Investigating magnetic susceptibility of human knee joint at 7 Tesla.


Journal Article

PURPOSE: To evaluate the magnetic susceptibility properties of different anatomical structures within the knee joint using quantitative susceptibility mapping (QSM). METHODS: A collagen tissue model was simulated and ex vivo animal cartilage experiments were conducted at 9.4 Tesla (T) to evaluate the B0 orientation-dependent magnetic susceptibility contrast observed in cartilage. Furthermore, nine volunteers (six healthy subjects without knee pain history and three patients with known knee injury, between 29 and 58 years old) were scanned using gradient-echo acquisitions on a high-field 7T MR scanner. Susceptibility values of different tissues were quantified and diseased cartilage and meniscus were compared against that of healthy volunteers. RESULTS: Simulation and ex vivo animal cartilage experiments demonstrated that collagen fibrils exhibit an anisotropic susceptibility. A gradual change of magnetic susceptibility was observed in the articular cartilage from the superficial zone to the deep zone, forming a multilayer ultrastructure consistent with anisotropy of collagen fibrils. Meniscal tears caused a clear reduction of susceptibility contrast between the injured meniscus and surrounding cartilage illustrated by a loss of the sharp boundaries between the two. Moreover, QSM showed more dramatic contrast in the focal degenerated articular cartilage than R2* mapping. CONCLUSION: The arrangement of the collagen fibrils is significant, and likely the most dominant source of magnetic susceptibility anisotropy. Quantitative susceptibility mapping offers a means to characterize magnetic susceptibility properties of tissues in the knee joint. It is sensitive to collagen damage or degeneration and may be useful for evaluating the status of knee diseases, such as meniscal tears and cartilage disease. Magn Reson Med 78:1933-1943, 2017. © 2017 International Society for Magnetic Resonance in Medicine.

Full Text

Duke Authors

Cited Authors

  • Wei, H; Dibb, R; Decker, K; Wang, N; Zhang, Y; Zong, X; Lin, W; Nissman, DB; Liu, C

Published Date

  • November 2017

Published In

Volume / Issue

  • 78 / 5

Start / End Page

  • 1933 - 1943

PubMed ID

  • 28097689

Pubmed Central ID

  • 28097689

Electronic International Standard Serial Number (EISSN)

  • 1522-2594

Digital Object Identifier (DOI)

  • 10.1002/mrm.26596


  • eng

Conference Location

  • United States