Pulpal responses to bacterial contamination following dentin bridging beneath hard-setting calcium hydroxide and self-etching adhesive resin system
Pulpal responses to bacterial contamination following dentin bridging beneath hard-setting calcium hydroxide and self-etching adhesive resin system
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DOI：
10.1111/j.1600-9657.2007.00517.x
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发表时间：
2008-04-01
影响因子：
2.5
通讯作者：
Tagami, Junji
中科院分区：
文献类型：
--
作者：
Kitasako, Yuichi;Ikeda, Masaomi;Tagami, Junji
为了评估在硬固化氢氧化钙（DY：Dycal，L.D.）Caulk Co.）和自蚀刻粘合剂树脂（2 V：Clearfil Liner Bond 2 V，Kuraray Medical Inc.）牙本质桥形成后。在30颗猴牙上制备V类洞，用硬质合金钻穿过洞底暴露牙髓。每个暴露的牙髓用DY或2 V覆盖。用混合树脂复合材料修复这些洞。在加盖后180天除去树脂复合物，然后使腔体对口腔环境开放2周以获得细菌污染DY（BDY）和2 V（B2 V; n = 10）。用DY覆盖的非细菌污染组用作对照。在细菌攻击后，组织学上评估炎性细胞浸润、牙本质桥的发生率和分化。各组间炎性细胞浸润差异有统计学意义（P < 0.05）。DY组未见中、重度炎症反应。BDY组50%可见中、重度炎性细胞浸润，4例坏死。虽然各组牙本质桥的形成和分化无统计学差异，但在70%（DY），80%（BDY）和50%（B2 V）的牙本质桥中检测到隧道缺陷。B2 V组炎性细胞浸润明显低于BDY组（P < 0.05）。粘合剂应该密封暴露部位，并且腔体上剩余的粘合剂在细菌挑战后有效地作为牙本质中的屏障。
To evaluate the pulp healing to bacterial contamination beneath a hard-setting calcium hydroxide (DY: Dycal, L.D. Caulk Co.) and a self-etching adhesive resin (2V: Clearfil Liner Bond 2V, Kuraray Medical Inc.) following dentin bridge formation. Class V cavities were prepared on 30 monkey teeth, and the pulps were exposed with a carbide bur through the cavity floor. Each exposed pulp was capped with either DY or 2V. The cavities were restored with a hybrid resin composite. The resin composite was removed at 180 days after capping, and then cavities were left open to the oral environment for 2 weeks to obtain bacteria contamination DY (BDY) and 2V (B2V; n = 10). A non-bacterial-contaminated group capped with DY was used as control. After bacterial challenges, inflammatory cell infiltration, incidence and differentiation of dentin bridges were evaluated histologically. There were significant differences in the presence of inflammatory cell infiltration among all groups (P < 0.05). No moderate or severe inflammatory reaction was found in Group DY. Group BDY showed moderate or severe inflammatory cell infiltration in 50%, and showed four necrotic specimens. Although no statistically significant difference was found in the formation and differentiation of dentin bridges among all groups, tunnel defects in dentin bridges were detected in 70% (DY), 80% (BDY), and 50% (B2V). Group B2V showed a significantly lower presence of inflammatory cell infiltration than Group BDY (P < 0.05). Bonding agent is supposed to seal the exposure site, and the remaining bonding agent on the cavities was effective as the barrier in the dentin bridges after bacterial challenges.