Head injuries resulting from motor vehicle crashes (MVC) are extremely common, yet the details of the mechanism of injury remain to be well characterized. Skull deformation is believed to be a contributing factor to some types of traumatic brain injury (TBI). Understanding biomechanical contributors to skull deformation would provide further insight into the mechanism of head injury resulting from blunt trauma. In particular, skull thickness is thought be a very important factor governing deformation of the skull and its propensity for fracture. Previously, age-and sex-based skull cortical thickness changes were difficult to evaluate based on the need for cadaveric skulls. In this cross-sectional study, skull thickness changes with age and sex have been evaluated at homologous locations using a validated cortical density-based algorithm to accurately quantify cortical thickness from 123 high-resolution clinical computed tomography (CT) scans. The flat bones of the skull have a sandwich structure; therefore, skull thickness was evaluated for the inner and outer tables as well the full thickness. General trends indicated an increase in the full skull thickness, mostly attributed to an increase in the thickness of the diploic layer; however, these trends were not found to be statistically significant. There was a significant relationship between cortical thinning and age for both tables of the frontal, occipital, and parietal bones ranging between a 36% and 60% decrease from ages 20 to 100 years in females, whereas males exhibited no significant changes. Understanding how cortical and full skull thickness changes with age from a wide range of subjects can have implications in improving the biofidelity of age-and sex-specific finite element models and therefore aid in the prediction and understanding of TBI from impact and blast injuries.

Rib cage morphology changes with age and sex are expected to affect thoracic injury mechanisms and tolerance, particularly for vulnerable populations such as pediatrics and the elderly. The size and shape variation of the external geometry of the ribs was characterized for males and females aged 0-100 years. Computed tomography (CT) scans from 339 subjects were analyzed to collect between 2700 and 10 400 homologous landmarks from each rib. Rib landmarks were analyzed using the geometric morphometric technique known as Procrustes superimposition. Age-and sex-specific functions of 3D rib morphology were produced representing the combined size and shape variation and the isolated shape variation. Statistically significant changes in the size and shape variation (P < 0.0001) and shape variation (P < 0.0053) of all 24 ribs were found to occur with age in males and females. Rib geometry, location, and orientation varied according to the rib level. From birth through adolescence, the rib cage experienced an increase in size, a decrease in thoracic kyphosis, and inferior rotation of the ribs relative to the spine within the sagittal plane. From young adulthood into elderly age, the rib cage experienced increased thoracic kyphosis and superior rotation of the ribs relative to the spine within the sagittal plane. The increased roundedness of the rib cage and horizontal angling of the ribs relative to the spine with age influences the biomechanical response of the thorax. With the plane of the rib oriented more horizontally, loading applied in the anterior-posterior direction will result in increased deformation within the plane of the rib and an increased risk for rib fractures. Thus, morphological changes may be a contributing factor to the increased incidence of rib fractures in the elderly. The morphological functions derived in this study capture substantially more information on thoracic skeleton morphology variation with age and sex than is currently available in the literature. The developed models of rib cage anatomy can be used to study age and sex variations in thoracic injury patterns due to motor vehicle crashes or falls, and clinically relevant changes due to chronic obstructive pulmonary disease or other diseases evidenced by structural and anatomic changes to the chest.

No abstract

The objective of this study was to determine the ability of either aerobic or resistance training to counter weight-loss-associated bone loss in older adults. There were 187 older adults (67 years, 70% women, 64% white) with obesity (BMI = 34.5 ± 3.7 kg/m ) and cardiovascular disease and/or metabolic syndrome who were randomized to participate in an 18-month, community-based trial, with a follow-up assessment at 30 months. Intervention arms included: weight loss alone (WL; 7% to 10% baseline weight), WL plus aerobic training (WL + AT), and WL plus resistance training (WL + RT), as well as DXA-acquired total hip, femoral neck, and lumbar spine areal bone mineral density (aBMD), and trabecular bone score (TBS). Biomarkers of bone turnover (procollagen type 1 N-terminal propeptide, C-terminal telopeptide of type 1 collagen) were measured at baseline, 6, 18, and 30 (aBMD and TBS only) months. CT-acquired hip and spine volumetric BMD (vBMD), cortical thickness, and bone strength were measured in a subset at baseline (n = 55) and 18 months. Total hip aBMD was reduced by 2% in all groups at 18 months, with a primary analysis showing no significant treatment effects for any DXA, biomarker, or CT outcome. After adjustment for WL and follow-up at 30 months, secondary analyses revealed that total hip [-0.018 (-0.023 to -0.012) g/cm versus -0.025 (-0.031 to -0.019) g/cm ; p = 0.05] and femoral neck [-0.01 (-0.009 to 0.008) g/cm versus -0.011 (-0.020 to -0.002) g/cm ; p = 0.06] aBMD estimates were modestly attenuated in the WL + RT group compared with the WL group. Additionally, lumbar spine aBMD was increased in the WL [0.015 (0.007 to 0.024) g/cm ] and the WL + RT [0.009 (0.000 to 0.017) g/cm ] groups compared with the WL + AT [-0.003 (-0.012 to 0.005)g/cm ] group; both p ≤ 0.01. Community-based exercise does not prevent bone loss during active WL in older adults; however, adding RT may help minimize long-term hip bone loss. © 2018 American Society for Bone and Mineral Research.