Center for Biologically Inspired Materials and Material Systems Center for Biologically Inspired Materials and Material Systems
Pratt School of Engineering
Duke University

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Publications [#263337] of Stefan Zauscher

Papers Published

  1. Wilusz, RE; Zauscher, S; Guilak, F, Micromechanical mapping of early osteoarthritic changes in the pericellular matrix of human articular cartilage., Osteoarthritis and Cartilage, vol. 21 no. 12 (December, 2013), pp. 1895-1903 [24025318], [doi]
    (last updated on 2017/11/18)

    Abstract:
    OBJECTIVE: Osteoarthritis (OA) is a degenerative joint disease characterized by the progressive loss of articular cartilage. While macroscale degradation of the cartilage extracellular matrix (ECM) has been extensively studied, microscale changes in the chondrocyte pericellular matrix (PCM) and immediate microenvironment with OA are not fully understood. The objective of this study was to quantify osteoarthritic changes in the micromechanical properties of the ECM and PCM of human articular cartilage in situ using atomic force microscopy (AFM). METHOD: AFM elastic mapping was performed on cryosections of human cartilage harvested from both condyles of macroscopically normal and osteoarthritic knee joints. This method was used to test the hypotheses that both ECM and PCM regions exhibit a loss of mechanical properties with OA and that the size of the PCM is enlarged in OA cartilage as compared to normal tissue. RESULTS: Significant decreases were observed in both ECM and PCM moduli of 45% and 30%, respectively, on the medial condyle of OA knee joints as compared to cartilage from macroscopically normal joints. Enlargement of the PCM, as measured biomechanically, was also observed in medial condyle OA cartilage, reflecting the underlying distribution of type VI collagen in the region. No significant differences were observed in elastic moduli or their spatial distribution on the lateral condyle between normal and OA joints. CONCLUSION: Our findings provide new evidence of significant site-specific degenerative changes in the chondrocyte micromechanical environment with OA.


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