RESEARCH ARTICLE


Histological Examination of Collagen and Proteoglycan Changes in Osteoarthritic Menisci



Yubo Sun*, 1, David R Mauerhan1, Jeffrey S Kneisl1, H James Norton2, Natalia Zinchenko1, Jane Ingram1, Edward N Hanley, Jr1, Helen E Gruber1
1 Department of Orthopedic Surgery, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232, USA
2 Department of Biostatistics, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232, USA


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Creative Commons License
© Sun et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Cannon Research 303, Department of Orthopedic Surgery, Carolinas Medical Center, PO Box 32861, Charlotte, NC 28232, USA; Tel: 704/355-5656; Fax: 704/355-5620; E-mail: yubo.sun@carolinashealthcare.org


Abstract

This study sought to examine collagen and proteoglycan changes in the menisci of patients with osteoarthritis (OA). Collagens were examined using picrosirius red, and hematoxylin and eosin. Proteoglycans were examined using safranin-O and alcian blue. Types I and II collagens and aggrecan were examined using immunochemistry. Severe loss of collagens was observed to occur in OA menisci, particularly in the middle and deep zones and collagen networks were less organized than those of normal menisci. In contrast, proteoglycan staining in the middle and deep zones of OA meniscus increased compared to normal control menisci. Immunohistochemistry indicated that types I and II collagens were co-localized and the loss of types I collagen in OA menisci appeared more severe in the middle and deep zones than that in the surface zones. The loss of type II collagen however was severe across all three zones. Immunohistochemistry also indicated elevated aggrecan staining in OA menisci. These findings together indicate that severe loss of collagens and intrameniscal degeneration are hallmarks of OA menisci and that extracellular matrix degeneration occurred in OA menisci follows a pathway different from that occurred in OA articular cartilage. These findings are not only important for a better understanding of the disease process but also important for the development of novel structure-modifying drugs for OA therapy.

Keywords: Aggrecan, collagen I, collagen II, meniscus, osteoarthritis, proteoglycan..