Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases

Bone remodeling is a lifelong process in vertebrates that relies on the correct balance between bone resorption by osteoclasts and bone formation by osteoblasts. Bone loss and fracture risk are implicated in inflammatory autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis, infla...

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Main Authors: Dulshara Sachini Amarasekara, Jiyeon Yu, Jaerang Rho
Format: Article
Language:English
Published: Hindawi Limited 2015-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2015/832127
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spelling doaj-92f9e887112d4cc7909d98babb2eea102020-11-24T21:03:58ZengHindawi LimitedJournal of Immunology Research2314-88612314-71562015-01-01201510.1155/2015/832127832127Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune DiseasesDulshara Sachini Amarasekara0Jiyeon Yu1Jaerang Rho2Department of Bioscience and Biotechnology, College of Biological Sciences and Biotechnology, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 305-764, Republic of KoreaDepartment of Bioscience and Biotechnology, College of Biological Sciences and Biotechnology, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 305-764, Republic of KoreaDepartment of Bioscience and Biotechnology, College of Biological Sciences and Biotechnology, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 305-764, Republic of KoreaBone remodeling is a lifelong process in vertebrates that relies on the correct balance between bone resorption by osteoclasts and bone formation by osteoblasts. Bone loss and fracture risk are implicated in inflammatory autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, and systemic lupus erythematosus. The network of inflammatory cytokines produced during chronic inflammation induces an uncoupling of bone formation and resorption, resulting in significant bone loss in patients with inflammatory autoimmune diseases. Here, we review and discuss the involvement of the inflammatory cytokine network in the pathophysiological aspects and the therapeutic advances in inflammatory autoimmune diseases.http://dx.doi.org/10.1155/2015/832127
collection DOAJ
language English
format Article
sources DOAJ
author Dulshara Sachini Amarasekara
Jiyeon Yu
Jaerang Rho
spellingShingle Dulshara Sachini Amarasekara
Jiyeon Yu
Jaerang Rho
Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases
Journal of Immunology Research
author_facet Dulshara Sachini Amarasekara
Jiyeon Yu
Jaerang Rho
author_sort Dulshara Sachini Amarasekara
title Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases
title_short Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases
title_full Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases
title_fullStr Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases
title_full_unstemmed Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases
title_sort bone loss triggered by the cytokine network in inflammatory autoimmune diseases
publisher Hindawi Limited
series Journal of Immunology Research
issn 2314-8861
2314-7156
publishDate 2015-01-01
description Bone remodeling is a lifelong process in vertebrates that relies on the correct balance between bone resorption by osteoclasts and bone formation by osteoblasts. Bone loss and fracture risk are implicated in inflammatory autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, and systemic lupus erythematosus. The network of inflammatory cytokines produced during chronic inflammation induces an uncoupling of bone formation and resorption, resulting in significant bone loss in patients with inflammatory autoimmune diseases. Here, we review and discuss the involvement of the inflammatory cytokine network in the pathophysiological aspects and the therapeutic advances in inflammatory autoimmune diseases.
url http://dx.doi.org/10.1155/2015/832127
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