title: Osteoprotegerin reduces the loss of periarticular bone mass in primary and secondary spongiosa but does not influence inflammation in rat antigen-induced arthritis.
abstract: OBJECTIVE
  To assess the effect of osteoprotegerin (OPG) on joint swelling, synovial inflammation and cartilage destruction, periarticular and axial bone volume, and bone turnover in rat antigen-induced arthritis (AIA).
  
  
  METHODS
  Rats were treated with OPG (3 mg/kg/day) at regular intervals from day 1 to day 20 of AIA. Disease activity was evaluated by measurement of joint swelling as well as, joint inflammation and destruction by histology. Bone volume and cellular turnover parameters of secondary spongiosa of the right tibia head and the third lumbar vertebra were evaluated by histomorphometry. Periarticular bone volume of the primary spongiosa at the right tibia head was measured by linear scanning. The findings were compared with those of PBS-treated AIA and healthy animals.
  
  
  RESULTS
  OPG treatment did not reduce joint swelling or histological signs of inflammation. Cartilage destruction was reduced. However, this effect did not reach statistical significance . In the secondary spongiosa OPG treatment reduced the loss of periarticular bone volume. However, the latter did not reach the level of healthy controls. OPG treatment significantly reduced parameters of bone formation and bone resorption. In the primary spongiosa, OPG-treatment led to a higher amount of mineralized tissue and a greater number of trabeculae compared to PBS-treated animals with AIA or healthy controls. In the axial skeleton, OPG treatment reduced bone formation and bone resorption parameters compared to healthy animals. This treatment had no influence on bone volume.
  
  
  CONCLUSIONS
  In periarticular bone of AIA rats, OPG treatment reduced the loss of bone volume and decreased the bone turnover, thus preventing periarticular bone destruction. OPG treatment had no influence on inflammatory process or on cartilage destruction.
authors.affiliation: Department of Internal Medicine III, Friedrich Schiller University of Jena, Division of Rheumatology/Osteology, Erlanger Allee 101, 07740 Jena, Germany. thomas.neumann@med.uni-jena.de
authors.forename: T
authors.initials: T
authors.lastname: Neumann
authors.forename: P
authors.initials: P
authors.lastname: Oelzner
authors.forename: P K
authors.initials: PK
authors.lastname: Petrow
authors.forename: K
authors.initials: K
authors.lastname: Thoss
authors.forename: G
authors.initials: G
authors.lastname: Hein
authors.forename: G
authors.initials: G
authors.lastname: Stein
authors.forename: R
authors.initials: R
authors.lastname: Bräuer
mesh_terms: D000818:Animals; D000941:Antigens / Q000737:chemistry*; D001169:Arthritis, Experimental / Q000473:pathology*; D001847:Bone Diseases / Q000378:metabolism* / Q000628:therapy*; D001842:Bone and Bones / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D007249:Inflammation; D007719:Knee Joint / Q000473:pathology; D053244:Osteoprotegerin / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D011917:Rats, Inbred Lew; D013997:Time Factors
chemical_list: D000941:Antigens; D053244:Osteoprotegerin