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Histomorphometric and molecular biologic comparison of bioactive glass granules and autogenous bone grafts in augmentation of bone defect healing

✍ Scribed by Virolainen, P. ;Heikkil�, J. ;Yli-Urpo, A. ;Vuorio, E. ;Aro, H. T.


Publisher
John Wiley and Sons
Year
1997
Tongue
English
Weight
311 KB
Volume
35
Category
Article
ISSN
0021-9304

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✦ Synopsis


The applicability of bioactive glass (BG) granules as a levels of TGF-ͱ1 and type I collagen mRNAs during the substitute for bone grafts was tested by comparing the first 2 weeks of healing, whereas BG-filled defects showed histologic, histomorphometric, and molecular biologic heal-biphasic expression patterns of the same genes. Spontaneing patterns to those of bone autografts and ungrafted ous new bone formation in ungrafted bone defects was bone defects in a rat model. The cellular response in defects also characterized by biphasic expression of type I collagen filled with BG granules was characterized by continuous gene. Osteonectin mRNA declined gradually over time in overexpression of type III collagen. Osteogenic mesenchy-autografted and BG filled defects, whereas unfilled defects mal cells, prior to their differentiation to osteoblasts, orga-showed a gradual increase of osteonectin mRNA during nized as a dense periosteumlike layer on the surface of healing. By 8 weeks, about 70% of the BG surface showed the BG granules. By day 14 new bone formation was more evidence of direct new bone contact. Energy-dispersing Xextensive in autografted defects than in BG filled defects ray analyses confirmed the presence of silica-rich and CaP-( p ϭ 0.039). No cartilage-specific type II collagen mRNA rich zones at the bonding interface. In conclusion, the was detectable, confirming the uniformity of intramembra-osteoconductive surface of bioactive glass granules effinous bone formation. The difference in the initiation of ciently bonds to ongrowing new bone but the material new bone formation was further confirmed by the mRNA does not reach the capacity of autogenous bone graft in analyses of the de novo production of TGF-ͱ1 and type I promotion of osteogenesis.


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