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dc.contributor.authorChapurlat, Roland
dc.contributor.authorGensburger, Deborah
dc.contributor.authorJimenez-Andrade, Juan
dc.contributor.authorGhilardi, Joseph
dc.contributor.authorKelly, Marilyn
dc.contributor.authorMantyh, Patrick
dc.date.accessioned2016-05-20T09:01:36Z
dc.date.available2016-05-20T09:01:36Z
dc.date.issued2012en
dc.identifier.citationChapurlat et al. Orphanet Journal of Rare Diseases 2012, 7(Suppl 1):S3 http://www.ojrd.com/content/7/S1/S3en
dc.identifier.doi10.1186/1750-1172-7-S1-S3en
dc.identifier.urihttp://hdl.handle.net/10150/610228
dc.description.abstractOne of the most common complications of fibrous dysplasia of bone (FD) is bone pain. Usual pain killers are often of inadequate efficacy to control this bone pain. The mechanism of bone pain in FD remains uncertain, but by analogy with bone tumors one may consider that ectopic sprouting and formation of neuroma-like structures by sensory and sympathetic nerve fibers also occur in the dysplastic skeleton. Bone pain has been reported in up to 81% of adults and 49% of children. It affects predominantly the lower limbs and the spine. The degree of pain is highly variable and adults reports more pain than children. Bisphosphonates have been shown to reduce bone pain in uncontrolled studies. Their influence on bone strength remains unknown. In a randomized trial testing alendronate, bone pain was not significantly improved. Another trial assessing the effect of risedronate is ongoing. Possible future therapies include tocilizumab, denosumab and drugs targeting nerve growth factor and its receptor TrkA.
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.ojrd.com/content/7/S1/S3en
dc.rights© 2012 Chapurlat et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).en
dc.rights.urihttps://creativecommons.org/licenses/by/2.0/
dc.titlePathophysiology and medical treatment of pain in fibrous dysplasia of boneen
dc.typeArticleen
dc.identifier.eissn1750-1172en
dc.contributor.departmentINSERM UMR 1033, Université de Lyon, Hospices Civils de Lyon, Hôpital E Herriot, 69437 Lyon, Franceen
dc.contributor.departmentNational Reference Center for Fibrous Dysplasia of Bone, Hôpital E Herriot, 69437 Lyon, Franceen
dc.contributor.departmentDepartment of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ 85724, USAen
dc.contributor.departmentResearch Service, VA Medical Center, Minneapolis, MN 55417, USAen
dc.contributor.departmentSkeletal Clinical Studies Unit, Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USAen
dc.contributor.departmentArizona Cancer Center, University of Arizona, Tucson, AZ 85724, USAen
dc.identifier.journalOrphanet Journal of Rare Diseasesen
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
refterms.dateFOA2018-06-12T12:51:56Z
html.description.abstractOne of the most common complications of fibrous dysplasia of bone (FD) is bone pain. Usual pain killers are often of inadequate efficacy to control this bone pain. The mechanism of bone pain in FD remains uncertain, but by analogy with bone tumors one may consider that ectopic sprouting and formation of neuroma-like structures by sensory and sympathetic nerve fibers also occur in the dysplastic skeleton. Bone pain has been reported in up to 81% of adults and 49% of children. It affects predominantly the lower limbs and the spine. The degree of pain is highly variable and adults reports more pain than children. Bisphosphonates have been shown to reduce bone pain in uncontrolled studies. Their influence on bone strength remains unknown. In a randomized trial testing alendronate, bone pain was not significantly improved. Another trial assessing the effect of risedronate is ongoing. Possible future therapies include tocilizumab, denosumab and drugs targeting nerve growth factor and its receptor TrkA.


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© 2012 Chapurlat et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).
Except where otherwise noted, this item's license is described as © 2012 Chapurlat et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0).