Shear-wave elastography is reproducible for assessment of the SSP muscle. Mean normal SSP SWV is 3.0 m/sec ± 0.5. SWV decreases with increasing fat content (Goutallier stage 0-III) and increases in the final stage of fatty infiltration (Goutallier stage IV).

Charcot foot refers to an inflammatory pedal disease based on polyneuropathy; the detailed pathomechanism of the disease is still unclear. Since the most common cause of polyneuropathy in industrialized countries is diabetes mellitus, the prevalence in this risk group is very high, up to 35%. Patients with Charcot foot typically present in their fifties or sixties and most of them have had diabetes mellitus for at least 10 years. If left untreated, the disease leads to massive foot deformation. This review discusses the typical course of Charcot foot disease including radiographic and MR imaging findings for diagnosis, treatment, and detection of complications.

Femoral and tibial torsion measurements in children using 3D models based on biplanar radiography are comparable to CT measurement results. Despite skeletal immaturity, torsion measurements in children on biplanar radiography seem to be as reliable as those on CT images.

The aim of this study was to quantitatively assess changes in collagen structure using MR T1-and T2*-mapping in a novel controlled ex vivo tendon model setup. MATERIALS AND METHODS Twenty-four cadaveric bovine flexor tendons underwent MRI at 3 T before and after chemical modifications, representing mechanical degeneration and augmentation. Collagen degradation (COL), augmenting collagen fiber cross-linking (CXL), and a control (phosphate-buffered saline [PBS]) were examined in experimental groups, using histopathology as standard of reference. Variable echo-time and variable-flip angle gradient-echo sequences were used for T2*-and T1-mapping, respectively. Standard T1-and T2-weighted spin-echo sequences were acquired for visual assessment of tendon texture. Tendons were assessed subsequently for their biomechanical properties and compared with quantitative MRI analysis. RESULTS T1-and T2*-mapping was feasible and repeatable for untreated (mean, 545 milliseconds, 2.0 milliseconds) and treated tendons. Mean T1 and T2* values of COL, CXL, and PBS tendons were 1459, 934, and 1017 milliseconds, and 5.5, 3.6, and 2.5 milliseconds, respectively. T2* values were significantly different between enzymatically degraded tendons, cross-linked tendons, and controls, and were significantly correlated with mechanical tendon properties (r =-0.74, P < 0.01). T1 values and visual assessment could not differentiate CXL from PBS tendons. Photo-spectroscopy showed increased autofluorescence of cross-linked tendons, whereas histopathology verified degenerative lesions of enzymatically degraded tendons. CONCLUSIONS T2*-mapping has the potential to detect and quantify subtle changes in tendon collagen structure not visible on conventional clinical MRI. Tendon T2* values might serve as a biomarker for biochemical alterations associated with tendon pathology.