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AB0144 EFFECTS OF AB501 (CERTOLIZUMAB MICE EQUIVALENT) IN ARTHRITIS INDUCED BONE LOSS

Authors :
João Eurico Fonseca
Rita Cascão
Bruno Vidal
Inês P Lopes
Mikko A. J. Finnilä
Source :
Abstracts Accepted for Publication.
Publication Year :
2019
Publisher :
BMJ Publishing Group Ltd and European League Against Rheumatism, 2019.

Abstract

Background: Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease, which causes local and systemic bone damage. Objectives: The main goal of this work was to analyze, how treatment intervention with Ab501 (certolizumab mice equivalent) prevents the disturbances on bone structure and mechanics induced by arthritis. Methods: Thirty one DBA/1 collagen-induced arthritis (CIA) mice were randomly housed in experimental groups, as follows: arthritic untreated (N=10), preventive intervention with ab501 2 days before arthritis induction (N=10) and treatment intervention upon arthritis onset with ab501 (N=11). A non-induced group (N=5) was used as a control. Mice were monitored during 70 days after disease induction for the inflammatory score, ankle perimeter and body weight. Non-induced mice were used as controls. After 70 days of disease progression mice were sacrificed and bone samples were collected for histology, micro-computed tomography (μCT) and 3-point bending analysis. In addition, blood samples were also collected for bone turnover markers quantification. Statistical differences were determined with Mann–Whitney tests using GraphPad Prism (GraphPad, California, USA). Data were expressed as median with interquartile range. Differences were considered statistically significant for p Results: Results showed that Ab501 administration was able to control and abrogate disease development both in preventive and early therapeutic intervention. μCT results revealed that ab501 was able to preserve bone structure when delivered before arthritis induction. Conclusion: Ab501 preventive administration was able to control inflammation and prevent the degradative effects of arthritis on trabecular bone structure. Acknowledgement: This work was supported by UCB in the context of an Investigator Initiated Study where UCB provided financial and product support. Disclosure of Interests: Bruno Vidal Grant/research support from: Aspire Pfizer 2013, Mikko A. Finnila: None declared, Ines Lopes: None declared, Rita Cascao: None declared, Joao Eurico Fonseca: None declared

Details

Database :
OpenAIRE
Journal :
Abstracts Accepted for Publication
Accession number :
edsair.doi...........1c4227f38345d6c8dfaa51b79d044c89