The articular cartilage surface is impaired by a loss of thick collagen fibers and formation of type I collagen in early osteoarthritis

Abstract: Osteoarthritis (OA) is a joint disease affecting millions of patients worldwide. During OA onset and progression, the articular cartilage is destroyed, but the underlying complex mechanisms remain unclear. Here we uncovered changes in the thickness of collagen fibers and their composition at the onset of OA. For articular cartilage explants from knee joints of OA we find that type I collagen-rich fibrocartilage-like tissue was formed in macroscopically intact cartilage, distant from OA lesions. Importantly, the number of thick fibers (>100 nm) had decreased early in the disease, followed by complete absence of thick fibers in advanced OA. These results became possible by a combination of high-resolution atomic force microscopy imaging under near-native conditions, immunofluorescence, scanning electron microscopy and a fluorescence-based classification of the superficial chondrocyte spatial organization. Taken together, our data suggests that the loss of tissue functionality in early OA cartilage is caused by a reduction of thick type II collagen fibers, likely due to the formation of type I collagen-rich fibrocartilage, followed by the development of focal defects in later OA stages. We anticipate that such an integrative characterization will be very beneficial for an in-depth understanding of other native biological tissues and the development of sustainable biomaterials

Angaben zum Objekt

• Standort: Deutsche Nationalbibliothek Frankfurt am Main
• Umfang: Online-Ressource
• Sprache: Englisch
• Anmerkungen: Acta biomaterialia. - 146 (2022) , 274-283, ISSN: 1878-7568

Beteiligte, Orts- und Zeitangaben

• Ereignis: Veröffentlichung
• (wo): Freiburg
• (wer): Universität
• (wann): 2022
• Urheber: Tschaikowsky, Mathäus ; Brander, Sofia ; Barth, Vanessa ; Thomann, Ralf ; Rolauffs, Bernd ; Balzer, Bizan N. ; Hugel, Thorsten

Weitere Informationen

• DOI: 10.1016/j.actbio.2022.04.036
• URN: urn:nbn:de:bsz:25-freidok-2265280
• Rechteinformation: Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
• Letzte Aktualisierung: 15.08.2025, 07:23 MESZ