bright-field immunohistochemistry and high-resolution fluorescence microscopy were used to investigate the distribution of RANK, RANKL, and OPG in healthy and arthritic joints. Results All 3 molecules were identified by immunostaining of canine bone tissue. In elbow dysplasia, the number of RANK-positive osteoclasts was increased. In their vicinity, cells expressing RANKL, a mediator of osteoclast activation, were abundant whereas the number of osteoblasts having the potential to limit osteoclastogenesis and bone resorption via OPG was few. Conclusions The RANK-RANKL-OPG system is active in bone remodeling in dogs. In elbow dysplasia, a surplus of molecules promoting osteoclastogenesis was evident and is indicative of an imbalance between the mediators regulating bone resorption and bone formation. Both OPG and neutralizing antibodies against RANKL have the potential to counterbalance bone resorption. Clinical Relevance Therapeutic use of neutralizing antibodies against RANKL to inhibit osteoclast activation warrants further investigation. © 2009 by The American College of Veterinary Surgeons.
Persistent Identifierhttp://hdl.handle.net/10722/154580
ISSN
2015 Impact Factor: 1.295
2015 SCImago Journal Rankings: 0.999
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSpahni, AIen_US
dc.contributor.authorSchawalder, Pen_US
dc.contributor.authorRothen, Ben_US
dc.contributor.authorBosshardt, DDen_US
dc.contributor.authorLang, Nen_US
dc.contributor.authorStoffel, MHen_US
dc.date.accessioned2012-08-08T08:26:17Z-
dc.date.available2012-08-08T08:26:17Z-
dc.date.issued2009en_US
dc.identifier.citationVeterinary Surgery, 2009, v. 38 n. 6, p. 780-786en_US
dc.identifier.issn0161-3499en_US
dc.identifier.urihttp://hdl.handle.net/10722/154580-
dc.description.abstractObjective To determine if the receptor activator of nuclear factor-κB-receptor activator of nuclear factor-κB ligand-osteoprotegerin (RANK-RANKL-OPG) system is active in bone remodeling in dogs and, if so, whether differences in expression of these mediators occur in healthy and arthritic joints. Study Design Experimental study. Sample Population Fragmented processus coronoidei (n=20) were surgically removed from dogs with elbow arthritis and 5 corresponding healthy samples from dogs euthanatized for reasons other than elbow joint disease. Methods Bright-field immunohistochemistry and high-resolution fluorescence microscopy were used to investigate the distribution of RANK, RANKL, and OPG in healthy and arthritic joints. Results All 3 molecules were identified by immunostaining of canine bone tissue. In elbow dysplasia, the number of RANK-positive osteoclasts was increased. In their vicinity, cells expressing RANKL, a mediator of osteoclast activation, were abundant whereas the number of osteoblasts having the potential to limit osteoclastogenesis and bone resorption via OPG was few. Conclusions The RANK-RANKL-OPG system is active in bone remodeling in dogs. In elbow dysplasia, a surplus of molecules promoting osteoclastogenesis was evident and is indicative of an imbalance between the mediators regulating bone resorption and bone formation. Both OPG and neutralizing antibodies against RANKL have the potential to counterbalance bone resorption. Clinical Relevance Therapeutic use of neutralizing antibodies against RANKL to inhibit osteoclast activation warrants further investigation. © 2009 by The American College of Veterinary Surgeons.en_US
dc.languageengen_US
dc.publisherBlackwell Publishing, Inc. The Journal's web site is located at http://www.blackwellpublishing.com/journals/VSUen_US
dc.relation.ispartofVeterinary Surgeryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBone Remodeling - Physiologyen_US
dc.subject.meshBone And Bones - Cytology - Metabolismen_US
dc.subject.meshDog Diseases - Metabolismen_US
dc.subject.meshDogsen_US
dc.subject.meshForelimb - Metabolismen_US
dc.subject.meshMicroscopy, Fluorescenceen_US
dc.subject.meshOsteoarthritis - Metabolism - Veterinaryen_US
dc.subject.meshOsteoprotegerin - Genetics - Metabolismen_US
dc.subject.meshRank Ligand - Genetics - Metabolismen_US
dc.subject.meshReceptor Activator Of Nuclear Factor-Kappa B - Genetics - Metabolismen_US
dc.titleImmunohistochemical localization of RANK, RANKL and OPG in healthy and arthritic canine elbow jointsen_US
dc.typeArticleen_US
dc.identifier.emailLang, N:nplang@hkucc.hku.hken_US
dc.identifier.authorityLang, N=rp00031en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1532-950X.2009.00566.xen_US
dc.identifier.pmid19674422-
dc.identifier.scopuseid_2-s2.0-68749105048en_US
dc.identifier.hkuros169066-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-68749105048&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume38en_US
dc.identifier.issue6en_US
dc.identifier.spage780en_US
dc.identifier.epage786en_US
dc.identifier.isiWOS:000268455700014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridSpahni, AI=40262667400en_US
dc.identifier.scopusauthoridSchawalder, P=40262445700en_US
dc.identifier.scopusauthoridRothen, B=6507626839en_US
dc.identifier.scopusauthoridBosshardt, DD=6603806230en_US
dc.identifier.scopusauthoridLang, N=7201577367en_US
dc.identifier.scopusauthoridStoffel, MH=7102900549en_US
dc.identifier.citeulike5383338-

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