Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapy

Hubert Marotte, Pierre MiossecClinical Immunology Unit, Departments of Immunology and Rheumatology, University of Lyon, and Unité Mixte Hospices Civils de Lyon–bioMérieux, Hôpital Edouard Herriot, Lyon, FranceAbstract: This review focuses on...

Full description

Bibliographic Details
Main Authors: Hubert Marotte, Pierre Miossec
Format: Article
Language:English
Published: Dove Medical Press 2008-08-01
Series:Biologics: Targets & Therapy
Online Access:http://www.dovepress.com/prevention-of-bone-mineral-density-loss-in-patients-with-rheumatoid-ar-a2035
_version_ 1818909212031320064
author Hubert Marotte
Pierre Miossec
author_facet Hubert Marotte
Pierre Miossec
author_sort Hubert Marotte
collection DOAJ
description Hubert Marotte, Pierre MiossecClinical Immunology Unit, Departments of Immunology and Rheumatology, University of Lyon, and Unité Mixte Hospices Civils de Lyon–bioMérieux, Hôpital Edouard Herriot, Lyon, FranceAbstract: This review focuses on recent advances in the effect of anti-TNFα therapy on bone metabolism and bone mineral density (BMD) in rheumatoid arthritis (RA). RA is a chronic disease characterized by inflammation of the synovial joint, cartilage degradation, and subsequent bone destruction. Bone damage is often manifested as erosions, localized juxta-articular bone loss, or generalized bone loss. Thus, blockade of TNFa not only serves to block inflammation, but also halts the erosive nature of RA and generalized/localized juxta-articular bone loss. Here, we review recent findings showing that anti-TNFa therapy is also effective on halting systemic bone loss. In vitro, TNFa reduces osteoblast activity and increases osteoclast activity through RANKL-RANK pathway. In arthritis animal models, an imbalance between bone formation and resorption is observed. In humans, this coupling of destruction is restored by anti-TNFα therapy early on, but only for a few months. Thus, anti-TNFα prevents the BMD loss in RA patients. In summary, TNFa blockade is not only able to prevent joint destruction, but it is also able to prevent bone loss in RA patients. Future studies are needed to address if TNFa blockers have an effect on bone fractures.Keywords: rheumatoid arthritis, TNFα, bone mineral density, infliximab
first_indexed 2024-12-19T22:23:19Z
format Article
id doaj.art-f894966d3ecc46ec8226c9d102eb9061
institution Directory Open Access Journal
issn 1177-5475
1177-5491
language English
last_indexed 2024-12-19T22:23:19Z
publishDate 2008-08-01
publisher Dove Medical Press
record_format Article
series Biologics: Targets & Therapy
spelling doaj.art-f894966d3ecc46ec8226c9d102eb90612022-12-21T20:03:34ZengDove Medical PressBiologics: Targets & Therapy1177-54751177-54912008-08-012008Issue 4663669Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapyHubert MarottePierre MiossecHubert Marotte, Pierre MiossecClinical Immunology Unit, Departments of Immunology and Rheumatology, University of Lyon, and Unité Mixte Hospices Civils de Lyon–bioMérieux, Hôpital Edouard Herriot, Lyon, FranceAbstract: This review focuses on recent advances in the effect of anti-TNFα therapy on bone metabolism and bone mineral density (BMD) in rheumatoid arthritis (RA). RA is a chronic disease characterized by inflammation of the synovial joint, cartilage degradation, and subsequent bone destruction. Bone damage is often manifested as erosions, localized juxta-articular bone loss, or generalized bone loss. Thus, blockade of TNFa not only serves to block inflammation, but also halts the erosive nature of RA and generalized/localized juxta-articular bone loss. Here, we review recent findings showing that anti-TNFa therapy is also effective on halting systemic bone loss. In vitro, TNFa reduces osteoblast activity and increases osteoclast activity through RANKL-RANK pathway. In arthritis animal models, an imbalance between bone formation and resorption is observed. In humans, this coupling of destruction is restored by anti-TNFα therapy early on, but only for a few months. Thus, anti-TNFα prevents the BMD loss in RA patients. In summary, TNFa blockade is not only able to prevent joint destruction, but it is also able to prevent bone loss in RA patients. Future studies are needed to address if TNFa blockers have an effect on bone fractures.Keywords: rheumatoid arthritis, TNFα, bone mineral density, infliximabhttp://www.dovepress.com/prevention-of-bone-mineral-density-loss-in-patients-with-rheumatoid-ar-a2035
spellingShingle Hubert Marotte
Pierre Miossec
Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapy
Biologics: Targets & Therapy
title Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapy
title_full Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapy
title_fullStr Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapy
title_full_unstemmed Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapy
title_short Prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti-TNFα therapy
title_sort prevention of bone mineral density loss in patients with rheumatoid arthritis treated with anti tnf amp alpha therapy
url http://www.dovepress.com/prevention-of-bone-mineral-density-loss-in-patients-with-rheumatoid-ar-a2035
work_keys_str_mv AT hubertmarotte preventionofbonemineraldensitylossinpatientswithrheumatoidarthritistreatedwithantitnfampalphatherapy
AT pierremiossec preventionofbonemineraldensitylossinpatientswithrheumatoidarthritistreatedwithantitnfampalphatherapy