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Pathophysiology and medical treatment of pain in fibrous dysplasia of bone.

Abstract
One 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.
AuthorsRoland D Chapurlat, Deborah Gensburger, Juan M Jimenez-Andrade, Joseph R Ghilardi, Marilyn Kelly, Patrick Mantyh
JournalOrphanet journal of rare diseases (Orphanet J Rare Dis) Vol. 7 Suppl 1 Pg. S3 (May 24 2012) ISSN: 1750-1172 [Electronic] England
PMID22640953 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Antibodies, Monoclonal, Humanized
  • tocilizumab
  • Alendronate
Topics
  • Alendronate (pharmacology)
  • Antibodies, Monoclonal, Humanized (pharmacology)
  • Bone Neoplasms (physiopathology)
  • Bone and Bones (innervation, physiopathology)
  • Fibrous Dysplasia of Bone (drug therapy, physiopathology)
  • Humans
  • Nerve Fibers (pathology)
  • Pain (drug therapy, physiopathology)
  • Pain Management (methods)
  • Pain Measurement (methods)
  • Self Report
  • Sensory Receptor Cells (pathology)

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