Abstract
Beta-tricalcium phosphate (β-TCP) has been used for bone regeneration in a variety of surgical procedures including dental implant therapy with satisfactory clinical results. However, very little is known about the molecular basis mechanisms enhancing the bone formation by β-TCP. To understand the molecular basis mechanism of β-TCP in bone formation, β-TCP was implanted into bone defects of mandible bones in beagle dogs. After 4, 7 and 14 days, bone tissues during the healing process were recovered and gene expression profiles were examined using an Affymetrix GeneChip system. A significantly higher high-temperature requirement protein A1 (HtrA1) mRNA level was found in the 4-day samples after β-TCP implantation compared with the controls. The elevated HtrA1 gene expressions in β-TCP-implanted bone tissues were confirmed by RT-PCR and real-time PCR. Because HtrA1 is known as a key regulator of physiological and pathological matrix mineralization, the enhancement of HtrA1 gene expression in β-TCP-implanted mandible bone might be one of the molecular mechanisms for stimulating bone formation.
