Journal of orthopaedic research : official publication of the Orthopaedic Research Society
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The rate of bone formation to bridge a fracture gap slows with age. To explore potential pathogenic mechanisms and possible negative-feedback responses by the skeleton to this reduced rate of healing, mRNA transcripts up-regulated more and/or longer were studied in older rats with delayed healing. Female rats at 6 (young), 26 (adult), and 52 (old) weeks of age received unilateral diaphyseal femoral fractures with intramedullary rod stabilization. ⋯ Of these, 60 were selected for more intense review. Significantly more and/or longer expression was seen in genes related to myofibroblasts, cell proliferation, calcification inhibition, TGF-beta activity, lipid metabolism, cell adhesion, and the cytoskeleton. Further study is needed to determine if these up-regulated transcripts are related to the pathological processes which slow healing or are related to attempts by the fracture tissue to stimulate bone to bridge the fracture gap.