Bone cancer pain and the role of RANKL/OPG

Denis R. Clohisy, P. W. Mantyh

Research output: Contribution to journalReview article

32 Scopus citations

Abstract

Cancer-induced bone diseases are common and can have a devastating impact at the end of life. One of the most difficult sequelae of cancer is metastases to the skeleton, an event that results in bone destruction and bone cancer pain. Bone cancer pain is usually progressive as the disease advances, and is particularly difficult to treat. Recently, experimental models of bone cancer pain have been developed and have provided seminal insight in understanding the pathophysiology of bone cancer pain. Animal models of bone cancer provided the finding that bone destruction (osteolysis) is associated with pain, and it has been determined that cancer-induced osteolysis is mediated by osteoclasts. Having established that RANK ligand contributed to cancer-induced osteoclastogenesis, it was determined that disruption of the RANKL-RANK axis with OPG inhibited tumor-induced osteoclastogenesis and decreased bone cancer pain.

Original languageEnglish (US)
Pages (from-to)293-300
Number of pages8
JournalJournal of Musculoskeletal Neuronal Interactions
Volume4
Issue number3
StatePublished - Sep 1 2004
Externally publishedYes

Keywords

  • Bone cancer
  • Osteolysis
  • Osteoprotegerin
  • Pain

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Orthopedics and Sports Medicine

Fingerprint Dive into the research topics of 'Bone cancer pain and the role of RANKL/OPG'. Together they form a unique fingerprint.

  • Cite this