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Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis

Osteoarthritis (OA) is a common age-related disease with complex pathophysiology. It is characterized by wide-ranging tissue damage and ultimate biomechanical failure of the whole joint. However, signs of tissue adaptation and attempted repair responses are evident in OA-affected osteochondral tissu...

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Autores principales: Ilas, Dragos C, Churchman, Sarah M, McGonagle, Dennis, Jones, Elena
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Future Science Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5674229/
https://www.ncbi.nlm.nih.gov/pubmed/29134116
http://dx.doi.org/10.4155/fsoa-2017-0055
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author Ilas, Dragos C
Churchman, Sarah M
McGonagle, Dennis
Jones, Elena
author_facet Ilas, Dragos C
Churchman, Sarah M
McGonagle, Dennis
Jones, Elena
author_sort Ilas, Dragos C
collection PubMed
description Osteoarthritis (OA) is a common age-related disease with complex pathophysiology. It is characterized by wide-ranging tissue damage and ultimate biomechanical failure of the whole joint. However, signs of tissue adaptation and attempted repair responses are evident in OA-affected osteochondral tissues. Highlighted in this review article is the role of bone-resident mesenchymal stem cells (MSCs) in these bone remodeling responses, and a proposal that targeting MSC activities in OA subchondral bone could represent a novel approach for intrinsic joint regeneration in OA. The development of these therapies will require better understanding of MSC proliferation, migration and differentiation patterns in relation to OA tissue damage and further clarification of the molecular signaling events in these MSCs during disease progression.
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spelling pubmed-56742292017-11-13 Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis Ilas, Dragos C Churchman, Sarah M McGonagle, Dennis Jones, Elena Future Sci OA Review Osteoarthritis (OA) is a common age-related disease with complex pathophysiology. It is characterized by wide-ranging tissue damage and ultimate biomechanical failure of the whole joint. However, signs of tissue adaptation and attempted repair responses are evident in OA-affected osteochondral tissues. Highlighted in this review article is the role of bone-resident mesenchymal stem cells (MSCs) in these bone remodeling responses, and a proposal that targeting MSC activities in OA subchondral bone could represent a novel approach for intrinsic joint regeneration in OA. The development of these therapies will require better understanding of MSC proliferation, migration and differentiation patterns in relation to OA tissue damage and further clarification of the molecular signaling events in these MSCs during disease progression. Future Science Ltd 2017-09-06 /pmc/articles/PMC5674229/ /pubmed/29134116 http://dx.doi.org/10.4155/fsoa-2017-0055 Text en © 2017 Ilas, Churchman, McGonagle, Jones This work is licensed under a Creative Commons Attribution 4.0 License (http://creativecommons.org/licenses/by/4.0/)
spellingShingle Review
Ilas, Dragos C
Churchman, Sarah M
McGonagle, Dennis
Jones, Elena
Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis
title Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis
title_full Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis
title_fullStr Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis
title_full_unstemmed Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis
title_short Targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis
title_sort targeting subchondral bone mesenchymal stem cell activities for intrinsic joint repair in osteoarthritis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5674229/
https://www.ncbi.nlm.nih.gov/pubmed/29134116
http://dx.doi.org/10.4155/fsoa-2017-0055
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