Various tissues in the human body, including cartilage, are known to calcify with aging. In cartilage, calcified regions may be thought of as inclusions within a cartilage substrate. Their presence undoubtedly affects the bulk mechanical response of the cartilage, but neither the nature of the calcifications nor their effect on mechanical response has been quantified. An understanding of these phenomena is important;​ for example, in the case of restraint loading in an automotive crash. Studies have found that in automotive crashes, older drivers are more prone to thoracic injuries and also are more likely to die from a chest injury. Costal cartilage calcification may be one aspect of aging that contributes to a decreased injury tolerance, so understanding its nature and mechanics can aid in the development of safety measures to help protect older drivers. There currently is no material model that accounts for the calcification in the costal cartilage, which could affect the structural response of the rib cage, and thus change the mechanisms and tolerance of injury.

The primary goal of this dissertation is to investigate, through the development of a calcifying cartilage model, whether the calcifications morphologies present in the costal cartilage change its effective material properties. In accomplishing this goal, the material properties of aging human costal cartilage were characterized through displacement controlled spherical indentation testing. MicroCT imaging was used to investigate the qualitative and quantitative properties of the calcifying costal cartilage. Finally, using the material properties of the cartilage substrate from indentation testing, and the microstructures of calcifications from microCT, a microstructural model of the calcifying costal cartilage was developed using the Generalized Method of Cells micromechanical analysis.

Calcifications were found to be present throughout the costal cartilage and ranged from small diffuse calcifications, to nodes, rods, plates, and even large complex structures that exhibited microstructural morphology similar to the cross-section of diaphysial bone, with a dense shell surrounding a trabecular core. The solid microstructure was most common for calcifications (44.5%), and the morphologies were found to vary by location, with rods and plates being most prevalent on the periphery of the cartilage (91.7% of all rods, 98.4% of all plates). On average, the calcifications and adjacent rib bone exhibited similar mineral densities (660mgHA/cm³) and the calcification volume fraction (VF) was as high as 20%, comparable to that of the rib bone.

Localized regions of calcification had mineral densities as high as 1200 mgHA/cm³, which was much higher than exhibited in the rib bone (814 mgHA/cm³). On the structural level, the average length of contiguous calcification infiltrating from the costo-chondral junction into the costal cartilage was 19.21 ± 11.65 mm. A calcified cartilage material model was developed using the morphologies of calcifications obtained from microCT and the relaxed elastic modulus of the human costal cartilage obtained from indentation testing (E_∞ = 5.07 MPa). The homogenized model of calcifying cartilage found that the calcifications alter the effective material behavior of the cartilage, and the effect is highly dependent on the microstructural connectivity of the calcification. Floating calcifications with limited connectivity ranging from 0-18% VF resulted in effective elastic moduli up to 8MPa compared to the baseline value of 5 MPa for the cartilage. Attached calcification with high connectivity, typically corresponding to higher VF 18-25% resulted in effective moduli of 20-66 MPa, and depending on the microstructure, began to introduce anisotropy to the material. The calcifying cartilage model developed in this dissertation can be incorporated into biomechamical models of the aging thorax to better understand how calcifications in the aging thorax affect the structural response of the rib cage.