Oral Biology, School of Dentistry, University of Birmingham, St Chad's Queensway, Birmingham B4 6NN, UK.
J Dent. 2010 Sep;38(9):687-97. doi: 10.1016/j.jdent.2010.05.016. Epub 2010 May 24.
Dental tissue disease and trauma provides an excellent model for the interaction between tissue defence and regenerative processes and has application to many of the body's other tissues. Following dental tissue infection, characterised by caries, the molecular and cellular mediators of the immune/inflammatory processes clearly impact on the dental tissues' natural regenerative responses. This review of the literature was performed to better understand how these two processes interact and identify whether cross-talk may provide novel areas for future research and subsequent translation into clinical application.
A review of the literature was performed using the PubMed database resource and this was followed by extensive hand searching using reference lists from relevant articles.
Frequently, the dental tissue inflammatory and regenerative processes are seen as both distinct and antagonistic and subsequently have often been studied in isolation; however, both direct and indirect data are now emerging which indicate significant inter-relationship. Whilst the ensuing inflammatory process will result in dental tissue breakdown and molecular signalling which may impede regeneration, low grade inflammation, potentially induced by mechanical trauma and tissue necrosis, may promote regenerative mechanisms, including angiogenic and stem cell processes. Notably, the locally derived growth factors, neuropeptides, cytokines and chemokines, released from the host dentine matrix and by resident pulpal cells, immune cells, neurons and/or dying cells, will modulate defence and repair processes within the tissue.
牙齿组织疾病和损伤为组织防御和再生过程的相互作用提供了一个极好的模型，并且可应用于人体的许多其他组织。在以龋齿为特征的牙齿组织感染之后，免疫/炎症过程的分子和细胞介质显然会影响牙齿组织的自然再生反应。进行本次文献回顾是为了更好地了解这两个过程如何相互作用，并确定是否可以进行交流以提供新的研究领域，随后将其转化为临床应用。
使用 PubMed 数据库资源进行文献回顾，然后使用相关文章的参考文献进行广泛的手动搜索。
通常，牙齿组织的炎症和再生过程被视为既独特又对立，因此通常是分开研究的；但是，现在直接和间接的数据都表明存在重要的相互关系。虽然随后的炎症过程将导致牙齿组织的破坏和可能阻碍再生的分子信号，但由机械创伤和组织坏死引起的低度炎症可能会促进包括血管生成和干细胞过程在内的再生机制。值得注意的是，从宿主牙本质基质以及常驻牙髓细胞、免疫细胞、神经元和/或死亡细胞中释放的局部来源的生长因子、神经肽、细胞因子和趋化因子将调节组织内的防御和修复过程。
