Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation?

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Oxidative stress in secondary osteoarthritis : from cartilage destruction to clinical presentation? / Ziskoven, Christoph; Jäger, Marcus; Zilkens, Christoph; Bloch, Wilhelm; Brixius, Klara; Krauspe, Rüdiger.

in: Orthopedic reviews, Jahrgang 2, Nr. 2, 23.09.2010, S. e23.

Publikationen: Beitrag in FachzeitschriftZeitschriftenaufsätzeForschung

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@article{002d3b1cb2044750ae4a4e72e747ea4e,
title = "Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation?",
abstract = "Due to an increasing life expectance, osteoarthritis (OA) is one of the most common chronic diseases. Although strong efforts have been made to regenerate degenerated joint cartilage, OA is a progressive and irreversible disease up to date. Among other factors the dysbalance between free radical burden and cellular scavenging mechanisms defined as oxidative stress is a relevant part of OA pathogenesis. Here, only little data are available about the mediation and interaction between different joint compartments. The article provides a review of the current literature regarding the influence of oxidative stress on cellular aging, senescence and apoptosis in different joint compartments (cartilage, synovial tissue and subchondral bone). Free radical exposure is known to promote cellular senescence and apoptosis. Radical oxygen species (ROS) involvement in inflammation, fibrosis control and pain nociception has been proven. The data from literature indicates a link between free radical burden and OA pathogenesis mediating local tissue reactions between the joint compartments. Hence, oxidative stress is likely not only to promote cartilage destruction but also to be involved in inflammative transformation, promoting the transition from clinically silent cartilage destruction to apparent OA. ROS induced by exogenous factors such as overload, trauma, local intraarticular lesion and consecutive synovial inflammation cause cartilage degradation. In the affected joint, free radicals mediate disease progression. The interrelationship between oxidative stress and OA etiology might provide a novel approach to the comprehension and therefore modification of disease progression and symptom control.",
author = "Christoph Ziskoven and Marcus J{\"a}ger and Christoph Zilkens and Wilhelm Bloch and Klara Brixius and R{\"u}diger Krauspe",
year = "2010",
month = "9",
day = "23",
doi = "10.4081/or.2010.e23",
language = "English",
volume = "2",
pages = "e23",
journal = "Orthopedic reviews",
issn = "2035-8237",
publisher = "PagePress Publications",
number = "2",

}

RIS

TY - JOUR

T1 - Oxidative stress in secondary osteoarthritis

T2 - from cartilage destruction to clinical presentation?

AU - Ziskoven, Christoph

AU - Jäger, Marcus

AU - Zilkens, Christoph

AU - Bloch, Wilhelm

AU - Brixius, Klara

AU - Krauspe, Rüdiger

PY - 2010/9/23

Y1 - 2010/9/23

N2 - Due to an increasing life expectance, osteoarthritis (OA) is one of the most common chronic diseases. Although strong efforts have been made to regenerate degenerated joint cartilage, OA is a progressive and irreversible disease up to date. Among other factors the dysbalance between free radical burden and cellular scavenging mechanisms defined as oxidative stress is a relevant part of OA pathogenesis. Here, only little data are available about the mediation and interaction between different joint compartments. The article provides a review of the current literature regarding the influence of oxidative stress on cellular aging, senescence and apoptosis in different joint compartments (cartilage, synovial tissue and subchondral bone). Free radical exposure is known to promote cellular senescence and apoptosis. Radical oxygen species (ROS) involvement in inflammation, fibrosis control and pain nociception has been proven. The data from literature indicates a link between free radical burden and OA pathogenesis mediating local tissue reactions between the joint compartments. Hence, oxidative stress is likely not only to promote cartilage destruction but also to be involved in inflammative transformation, promoting the transition from clinically silent cartilage destruction to apparent OA. ROS induced by exogenous factors such as overload, trauma, local intraarticular lesion and consecutive synovial inflammation cause cartilage degradation. In the affected joint, free radicals mediate disease progression. The interrelationship between oxidative stress and OA etiology might provide a novel approach to the comprehension and therefore modification of disease progression and symptom control.

AB - Due to an increasing life expectance, osteoarthritis (OA) is one of the most common chronic diseases. Although strong efforts have been made to regenerate degenerated joint cartilage, OA is a progressive and irreversible disease up to date. Among other factors the dysbalance between free radical burden and cellular scavenging mechanisms defined as oxidative stress is a relevant part of OA pathogenesis. Here, only little data are available about the mediation and interaction between different joint compartments. The article provides a review of the current literature regarding the influence of oxidative stress on cellular aging, senescence and apoptosis in different joint compartments (cartilage, synovial tissue and subchondral bone). Free radical exposure is known to promote cellular senescence and apoptosis. Radical oxygen species (ROS) involvement in inflammation, fibrosis control and pain nociception has been proven. The data from literature indicates a link between free radical burden and OA pathogenesis mediating local tissue reactions between the joint compartments. Hence, oxidative stress is likely not only to promote cartilage destruction but also to be involved in inflammative transformation, promoting the transition from clinically silent cartilage destruction to apparent OA. ROS induced by exogenous factors such as overload, trauma, local intraarticular lesion and consecutive synovial inflammation cause cartilage degradation. In the affected joint, free radicals mediate disease progression. The interrelationship between oxidative stress and OA etiology might provide a novel approach to the comprehension and therefore modification of disease progression and symptom control.

U2 - 10.4081/or.2010.e23

DO - 10.4081/or.2010.e23

M3 - Journal articles

VL - 2

SP - e23

JO - Orthopedic reviews

JF - Orthopedic reviews

SN - 2035-8237

IS - 2

ER -

ID: 66394