Conrads Georg, About Imad
Monogr Oral Sci. 2018;27:1-10. doi: 10.1159/000487826. Epub 2018 May 24.
Carious lesion dynamics are dependent predominantly on the availability of fermentable sugars, other environmental conditions, bacteria, and host factors. Our current understanding of the microorganisms involved in the initiation and progression of caries is still rather incomplete. The most relevant acidogenic-aciduric bacterial species known to date are Streptococcus mutans, bifidobacteria, and lactobacilli. Whereas mutans streptococci are initiators, bifidobacteria and lactobacilli are more enhancers for progression. Boosters for microbial activity are specific environmental conditions, such as the presence of fermentable dietary sugars and the absence of oxygen. Based on these conditions, the necrotic and/or contaminated zone fulfils all criteria for disease progression and has to be removed. For those deep lesions where the pulp vitality is not affected, a selective removal of the contaminated leathery dentine should take place as this approach lowers the risk of regrowth of the few embedded microbial cells here. In repelling the microbial attack and repairing damage, the host has developed several ingenious strategies. A major resistance to carious lesion progression is mounted by the dentine-pulp tissues. The signalling molecules and growth factors released upon dentine demineralisation upregulate the odontoblast activity and act as sensor cells. After carious stimulation, odontoblasts initiate an inflammatory reaction by producing chemokines and synthesise a protective tertiary dentine. After the destruction of these cells, the pulp still has a high capacity to synthesise this tertiary dentine thanks to the presence of adult stem cells within the pulp. Also, in addition to the systemic regulation, the pulp which is located within inextensible the confines of the dentine walls has a well-developed local regulation of its inflammation, regeneration, and vascularisation. This local regulation is due to the activity of different pulp cell types, mainly the fibroblasts, which secrete soluble molecules that regulate all these processes.
龋损动态主要取决于可发酵糖的可用性、其他环境条件、细菌和宿主因素。我们目前对参与龋齿发生和发展的微生物的理解仍然相当不完整。迄今为止已知的最相关的产酸耐酸细菌种类是变形链球菌、双歧杆菌和乳酸杆菌。变形链球菌是引发剂，而双歧杆菌和乳酸杆菌更多地是促进进展。微生物活性的增强剂是特定的环境条件，例如可发酵膳食糖的存在和无氧环境。基于这些条件，坏死和/或污染区域满足疾病进展的所有标准，必须予以清除。对于那些牙髓活力未受影响的深层病变，应选择性去除受污染的坚韧牙本质，因为这种方法可降低此处少数嵌入微生物细胞再生长的风险。在抵御微生物攻击和修复损伤方面，宿主已开发出几种巧妙的策略。牙本质-牙髓组织对龋损进展形成主要抵抗力。牙本质脱矿时释放的信号分子和生长因子上调成牙本质细胞活性并充当传感细胞。在受到龋病刺激后，成牙本质细胞通过产生趋化因子引发炎症反应并合成保护性第三期牙本质。这些细胞被破坏后，由于牙髓内存在成体干细胞，牙髓仍具有合成这种第三期牙本质的高能力。此外，除了全身调节外，位于不可伸展的牙本质壁范围内的牙髓对其炎症反应、再生和血管生成具有完善的局部调节机制。这种局部调节是由于不同牙髓细胞类型的活性，主要是成纤维细胞，它们分泌调节所有这些过程的可溶性分子。
