| Autor: |
Wehrhan, F, Hyckel, P, Amann, K, Ries, J, Stockmann, P, Schlegel, KA, Neukam, FW, Nkenke, E |
| Předmět: |
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| Zdroj: |
Oral Diseases; May2011, Vol. 17 Issue 4, p433-442, 10p, 3 Color Photographs |
| Abstrakt: |
Oral Diseases (2011) , 433-442 Bone-destructive disease treatments include bisphosphonates and antibodies against receptor activator for nuclear factor κB ligand (aRANKL). Osteonecrosis of the jaw (ONJ) is a side-effect. Aetiopathology models failed to explain their restriction to the jaw. The osteoproliferative transcription factor Msx-1 is expressed constitutively only in mature jaw bone. Msx-1 expression might be impaired in bisphosphonate-related ONJ. This study compared the expression of Msx-1, Bone Morphogenetic Protein (BMP)-2 and RANKL, in ONJ-affected and healthy jaw bone. An automated immunohistochemistry-based alkaline phosphatase-anti-alkaline phosphatase method was used on ONJ-affected and healthy jaw bone samples ( n = 20 each): cell-number ratio (labelling index, Bonferroni adjustment). Real-time RT-PCR was performed to quantitatively compare Msx-1, BMP-2, RANKL and GAPDH mRNA levels. Labelling indices were significantly lower for Msx-1 ( P < 0.03) and RANKL ( P < 0.003) and significantly higher ( P < 0.02) for BMP-2 in ONJ compared with healthy bone. Expression was sevenfold lower ( P < 0.03) for Msx-1, 22-fold lower ( P < 0.001) for RANKL and eightfold higher ( P < 0.02) for BMP-2 in ONJ bone. Msx-1, RANKL suppression and BMP-2 induction were consistent with the bisphosphonate-associated osteopetrosis and impaired bone remodelling in BP- and aRANKL-induced ONJ. Msx-1 suppression suggested a possible explanation of the exclusivity of ONJ in jaw bone. Functional analyses of Msx-1- RANKL interaction during bone remodelling should be performed in the future. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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