Abstract
Critical size defects (CSD) fail to heal and regenerate bone while noncritical defects produce an acceptable repair after bone loss. To improve outcome following significant bone loss we sought to identify genes differentially expressed between a 4 mm (noncritical) and 8 mm (critical) size defect in a rat calvarial model. Calvarial defects were created in 12 week‐old rats (6 per group) and RNA was extracted from the defect at 1, 3, 5, 7, 10, 14 and 21 days after injury. Following labeling and hybridization to Agilent rat whole genome microarrays, analysis with GeneSpring® software indicated 3,564 genes were significantly altered in their expression over all time points, 299 were unidentified genes and ESTs. Gene ontology and functional classification of genes altered in expression between the CSD and non‐CSD identified 122 statistically significant, differentially expressed genes related to bone and muscular development, function, and disorders. Microarray findings were validated with RT‐PCR. By reference to Ingenuity Pathway Analysis many of these 122 genes were related to the canonical Wnt/β‐catenin and Runx2 signaling pathways. Knowledge acquired through analysis of gene activity at each stage of bone healing and non‐healing is contributing to our understanding of bone repair and regeneration, and may provide the basis for healing critical size defects.
Published Version
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