TNF-alpha modulates alveolar bone repair under homeostatic conditions in mice (44.1)

Abstract

Abstract Cytokines have been implicated in the pathogenesis of bone diseases, but its role in bone repair process remains unknown. Our objective was to characterize the role of TNF-alpha in alveolar bone healing after tooth extraction in mice. Following the extraction of the right upper incisor of C57Bl/6(WT) and TNFp55KO strains, the maxilla containing the remaining alveolus was collected for histomorphometric and molecular (RealTimePCR) analysis. In WT mice the initial formation of clot was followed by the transient inflammatory infiltrate and a granulation tissue, gradually substituted by bone. In WT mice TNF-a mRNA was detected with an initial peak at 7 days, followed by a decreasing expression over time and a second peak at 28 days. Bone markers expression presented an initial high expression of COL-I, followed by CBFA-1 and ALP and subsequently by OCN and PHEX. TNFp55KO strain presented a delayed angiogenesis and osteogenesis processes, increased inflammatory reaction, despite of a decrease in CXCL1, CCL-2 and CCL3 levels; and increased COL-I mRNA levels and decreased CBFA-1, ALP, OCN and PHEX expression. The results presented here demonstrate that the absence of TNF-alpha interferes in alveolar bone repair through mechanisms that involve the modulation of inflammatory cell migration and osteogenic markers expression during the course of alveolar bone repair.