Osteoarthritis and cartilage · 2003
Presence and mechanism of knee articular cartilage degeneration after meniscal reconstruction in dogs.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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van Tienen T G, Heijkants R G J C, de Groot J H, Pennings A J, Poole A R, Veth R P H, Buma P
Аннотация
OBJECTIVE: Partial meniscectomy is the golden standard for treating a bucket-handle tear in the meniscus of the knee, but it inevitably leads to articular cartilage degeneration. Surgical creation of an access channel between the lesion and the vascularized synovial lining is intended to induce ingrowth of repair tissue and thus avoid degeneration of articular cartilage.
DESIGN: The presence and mechanism of cartilage degeneration were evaluated in 24 canine menisci after a longitudinal lesion and access channel had been created in the avascular part of the meniscus. In 12 menisci the channel was implanted with a porous polymer scaffold, while the remaining 12 were left empty. Evaluation was performed using routine histology and antibodies directed against denatured type II collagen (Col2-3/4M).
RESULTS: Articular degeneration was apparent in the polymer implant group and the empty channel group. This consisted of fibrillation, loss of chondrocytes and decreased proteoglycan content. Areas of fibrillated cartilage always showed positive labeling with the collagen degradation antibody Col2-3/4M. Collagen degradation was also visible in non-fibrillated areas. The upper zone of the cartilage showed swelling especially in the implant group, with empty cell lacunae and moderate levels of Col2-3/4M antibody labeling.
DISCUSSION: This reconstruction technique cannot be considered superior to partial meniscectomy. We propose that degradation of the collagen type II network is a result of cartilage fibrillation and vice versa.
DESIGN: The presence and mechanism of cartilage degeneration were evaluated in 24 canine menisci after a longitudinal lesion and access channel had been created in the avascular part of the meniscus. In 12 menisci the channel was implanted with a porous polymer scaffold, while the remaining 12 were left empty. Evaluation was performed using routine histology and antibodies directed against denatured type II collagen (Col2-3/4M).
RESULTS: Articular degeneration was apparent in the polymer implant group and the empty channel group. This consisted of fibrillation, loss of chondrocytes and decreased proteoglycan content. Areas of fibrillated cartilage always showed positive labeling with the collagen degradation antibody Col2-3/4M. Collagen degradation was also visible in non-fibrillated areas. The upper zone of the cartilage showed swelling especially in the implant group, with empty cell lacunae and moderate levels of Col2-3/4M antibody labeling.
DISCUSSION: This reconstruction technique cannot be considered superior to partial meniscectomy. We propose that degradation of the collagen type II network is a result of cartilage fibrillation and vice versa.