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Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures

BACKGROUND: The primary goal of this study was to identify nitric oxide (NO)-induced apoptosis in traumatized chondrocytes in intra-articular lower extremity fractures and the secondary goal was to identify the timeline of NO-induced apoptosis after injury. MATERIALS AND METHODS: This is a prospecti...

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Autores principales: Prince, Daniel E., Greisberg, Justin K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633420/
https://www.ncbi.nlm.nih.gov/pubmed/25957508
http://dx.doi.org/10.1007/s10195-015-0350-2
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author Prince, Daniel E.
Greisberg, Justin K.
author_facet Prince, Daniel E.
Greisberg, Justin K.
author_sort Prince, Daniel E.
collection PubMed
description BACKGROUND: The primary goal of this study was to identify nitric oxide (NO)-induced apoptosis in traumatized chondrocytes in intra-articular lower extremity fractures and the secondary goal was to identify the timeline of NO-induced apoptosis after injury. MATERIALS AND METHODS: This is a prospective collection of samples of human cartilage harvested at the time of surgery to measure apoptotic cell death and the presence of NO by immunohistochemistry. Three patients met the criteria for control subjects and eight patients sustained high-energy intra-articular fractures and were included in the study. Subjects who sustained intra-articular acetabular, tibial, calcaneal and talus fracture had articular cartilage harvested at the time of surgical intervention. All 8 patients underwent open reduction and internal fixation of the displaced intra-articular fractures. The main outcome measures were rate of apoptosis, degree of NO-induced apoptosis in chondrocytes, and the timeline of NO-induced apoptosis after high-energy trauma. RESULTS: The percentage of apoptotic chondrocytes was higher in impacted samples than in normal cartilage (56 vs 4 %), confirming the presence of apoptosis after intra-articular fracture. The percentage of cells with NO was greater in apoptotic cells than in normal cells (59 vs 20 %), implicating NO-induction of apoptosis. The correlation between chondrocyte apoptosis and increasing time from injury was found to be −0.615, indicating a decreasing rate of apoptosis post injury. CONCLUSIONS: The data showed the involvement of NO-induced apoptosis of chondrocytes after high-energy trauma, which decreased with time from injury.
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spelling pubmed-46334202015-11-10 Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures Prince, Daniel E. Greisberg, Justin K. J Orthop Traumatol Original Article BACKGROUND: The primary goal of this study was to identify nitric oxide (NO)-induced apoptosis in traumatized chondrocytes in intra-articular lower extremity fractures and the secondary goal was to identify the timeline of NO-induced apoptosis after injury. MATERIALS AND METHODS: This is a prospective collection of samples of human cartilage harvested at the time of surgery to measure apoptotic cell death and the presence of NO by immunohistochemistry. Three patients met the criteria for control subjects and eight patients sustained high-energy intra-articular fractures and were included in the study. Subjects who sustained intra-articular acetabular, tibial, calcaneal and talus fracture had articular cartilage harvested at the time of surgical intervention. All 8 patients underwent open reduction and internal fixation of the displaced intra-articular fractures. The main outcome measures were rate of apoptosis, degree of NO-induced apoptosis in chondrocytes, and the timeline of NO-induced apoptosis after high-energy trauma. RESULTS: The percentage of apoptotic chondrocytes was higher in impacted samples than in normal cartilage (56 vs 4 %), confirming the presence of apoptosis after intra-articular fracture. The percentage of cells with NO was greater in apoptotic cells than in normal cells (59 vs 20 %), implicating NO-induction of apoptosis. The correlation between chondrocyte apoptosis and increasing time from injury was found to be −0.615, indicating a decreasing rate of apoptosis post injury. CONCLUSIONS: The data showed the involvement of NO-induced apoptosis of chondrocytes after high-energy trauma, which decreased with time from injury. Springer International Publishing 2015-05-10 2015-12 /pmc/articles/PMC4633420/ /pubmed/25957508 http://dx.doi.org/10.1007/s10195-015-0350-2 Text en © The Author(s) 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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.
spellingShingle Original Article
Prince, Daniel E.
Greisberg, Justin K.
Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures
title Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures
title_full Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures
title_fullStr Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures
title_full_unstemmed Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures
title_short Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures
title_sort nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4633420/
https://www.ncbi.nlm.nih.gov/pubmed/25957508
http://dx.doi.org/10.1007/s10195-015-0350-2
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