Effect of osteocalcin deficiency on the nanomechanics and chemistry of mouse bones.

In healthy bone there is a balance between bone resorption and formation. When an imbalance occurs there is an overall loss of bone mass leading to an increased risk of fracture. The deterioration is typically accompanied by changes in the non-collagenous proteins in the bone. Osteocalcin (OC) is the most abundant noncollageneous bone matrix protein and it is believed to play a role in bone formation and resorption. Nanoindentation and Raman microspectroscopy have been used to correlate the mechanical and chemical properties of cortical bone from femora of OC -/- (osteocalcin deficient) mice and their wild-type controls (OC +/+). There are significant intra-bone variations in mechanics and crystallinity especially in the mid-cortical section for OC -/- mice compared to OC +/+ mice. Type-B carbonate substitution decreased significantly in the absence of osteocalcin and this appears to affect the hardness more than the elasticity. The results suggest that OC plays a role in the growth of apatite crystals in bone by increasing the degree of carbonate substitutions. The addition of these defects to the apatite's crystal lattice has little effect on elasticity, but does appear to reduce the bone's hardness.