The Impact of Aging on Bone Regeneration in Mice

Abstract

Older people are projected to outnumber children for the first time in U.S. history by 2030 (U.S. Census Bureau, 2017), creating a tsunami of people with reduced bone strength who are more susceptible to bone injury and fracture. Decreased bone quality has a multivariate causal path including loss of progenitor cells, reduced anabolic and catabolic capabilities of cells, and increased senescence. The age‐related cellular decline of bone begins prior to the onset of bone diseases such as osteoporosis. Thus, aging models exclusive of disease can be immensely beneficial in finding novel angles of approach for better bone healing during aging. With this in mind, our study uses the well‐characterized mouse digit amputation model. After amputation of the digit tip young mice are able to regrow patterned bone via direct ossification and soft tissue. However, regeneration in aged mice is delayed, and the regenerated bone is architecturally inferior showing decreased trabecular thickness, increased trabecular spacing, and an attenuated distal growth of the bone. Here we explore the impact of aging on regeneration and bone architecture, introduce a new method of analysis for bone architecture and discuss the advantages to alternative analysis for bone regeneration in the digit model.Support or Funding InformationCOBRE Grant ‐ 2P20GM103629 in addition to CELT LS‐LAMP Grant