Morphology, localization and accumulation of in vivo microdamage in human cortical bone

Abstract

In vivo, microdamage occurs in the form of linear microcracks and diffuse damage. However, it is unknown whether the age-related changes in bone quality predispose bone to form one type of damage morphology over the other during in vivo loading. In this study, histological and histomorphometrical analyses were conducted on transverse cross sections, obtained from the tibiae of aging human bone (age 19 to 89), to investigate the in vivo accumulation and localization of damage morphologies. The results demonstrate that old donor bone (83+/-3 years) contains more linear microcracks than younger donor bone in the cortices predominantly subjected to compressive (p<0.01) and tensile loading (p<0.01). In contrast, young donor bone (40+/-10 years) contains more diffuse damage than older donor bone in the cortex predominantly subjected to tensile loading (p<0.01). The formation of damage morphology showed no correlation with bone geometry parameters and exhibited distinct preferences with bone microstructure. Linear microcracks formed in the interstitial bone (p<0.01) and were either trapped or arrested by the microstructural interfaces (cement line and lamellar interface) (p<0.05). Areas of diffuse damage, however, were preferentially associated with secondary osteonal bone (p<0.01) and had no relationship with the microstructural interfaces (p<0.01). Based upon these findings, we conclude that age-related changes in bone microstructure, but not bone geometry, play a key role in the propensity of old donors to form linear microcrack over diffuse damage under in vivo loading conditions.

Figure 1

In vivo linear microcracks (a: under bright-field microscopy; b: under a laser confocal microscope) and diffuse damage (c: under bright-field microscopy; d: under a laser confocal microscope) in human cortical bone. Scale bars = 50 μm.

Figure 2

Schematic representation of microdamage morphologies and their relationship with the microstructural interfaces. LM₁: linear microcrack that either formed at the lamellar interface or was stopped at the cement line. LM₂: linear microcrack that neither formed at the lamellar interface nor was stopped at the cement line. DD₁: diffuse damage patch that was either limited to one lamella or was stopped at the cement line. DD₂: diffuse damage patch that was neither limited to one lamella nor was stopped at the cement line.

Figure 3

Bones obtained from old donors contained more linear microcracks than the bones from young donors in both the anterior and posterior cortices (a). In contrast, bones obtained young donors contained more diffuse damage than bones from old donors in the anterior cortex (b). * indicates p < 0.05.

Figure 4

More linear microcracks formed in interstitial bone than secondary osteonal bone (a), while more diffuse damage developed in secondary osteonal bone than interstitial bone (b). * indicates p < 0.05.

Figure 5

More linear microcracks either formed at the lamellar interface or were stopped at the cement line (LM₁) (a). In contrast, diffuse damage patches were neither limited to one lamella nor were stopped at the cement line (DD₂) (b). * indicates p < 0.05.