Bone healing in an aged murine fracture model is characterized by sustained callus inflammation and decreased cell proliferation

We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Geriatric fractures take longer to heal and heal with more complications than those of younger patients; however, the mechanistic basis for this difference in healing is not well understood. To improve this understanding, we investigated cell and molecular differences in fracture healing between 5 month-old (young adult) and 25 month-old (geriatric) mice healing utilizing high-throughput analysis of gene expression. Mice aged 5 months “young” or 25 months “geriatric” underwent bilateral tibial fractures and fracture calluses were harvested at 0, 5, 10, and 20 days post fracture (DPF) for analysis, yielding a total of 41 samples. For each time point and DPF, a group of 5 to 6 unique mice were harvested. Global gene expression analysis was performed using Affymetrix MoGene 1.0 ST microarrays. After normalization, data were compared using ANOVA and evaluated using Principal Component Analysis (PCA), CTen, heatmap, and Incromaps analysis.