Numerical and experimental simulation of the effect of long bone fracture healing stages on ultrasound transmission across an idealized fracture.

The effect of various stages of fracture healing on the amplitude of 200 kHz ultrasonic waves propagating along cortical bone plates and across an idealized fracture has been modeled numerically and experimentally. A simple, water-filled, transverse fracture was used to simulate the inflammatory stage. Next, a symmetric external callus was added to represent the repair stage, while a callus of reducing size was used to simulate the remodeling stage. The variation in the first arrival signal amplitude across the fracture site was calculated and compared with data for an intact plate in order to calculate the fracture transmission loss (FTL) in decibels. The inclusion of the callus reduced the fracture loss. The most significant changes were calculated to occur from the initial inflammatory phase to the formation of a callus (with the FTL reducing from 6.3 to between 5.5 and 3.5 dB, depending on the properties of the callus) and in the remodeling phase where, after a 50% reduction in the size of the callus, the FTL reduced to between 2.0 and 1.3 dB. Qualitatively, the experimental results follow the model predictions. The change in signal amplitude with callus geometry and elastic properties could potentially be used to monitor the healing process.

Modelling the effects of different fracture geometries and healing stages on ultrasound signal loss across a long bone fracture.

The effect on the signal amplitude of ultrasonic waves propagating along cortical bone plates was modelled using a 2D Finite Difference code. Different healing stages, represented by modified fracture geometries were introduced to the plate model. A simple transverse and oblique fracture filled with water was introduced to simulate the inflammatory stage. Subsequently, a symmetric external callus surrounding a transverse fracture was modelled to represent an advanced stage of healing. In comparison to the baseline (intact plate) data, a large net loss in signal amplitude was produced for the simple transverse and oblique cases. Changing the geometry to an external callus with different mechanical properties caused the net loss in signal amplitude to reduce significantly. This relative change in signal amplitude as the geometry and mechanical properties of the fracture site change could potentially be used to monitor the healing process.

An in vitro study of ultrasound signal loss across simple fractures in cortical bone mimics and bovine cortical bone samples.

Measurements have been performed on Sawbones and bovine cortical bone samples at 200 kHz using an axial transmission technique to investigate the factors that determine how ultrasonic waves propagate across a simulated fracture. The peak amplitude of the first arrival signal (FAS) was studied. Results taken from intact specimens were compared with those produced when a simple transverse fracture was introduced. These fracture simulation experiments were found to be consistent with Finite Difference modelling of the experimental conditions. The peak amplitude showed a characteristic variation across the fracture caused by interference between reradiated and scattered/diffracted waves at the fracture site and a net Fracture Transmission Loss (FTL). For small fracture gaps, the change in amplitude was sensitive to the presence of the fracture. This sensitivity suggests that this parameter could be a good quantitative indicator for the fracture healing process assuming the relative change in this parameter brought about by healing is measurable.

Ultrasonic propagation in cortical bone mimics.

Understanding the velocity and attenuation characteristics of ultrasonic waves in cortical bone and bone mimics is important for studies of osteoporosis and fractures. Three complementary approaches have been used to help understand the ultrasound propagation in cortical bone and bone mimics immersed in water, which is used to simulate the surrounding tissue in vivo. The approaches used were Lamb wave propagation analysis, experimental measurement and two-dimensional (2D) finite difference modelling. First, the water loading effects on the free plate Lamb modes in acrylic and human cortical bone plates were examined. This theoretical study revealed that both the S0 and S1 mode velocity curves are significantly changed in acrylic: mode jumping occurs between the S0 and S1 dispersion curves. However, in human cortical bone plates, only the S1 mode curve is significantly altered by water loading, with the S0 mode exhibiting a small deviation from the unloaded curve. The Lamb wave theory predictions for velocity and attenuation were then tested experimentally on acrylic plates using an axial transmission technique. Finally, 2D finite difference numerical simulations of the experimental measurements were performed. The predictions from Lamb wave theory do not correspond to the measured and simulated first arrival signal (FAS) velocity and attenuation results for acrylic and human cortical bone plates obtained using the axial transmission technique, except in very thin plates.

Changes in sciatic nerve cathepsin D after ligation or exposure to neurotoxins.

The content and distribution of cathepsin D, a lysosomal acidic endopeptidase, were determined by immunochemical methods in rat sciatic nerve near the site of a ligature or after exposure of animals to neurotoxins. In normal sciatic nerve, cathepsin D was localized predominantly in the perinuclear regions of Schwann cells. In ligated nerve, cathepsin D increased equally in both the proximal and distal nerve segments adjacent to the ligature. Although orthograde and retrograde axonal transport of cathepsin D may have contributed to this increase, immunocytochemical methods indicated that Schwann cells or other phagocytic cells accounted for the bulk of the increased cathepsin D content of nerve. Axonal function was nontraumatically altered by the administration of 2,5-hexanedione, acrylamide, B,B'-iminodipropionitrile or zinc pyridinethione. Exposure to any of these neurotoxins raised cathepsin D content throughout the sciatic nerve twofold or more, and greater amounts of immunoreactive cathepsin D in the cytoplasm of Schwann cells could be demonstrated immunocytochemically. These results indicate that changes in cathepsin D content of Schwann cells may be a reflection of their catabolic activity. The increased Schwann cell cathepsin D content in toxic axonopathies is further proof for an enhanced Schwann cell role as a phagocyte resulting from axonal injury.