No abstract

We present an algorithm for automatic anatomical measurements in tomographic datasets of the knee. The algorithm uses a set of atlases, each consisting of a knee image, surface segmentations of the bones, and locations of landmarks required by the anatomical metrics. A multistage volume-to-volume and surface-tovolume registration is performed to transfer the landmarks from the atlases to the target volume. Manual segmentation of the target volume is not required in this approach. Metrics were computed from the transferred landmarks of a best-matching atlas member (different for each bone), identified based on a mutual information criterion. Leave-one-out validation of the algorithm was performed on 24 scans of the knee obtained using extremity cone-beam computed tomography. Intraclass correlation (ICC) between the algorithm and the expert who generated atlas landmarks was above 0.95 for all metrics. This compares favorably to inter-reader ICC, which varied from 0.19 to 0.95, depending on the metric. Absolute agreement with the expert was also good, with median errors below 0.25 deg for measurements of tibial slope and static alignment, and below 0.2 mm for tibial tuberosity-trochlear groove distance and medial tibial depth. The automatic approach is anticipated to improve measurement workflow and mitigate the effects of operator experience and training on reliability of the metrics.

Objective: Deleterious impact loading to cartilage initiates post-traumatic osteoarthritis (OA). While cytokine and enzyme levels regulate disease progression, specific mechanical cues that elucidate cellular OA origins merit further investigation. We defined the dominant pericellular and cellular strain/stress transfer mechanisms following bulk-tissue injury associated with cell death. Method: Using an in vitro model, we investigated rate-dependent loading and spatial localization of cell viability in acute indentation and time-course studies. Atomic force microscopy (AFM) and magnetic resonance imaging (MRI) confirmed depth-wise changes in cartilage micro-/macro-mechanics and structure post-indentation. To understand the transfer of loading to cartilage domains, we computationally modeled full-field strain and stress measures in interstitial matrix, pericellular and cellular regions. Results: Chondrocyte viability decreased following rapid impact (80%/s) vs slow loading (0.1%/s) or unloaded controls. Viability was lost immediately during impact within regions near the indenter-tissue contact but did not change over 7 days of tissue culture. AFM studies revealed a loss of stiffness following 80%/s loading, and MRI studies confirmed an increased tensile and shear strain, but not relaxometry. Image-based patterns of chondrocyte viability closely matched computational estimates of amplified maximum principal and shear strain in interstitial matrix, pericellular and cellular regions. Conclusion: Rapid indentation worsens chondrocyte death and degrades cartilage matrix stiffness in indentation regions. Cell death at high strain rates may be driven by elevated tensile strains, but not matrix stress. Strain amplification beyond critical thresholds in the pericellular matrix and cells may define a point of origin for early damage in post-traumatic OA.