title: Prostaglandin levels of primary bone tumor tissues correlate with peritumoral edema demonstrated by magnetic resonance imaging.
abstract: BACKGROUND
  Several reports have shown peritumoral edema accompanying primary bone tumors demonstrated by magnetic resonance imaging (MRI). However, the mechanism of this inflammatory reaction is still unclear. The authors postulated that the reaction was caused by some chemical mediators including prostanoids, because several investigators have observed that some types of bone tumors synthesize prostanoids. Therefore, the authors compared MRI findings and tumor prostaglandin (PG) levels.
  
  
  METHODS
  The subjects were 29 patients with primary bone tumor or tumor-like conditions: chondroblastoma (n = 5); chondrosarcoma, including rare variants (n = 8); giant cell tumor (n = 6); osteochondroma (n = 5); osteoblastoma (n = 2); Ewing's sarcoma (n = 2); and eosinophilic granuloma (n = 1). T1- and T2-weighted spin echo images were obtained in all but one patient before surgery. The tumor concentration of prostaglandin E2, 6-keto-PGF1 alpha, and thromboxane B2 were measured by radioimmunoassay.
  
  
  RESULTS
  MRI distinctly showed bone marrow edema in 9 and soft tissue edema in 12 of the 28 patients examined. These findings were significantly correlated with the PG levels. Moreover, the PG levels were correlated with the histologic classifications (P < 0.001). In particular, the chondroblastomas showed prominent concentrations of PGs compared with other cartilaginous tumors or giant cell tumors.
  
  
  CONCLUSIONS
  Although peritumoral edema accompanying benign and malignant bone tumors is not necessarily related to one single pathophysiologic mechanism, these results suggest that PG production was an important cause of the inflammatory reaction that was revealed by MRI. Recognition of this phenomenon is advantageous not only for strict diagnostic purposes but also for understanding the characteristic features of individual primary bone tumors.
authors.affiliation: Department of Orthopaedic Surgery, Nagoya University School of Medicine, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Yamamura
authors.forename: K
authors.initials: K
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Sugiura
authors.forename: H
authors.initials: H
authors.lastname: Katagiri
authors.forename: Y
authors.initials: Y
authors.lastname: Ando
authors.forename: H
authors.initials: H
authors.lastname: Fukatsu
authors.forename: H
authors.initials: H
authors.lastname: Iwata
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis*; D001859:Bone Neoplasms / Q000737:chemistry* / Q000150:complications; D002804:Chondroblastoma / Q000737:chemistry / Q000150:complications; D015232:Dinoprostone / Q000032:analysis*; D004487:Edema / Q000150:complications / Q000175:diagnosis*; D004803:Eosinophilic Granuloma / Q000150:complications; D006801:Humans; D008279:Magnetic Resonance Imaging; D009363:Neoplasm Proteins / Q000032:analysis*; D018215:Osteoblastoma / Q000737:chemistry / Q000150:complications; D012516:Osteosarcoma / Q000737:chemistry / Q000150:complications; D013929:Thromboxane B2 / Q000032:analysis*
chemical_list: D009363:Neoplasm Proteins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D015232:Dinoprostone