Aging and accumulation of microdamage in canine bone

Abstract

Fractures associated with minimal trauma are common in aged human beings. However, bone safety margins are better preserved in aged dogs, which are rarely affected with minimal trauma fractures. Although the hierarchical architecture of canine and human compact bone is similar, the precise reasons for this species difference are unclear. Cyclic loading of bone during normal daily activity leads to the formation of microcracks within the tissue matrix of compact bone. Using a standard bulk-staining technique with basic fuchsin, we examined calcified transverse sections of the mid-diaphysis of the canine humerus from dogs of varying ages. We found that the amount of microdamage and porosity increased exponentially with aging, although the increases were relatively small, compared with human bone. Gender (female, ovariohysterectomized female, male, castrated male) did not have a significant effect on the amount of microdamage or porosity in bone. Alterations to the local material properties of bone tissue, or alterations to the local tissue repair responses, may play a role in the accumulation of microdamage in bone with aging. Determination of osteocyte lacunar density (number of osteocyte lacunae per bone area) and activation frequency (number of actively remodeling osteons per bone area per year) indicated that these variables declined exponentially with aging. There also was a trend for bone from dogs with low osteocyte lacunar density to have a higher microcrack density, but not higher porosity. Furthermore, bones with a high activation frequency did not accumulate microcracks or porosity. Taken together, these data suggest that, in canine bone, although a certain minimum number of osteocytes may be essential for an operational network that forms part of the signaling pathways that orchestrate repair of bone microdamage, increases in porosity with aging may not be directly associated with impaired function of the osteocyte network within bone.