Trabecular bone is an essential load-bearing tissue that remodels in response to external loads, creating a self-optimizing, materially heterogeneous microstructure. Tissue material heterogeneity and microstructure are captured in detail in micro-computed tomography (micro-CT) images, which may be converted into 3D models for finite element analysis (FEA) to study trabecular bone mechanics. This approach combined with a recently-developed individual trabecular segmentation (ITS) algorithm revealed distinct, orientation-dependent mechanical roles for trabecular plates and rods, suggesting plate-rod organization may be important for trabecular bone mechanical function and indicative of healthy development. Conversely, plate-rod disorganization may indicate adaptation to pathological loads, such as following brachial plexus birth injury (BPBI), a nerve injury affecting 0.1-0.3% of newborns with a substantial risk of lifelong arm impairment.

Outcomes following BPBI depend on injury location:​ muscle contracture, moderate paralysis, substantial glenohumeral joint dysplasia and mild trabecular deficits, or severe paralysis, mild joint dysplasia and severe trabecular deficits are associated with postganglionic and preganglionic injuries, respectively. Altered joint forces due to contracture and abnormal loading are believed to cause joint dysplasia, but how changes in sub-surface trabecular bone influence this process remains unknown. Therefore, this work aims to explore this knowledge gap and provide a more complete description of injury location-dependent changes to joint forces and bone following BPBI.

The initial goals of this dissertation were to examine the effect of material heterogeneity on trabecular bone mechanical performance and develop new metrics describing trabecular plate-rod organization. Through combined FEA and ITS, we determined heterogeneity was not critical for predicting trabecular bone apparent modulus but contributed to early tissue failure concentration in trabecular rods. Using ITS data, the structural organization index (SOI) was developed to quantify plate-rod organization and its relationship to trabecular bone yield behavior was demonstrated.

Subsequently, we aimed to characterize differential changes in trabecular plates and rods in the scapula following preganglionic and postganglionic BPBI in a rat model, and examine relationships among plate-rod organization, glenoid dysplasia, glenohumeral joint reaction forces (JRFs), and trabecular tissue mechanics. By analyzing sub-glenoid micro-CT volumes of interest with ITS and SOI, trabecular deficits following BPBI were found to be most severe in plates, with the worst outcomes following preganglionic injury. Trabecular disorganization indicated by SOI ranged from severe to mild following postganglionic and preganglionic injury, respectively, and was somewhat associated with glenoid dysplasia. Through analyses ofspecimen-specific musculoskeletal models, passive shoulder internal rotation contracture was observed following postganglionic, but not preganglionic injury, consistent with expectations. Further analyses throughout the shoulder protraction range of motion (ROM) indicated that both injuries, but primarily postganglionic injury, increased JRF directional variability across different limb postures, which correlated with plate-rod disorganization. Across analyses, postganglionic and preganglionic injuries were associated with mildly and severely reduced JRF magnitudes, respectively. Finally, FEA simulating glenohumeral joint contact based on JRFs and joint postures from musculoskeletal modeling was used to examine changes in trabecular tissue mechanics following BPBI. While these analyses were inconclusive, likely resulting from few samples, a novel pipeline was developed bridging musculoskeletal modeling and FEA, with potential applications for studying joint contact in multiple postures.

Overall, this work demonstrates the influence of trabecular tissue heterogeneity on plate and rod mechanics and suggests trabecular disorganization following BPBI is linked to JRF directional variability without severely reduced magnitude and may be important for differentiating cases that result in glenoid dysplasia from those that do not. Though further work is needed to examine how trabecular disorganization, JRF variability, and glenoid dysplasia progress over time, this work contributes to a fuller understanding of bone development following BPBI that may eventually enable more effective and appropriately-timed clinical interventions to improve long-term outcomes