title: Calcitonin substitution in calcitonin deficiency reduces particle-induced osteolysis.
abstract: BACKGROUND
  Periprosthetic osteolysis is a major cause of aseptic loosening in joint arthroplasty. This study investigates the impact of CT (calcitonin) deficiency and CT substitution under in-vivo circumstances on particle-induced osteolysis in Calca -/- mice.
  
  
  METHODS
  We used the murine calvarial osteolysis model based on ultra-high molecular weight polyethylene (UHMWPE) particles in 10 C57BL/6J wild-type (WT) mice and twenty Calca -/- mice. The mice were divided into six groups: WT without UHMWPE particles (Group 1), WT with UHMWPE particles (Group 2), Calca -/- mice without UHMWPE particles (Group 3), Calca -/- mice with UHMWPE particles (Group 4), Calca -/- mice without UHMWPE particles and calcitonin substitution (Group 5), and Calca -/- mice with UHMWPE particle implantation and calcitonin substitution (Group 6). Analytes were extracted from serum and urine. Bone resorption was measured by bone histomorphometry. The number of osteoclasts was determined by counting the tartrate-resistant acid phosphatase (TRACP) + cells.
  
  
  RESULTS
  Bone resorption was significantly increased in Calca -/- mice compared with their corresponding WT. The eroded surface in Calca -/- mice with particle implantation was reduced by 20.6% after CT substitution. Osteoclast numbers were significantly increased in Calca -/- mice after particle implantation. Serum OPG (osteoprotegerin) increased significantly after CT substitution.
  
  
  CONCLUSIONS
  As anticipated, Calca -/- mice show extensive osteolysis compared with wild-type mice, and CT substitution reduces particle-induced osteolysis.
authors.affiliation: Department of Trauma Surgery, University Duisburg-Essen, Hufelandstr. 55, 45147 Essen, Germany. maxdaniel.kauther@uk-essen.de
authors.forename: Max D
authors.initials: MD
authors.lastname: Kauther
authors.forename: Hagen S
authors.initials: HS
authors.lastname: Bachmann
authors.forename: Laura
authors.initials: L
authors.lastname: Neuerburg
authors.forename: Martina
authors.initials: M
authors.lastname: Broecker-Preuss
authors.forename: Gero
authors.initials: G
authors.lastname: Hilken
authors.forename: Florian
authors.initials: F
authors.lastname: Grabellus
authors.forename: Gabriele
authors.initials: G
authors.lastname: Koehler
authors.forename: Marius
authors.initials: M
authors.lastname: von Knoch
authors.forename: Christian
authors.initials: C
authors.lastname: Wedemeyer
mesh_terms: D000818:Animals; D050071:Bone Density Conservation Agents / Q000494:pharmacology*; D001862:Bone Resorption / Q000188:drug therapy / Q000517:prevention & control; D002116:Calcitonin / Q000172:deficiency* / Q000235:genetics / Q000502:physiology; D002452:Cell Count; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008863:Microspheres; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism; D010014:Osteolysis / Q000188:drug therapy* / Q000473:pathology / Q000517:prevention & control; D053244:Osteoprotegerin / Q000097:blood; D020959:Polyethylene / Q000633:toxicity; D011475:Prosthesis Failure / Q000009:adverse effects*; D012886:Skull / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016896:Treatment Outcome
chemical_list: D050071:Bone Density Conservation Agents; D053244:Osteoprotegerin; D020959:Polyethylene; D002116:Calcitonin