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Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis
Osteoarthritis (OA) is the most common arthritis and its hallmark is degradation of articular cartilage by proteolytic enzymes leading to loss of joint function. It is challenging to monitor the status of cartilage in vivo and this study explores the use of autofluorescence lifetime (AFL) measuremen...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7005742/ https://www.ncbi.nlm.nih.gov/pubmed/32034262 http://dx.doi.org/10.1038/s41598-020-59219-5 |
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author | Lagarto, João L. Nickdel, Mohammad B. Kelly, Douglas J. Price, Andrew Nanchahal, Jagdeep Dunsby, Chris French, Paul Itoh, Yoshifumi |
author_facet | Lagarto, João L. Nickdel, Mohammad B. Kelly, Douglas J. Price, Andrew Nanchahal, Jagdeep Dunsby, Chris French, Paul Itoh, Yoshifumi |
author_sort | Lagarto, João L. |
collection | PubMed |
description | Osteoarthritis (OA) is the most common arthritis and its hallmark is degradation of articular cartilage by proteolytic enzymes leading to loss of joint function. It is challenging to monitor the status of cartilage in vivo and this study explores the use of autofluorescence lifetime (AFL) measurements to provide a label-free optical readout of cartilage degradation that could enable earlier detection and evaluation of potential therapies. We previously reported that treatment of ex vivo porcine cartilage with proteolytic enzymes resulted in decreased AFL. Here we report changes in AFL of ex vivo mouse knee joints, porcine metacarpophalangeal joints, normal human metatarsophalangeal articular tissue and human OA tibial plateau tissues measured with or without treatment using a compact single-point time resolved spectrofluorometer. Our data show that proteolytically damaged areas in porcine metacarpophalangeal joints present a reduced AFL and that inducing aggrecanases in mouse and human joints also significantly reduces AFL. Further, human cartilage from OA patients presents a significantly lower AFL compared to normal human cartilage. Our data suggest that AFL can detect areas of cartilage erosion and may potentially be utilised as a minimally-invasive diagnostic readout for early stage OA in combination with arthroscopy devices. |
format | Online Article Text |
id | pubmed-7005742 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-70057422020-02-18 Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis Lagarto, João L. Nickdel, Mohammad B. Kelly, Douglas J. Price, Andrew Nanchahal, Jagdeep Dunsby, Chris French, Paul Itoh, Yoshifumi Sci Rep Article Osteoarthritis (OA) is the most common arthritis and its hallmark is degradation of articular cartilage by proteolytic enzymes leading to loss of joint function. It is challenging to monitor the status of cartilage in vivo and this study explores the use of autofluorescence lifetime (AFL) measurements to provide a label-free optical readout of cartilage degradation that could enable earlier detection and evaluation of potential therapies. We previously reported that treatment of ex vivo porcine cartilage with proteolytic enzymes resulted in decreased AFL. Here we report changes in AFL of ex vivo mouse knee joints, porcine metacarpophalangeal joints, normal human metatarsophalangeal articular tissue and human OA tibial plateau tissues measured with or without treatment using a compact single-point time resolved spectrofluorometer. Our data show that proteolytically damaged areas in porcine metacarpophalangeal joints present a reduced AFL and that inducing aggrecanases in mouse and human joints also significantly reduces AFL. Further, human cartilage from OA patients presents a significantly lower AFL compared to normal human cartilage. Our data suggest that AFL can detect areas of cartilage erosion and may potentially be utilised as a minimally-invasive diagnostic readout for early stage OA in combination with arthroscopy devices. Nature Publishing Group UK 2020-02-07 /pmc/articles/PMC7005742/ /pubmed/32034262 http://dx.doi.org/10.1038/s41598-020-59219-5 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Lagarto, João L. Nickdel, Mohammad B. Kelly, Douglas J. Price, Andrew Nanchahal, Jagdeep Dunsby, Chris French, Paul Itoh, Yoshifumi Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis |
title | Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis |
title_full | Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis |
title_fullStr | Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis |
title_full_unstemmed | Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis |
title_short | Autofluorescence Lifetime Reports Cartilage Damage in Osteoarthritis |
title_sort | autofluorescence lifetime reports cartilage damage in osteoarthritis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7005742/ https://www.ncbi.nlm.nih.gov/pubmed/32034262 http://dx.doi.org/10.1038/s41598-020-59219-5 |
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