title: Trabecular bone loss in collagen antibody-induced arthritis.
abstract: BACKGROUND
  Postmenopausal women with rheumatoid arthritis (RA) have increased risk of developing osteoporosis due to chronic inflammation and estrogen deprivation. Collagen antibody-induced arthritis (CAIA), an experimental polyarthritis model representing the effector phase of arthritis, is mainly mediated by the innate immune system. Compared to the widely used collagen-induced arthritis model, CAIA is conveniently short and can be used in C57BL/6 mice, enabling studies with knock-out mice. However, the impact on bone of the CAIA model in C57BL/6 mice has not previously been studied. Therefore, the aim of this study was to determine if CAIA can be used to study postmenopausal arthritis-induced osteoporosis.
  
  
  METHODS
  CAIA was induced by administration of collagen-type II antibodies and lipopolysaccharide to ovariectomized female C57BL/6J mice. Control mice received lipopolysaccharide, but no antibodies. Nine days later, femurs were collected for high-resolution micro-CT and histomorphometry. Serum was used to assess cartilage breakdown and levels of complement. Frequencies of immune cell subsets from bone marrow and lymph nodes were analyzed by flow cytometery.
  
  
  RESULTS
  Trabecular bone mass was decreased and associated with increased number of osteoclasts per bone surface in the CAIA model. Also, the frequency of interleukin-17(+) cells in lymph nodes was increased in CAIA.
  
  
  CONCLUSIONS
  The present study show that CAIA, a short reproducible arthritis model that is compatible with C57BL/6 mice, is associated with increased number of osteoclasts and trabecular bone loss.
authors.affiliation: Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. louise.grahnemo@gu.se.
authors.forename: Louise
authors.initials: L
authors.lastname: Grahnemo
authors.affiliation: Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. annica.andersson@rheuma.gu.se.
authors.forename: Annica
authors.initials: A
authors.lastname: Andersson
authors.affiliation: Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. merja.nurkkala@rheuma.gu.se.
authors.forename: Merja
authors.initials: M
authors.lastname: Nurkkala-Karlsson
authors.affiliation: Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. alexandra.stubelius@rheuma.gu.se.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Stubelius
authors.affiliation: Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Su Sahlgrenska, 413 45, Gothenburg, Sweden. marie.lagerquist@medic.gu.se.
authors.forename: Marie K
authors.initials: MK
authors.lastname: Lagerquist
authors.affiliation: Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. mattias.svensson@rheuma.gu.se.
authors.forename: Mattias N D
authors.initials: MN
authors.lastname: Svensson
authors.affiliation: Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Su Sahlgrenska, 413 45, Gothenburg, Sweden. claes.ohlsson@medic.gu.se.
authors.forename: Claes
authors.initials: C
authors.lastname: Ohlsson
authors.affiliation: Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. hans.carlsten@rheuma.gu.se.
authors.forename: Hans
authors.initials: H
authors.lastname: Carlsten
authors.affiliation: Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Box 480, 405 30, Gothenburg, Sweden. ulrika.islander@gu.se.
authors.forename: Ulrika
authors.initials: U
authors.lastname: Islander
mesh_terms: D000818:Animals; D000906:Antibodies / Q000276:immunology / Q000633:toxicity; D001169:Arthritis, Experimental / Q000139:chemically induced / Q000276:immunology / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D015663:Osteoporosis, Postmenopausal / Q000139:chemically induced / Q000276:immunology / Q000473:pathology*
chemical_list: D000906:Antibodies