ラットの象牙質とエナメル質の形成に及ぼすメチルプレドニゾロン長期投与の影響

メチルプレドニゾロン(mPSL)の長期投与が, 歯の形成にどのような影響を及ぼすかについてラットを用いて検討した。0,2.5,5,10,20mg/kg/dayのmPSLを5週齢のラットに4週間, 皮下投与した。象牙質形成量を測定するためニトリロトリ酢酸鉛による硬組織内時刻描記を適宜施した。下顎切歯について切端側と歯根側の2ヶ所から脱灰横断標本を作製した。また, 0および10mg/kg/dayのmPSLを4週間投与した別のラットについて, 屠殺1時間前に3H-プロリンを投与し, 下顎切歯矢状縦断標本のラジオオートグラフを作製した。象牙芽細胞とエナメル芽細胞の基質合成・分泌活性を測定するために, 細胞上および基質上にみられる銀粒子数を測定した。その結果, (1)象牙質の形成量と幅径はmPSLにより用量依存的に抑制された。また, 象牙質幅径の抑制に比例して歯髄径は用量依存的に拡大した。(2)象牙芽細胞による3H-プロリンの取り込みと基質中への分泌はmPSLの投与により抑制された。この抑制は基質形成前期の象牙芽細胞ではみられず, 基質形成後期の象牙芽細胞においてみられた。また, 象牙芽細胞の高さと象牙前質の幅についても基質形成前期には影響はみられず, 基質形成後期に減少がみられた。(3)mPSLの投与によりエナメル芽細胞の3H-プロリンの取り込みと分泌量には対照群との間に差はみられず, エナメル質の厚さにも変化はみられなかった。以上の結果からmPSLは象牙質の形成を用量依存的に抑制することが示された。一方, エナメル質の形成は象牙質形成に較べて影響を受けにくいと考えられた。

The present study was undertaken to investigate whether long-term administration of methylprednisolone (mPSL) inhibits formation of dentin and enamel. Fifty male Wistar rats were given O, 2.5,5,10,or 20 mg/kg/day of mPSL by subcutaneous injection for 4 weeks. All rats received lead nitrilotriacetate to chronologically label the growing dentin. Decalcified transverse sections were prepared from the apical and incisal portions of mandibular incisors. In another experiment, 12 rats were given either 0 or 10 mg/kg/day of mPSL by subcutaneous injection for 4 weeks. They were given 3H-proline I hour before sacrifice. To examine the matrix synthetic and secretory activities of odontoblasts and ameloblasts, radioautographs of longitudinal specimens of incisor dentin and enamel were prepared. Silver grains over the odontoblasts, amelob-lasts and matrices were counted at different stages of cell maturation. The following results were obtained : (1) mPSL inhibited dentin formation in a dose-dependent fashion. The inhibition was accompanied by a proportional decrease in the thickness of dentin and an inversely proportional increase in the dental pulp. The above changes were observed in specimens from the incisal portion, but not in those from the apical portion. (2) Incorporation and secretion of 3H-proline by odontoblasts was inhibited by mPSL. This inhibition was observed in odontoblasts during late, but not early, dentin formation. The width of predentin and height of odontoblasts also decreased during late dentin formation. (3) Throughout maturation of ameloblasts, incorporation and secretion of 3H-proline by ameloblasts was not affected by mPSL. Enamel thickness was also unaffected by mPSL. These findings indicate that long-term administration of mPSL dose-dependently inhibits dentin formation, especially during the late stage. However mPSL might not affect enamel formation.