Takahashi Nobuhiro, Nyvad Bente
Division of Oral Ecology and Biochemistry, Tohoku University Graduate School of Dentistry, Sendai, Japan.
Caries Res. 2016;50(4):422-31. doi: 10.1159/000447309. Epub 2016 Jul 27.
Recent advances regarding the caries process indicate that ecological phenomena induced by bacterial acid production tilt the de- and remineralization balance of the dental hard tissues towards demineralization through bacterial acid-induced adaptation and selection within the microbiota - from the dynamic stability stage to the aciduric stage via the acidogenic stage [Takahashi and Nyvad, 2008]. Dentin and root caries can also be partly explained by this hypothesis; however, the fact that these tissues contain a considerable amount of organic material suggests that protein degradation is involved in caries formation. In this review, we compiled relevant histological, biochemical, and microbiological information about dentin/root caries and refined the hypothesis by adding degradation of the organic matrix (the proteolytic stage) to the abovementioned stages. Bacterial acidification not only induces demineralization and exposure of the organic matrix in dentin/root surfaces but also activation of dentin-embedded and salivary matrix metalloproteinases and cathepsins. These phenomena initiate degradation of the demineralized organic matrix in dentin/root surfaces. While a bacterial involvement has never been confirmed in the initial degradation of organic material, the detection of proteolytic/amino acid-degrading bacteria and bacterial metabolites in dentin and root caries suggests a bacterial digestion and metabolism of partly degraded matrix. Moreover, bacterial metabolites might induce pulpitis as an inflammatory/immunomodulatory factor. Root and dentin surfaces are always at risk of becoming demineralized in the oral cavity, and exposed organic materials can be degraded by host-derived proteases contained in saliva and dentin itself. New approaches to the prevention and treatment of root/dentin caries are required.
近期关于龋病进程的研究进展表明，细菌产酸引发的生态现象会通过微生物群内细菌酸诱导的适应和选择，使牙体硬组织的脱矿和再矿化平衡向脱矿倾斜，即从动态稳定阶段经产酸阶段到耐酸阶段[高桥和尼瓦德，2008年]。牙本质龋和根龋也可部分用这一假说来解释；然而，这些组织含有大量有机物质这一事实表明，蛋白质降解参与了龋病形成。在本综述中，我们收集了有关牙本质/根龋的相关组织学、生物化学和微生物学信息，并通过在上述阶段中增加有机基质的降解（蛋白水解阶段）来完善这一假说。细菌酸化不仅会诱导牙本质/根表面的脱矿和有机基质暴露，还会激活牙本质中嵌入的和唾液中的基质金属蛋白酶及组织蛋白酶。这些现象引发牙本质/根表面脱矿有机基质的降解。虽然从未证实细菌参与有机物质的初始降解，但在牙本质和根龋中检测到蛋白水解/氨基酸降解细菌及细菌代谢产物，提示细菌对部分降解基质的消化和代谢。此外，细菌代谢产物可能作为炎症/免疫调节因子诱发牙髓炎。根面和牙本质表面在口腔中始终有脱矿的风险，暴露的有机物质可被唾液和牙本质自身所含的宿主来源蛋白酶降解。因此需要预防和治疗根龋/牙本质龋的新方法。
