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Erschienen in: Knee Surgery, Sports Traumatology, Arthroscopy 5/2007

01.05.2007 | Knee

Histological changes and apoptosis of cartilage layer in human anterior cruciate ligament tibial insertion after rupture

Erschienen in: Knee Surgery, Sports Traumatology, Arthroscopy | Ausgabe 5/2007

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Abstract

The purpose of this study is to investigate the histological changes and apoptosis of cartilaginous layers in human anterior cruciate ligament (ACL) tibial insertion at different time periods after rupture. By using a core reamer, 35 tibial insertions of ruptured ACLs were obtained during primary ACL reconstructions (number of days after injury: 19–206 days). A histological examination was performed and a terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) staining assay was carried out to detect apoptosis. The average thickness of the cartilage layer, the glycosaminoglycan-stained area and the number of chondrocytes per millimeter decreased with time. The percentage average of TUNEL-positive chondrocytes was 42.0 ± 16.2. The histological degenerative changes of the cartilage layer in the ruptured ACL tibial insertion progressed with time, especially in the first 2 months. Moreover, chondrocyte apoptosis continued from 19 to 206 days after rupture. The results may help elucidate the etiology of the histological changes of the insertion, and may help in devising optimal treatment protocols for ACL injuries if apoptosis is controlled. Moreover, we consider that using a surviving ligament and minimizing a debridement of ACL remnant during ACL reconstruction may be important for ACL reconstruction to maintain cartilage layers in ACL insertions.
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Metadaten
Titel
Histological changes and apoptosis of cartilage layer in human anterior cruciate ligament tibial insertion after rupture
Publikationsdatum
01.05.2007
Erschienen in
Knee Surgery, Sports Traumatology, Arthroscopy / Ausgabe 5/2007
Print ISSN: 0942-2056
Elektronische ISSN: 1433-7347
DOI
https://doi.org/10.1007/s00167-006-0264-x

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