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Developing clinical tools that assess bone matrix quality could improve the assessment of a person's fracture risk. To determine whether Raman spectroscopy (RS) has such potential, we acquired Raman spectra from human cortical bone using microscope- and fiber optic probe-based Raman systems and tested whether correlations between RS and fracture toughness properties were statistically significant. Calculated directly from intensities at wavenumbers identified by second derivative analysis, Amide I sub-peak ratio I 1670 /I 1640 , not I 1670 /I 1690 , was negatively correlated with K init (N = 58; R 2  = 32.4%) and J-integral (R 2  = 47.4%) when assessed by Raman micro-spectroscopy. Area ratios (A 1670 /A 1690 ) determined from sub-band fitting did not correlate with fracture toughness. There were fewer correlations between RS and fracture toughness when spectra were acquired by probe RS. Nonetheless, the I 1670 /I 1640 sub-peak ratio again negatively correlated with K init (N = 56; R 2  = 25.6%) and J-integral (R 2  = 39.0%). In best-fit general linear models, I 1670 /I 1640, age, and volumetric bone mineral density explained 50.2% (microscope) and 49.4% (probe) of the variance in K init . I 1670 /I 1640 and v 1 PO 4 /Amide I (microscope) or just I 1670 /I 1640 (probe) were negative predictors of J-integral (adjusted-R 2  = 54.9% or 37.9%, respectively). While Raman-derived matrix properties appear useful to the assessment of fracture resistance of bone, the acquisition strategy to resolve the Amide I band needs to be identified.

As in clinical studies, finite element analysis (FEA) developed from computed tomography (CT) images of bones are useful in pre-clinical rodent studies assessing treatment effects on vertebral body (VB) strength. Since strength predictions from microCT-derived FEAs (μFEA) have not been validated against experimental measurements of mouse VB strength, a parametric analysis exploring material and failure definitions was performed to determine whether elastic μFEAs with linear failure criteria could reasonably assess VB strength in two studies, treatment and genetic, with differences in bone volume fraction between the control and the experimental groups. VBs were scanned with a 12-μm voxel size, and voxels were directly converted to 8-node, hexahedral elements. The coefficient of determination or R (2) between predicted VB strength and experimental VB strength, as determined from compression tests, was 62.3% for the treatment study and 85.3% for the genetic study when using a homogenous tissue modulus (E t) of 18 GPa for all elements, a failure volume of 2%, and an equivalent failure strain of 0.007. The difference between prediction and measurement (that is, error) increased when lowering the failure volume to 0.1% or increasing it to 4%. Using inhomogeneous tissue density-specific moduli improved the R (2) between predicted and experimental strength when compared with uniform E t=18 GPa. Also, the optimum failure volume is higher for the inhomogeneous than for the homogeneous material definition. Regardless of model assumptions, μFEA can assess differences in murine VB strength between experimental groups when the expected difference in strength is at least 20%.