Pathomechanisms of posttraumatic osteoarthritis: chondrocyte behavior and fate in a precarious environment
peer-reviewed
Erstveröffentlichung
2020-01-18Authors
Riegger, Jana
Brenner, Rolf E.
Wissenschaftlicher Artikel
Published in
International Journal of Molecular Sciences ; 21 (2020). - Art.-Nr. 1560. - ISSN 1661-6596. - eISSN 1422-0067
Link to original publication
https://dx.doi.org/10.3390/ijms21051560Institutions
UKU. Klinik für OrthopädieDocument version
published version (publisher's PDF)Abstract
Traumatic injuries of the knee joint result in a wide variety of pathomechanisms, which
contribute to the development of so-called posttraumatic osteoarthritis (PTOA). These pathogenetic
processes include oxidative stress, excessive expression of catabolic enzymes, release of
damage-associated molecular patterns (DAMPs), and synovial inflammation. The present review
focuses on the underlying pathomechanisms of PTOA and in particular the behavior and fate of the
surviving chondrocytes, comprising chondrocyte metabolism, regulated cell death, and phenotypical
changes comprising hypertrophy and senescence. Moreover, possible therapeutic strategies, such
as chondroanabolic stimulation, anti-oxidative and anti-inflammatory treatment, as well as novel
therapeutic targets are discussed.
Subject headings
[GND]: Osteoarthritis | Kniegelenk | Entzündung | Pathomechanismus[MeSH]: Osteoarthritis; Therapy | Oxidative stress | Cell death | Metabolism | Chondrocytes
[Free subject headings]: Posttraumatic osteoarthritis | DAMP release | Synovial inflammation | CSPC | Catabolism | Anabolism
[DDC subject group]: DDC 610 / Medicine & health
Metadata
Show full item recordDOI & citation
Please use this identifier to cite or link to this item: http://dx.doi.org/10.18725/OPARU-35302
Riegger, Jana; Brenner, Rolf E. (2021): Pathomechanisms of posttraumatic osteoarthritis: chondrocyte behavior and fate in a precarious environment. Open Access Repositorium der Universität Ulm und Technischen Hochschule Ulm. http://dx.doi.org/10.18725/OPARU-35302
Citation formatter >