Dentin Degradation: From Tissue Breakdown to Possibilities for Therapeutic Intervention.
Dentin Degradation: From Tissue Breakdown to Possibilities for Therapeutic Intervention.
复制标题
牙本质降解：从组织破坏到治疗干预的可能性。
DOI：
10.1007/s40496-023-00341-4
复制
发表时间：
2023
影响因子：
--
通讯作者：
Carrilho,MarcelaR
中科院分区：
文献类型：
--
作者：
Vidal,CristinaMP;Carrilho,MarcelaR
目前，牙科材料科学的驱动力是寻找新的和改进的材料，这些材料可以引发受影响组织的特定反应，以刺激修复或再生，同时与口腔环境相互作用，以促进或保持口腔健康。同时，过去几十年的证据已经挑战了细菌在龋齿牙本质组织降解中的唯一作用，质疑了我们对龋齿发病机制的理解。这篇综述的目的是概括目前的证据对宿主和细菌的贡献的降解，炎症和修复的牙本质牙髓复合体在carrier.Recent FindingsContrasting发现属性牙本质分解的内源性酶的活性，如基质金属蛋白酶（MMPs）和组织蛋白酶，而细菌及其副产物在破坏牙本质有机基质和牙髓炎症中的作用几十年来一直被支持为不可否认的稳定范例。为了更好地理解龋齿中宿主酶降解胶原蛋白的机制，研究表明这些蛋白酶在成熟牙本质中表达（即，牙本质形成后），并在龋齿中由细菌代谢导致的酸性环境中的低pH下被活化。然而，除了牙本质结合蛋白酶之外，不同的宿主来源似乎也有助于龋齿的进展，例如唾液和牙髓。有趣的是，评估牙髓对龋齿中细菌入侵和炎症的反应的研究报告了发炎组织中更高水平的MMP和组织蛋白酶，但也显示了MMP解决炎症和刺激伤口愈合的潜力。值得注意的是，据报道，为其他组织，基质金属蛋白酶发挥双重作用，在牙本质牙髓复合体在龋齿，参与或调节降解和修复mechanism.SummaryThe的具体作用的主机和细菌及其副产品在龋齿的进展还有待澄清。龋病中炎症和修复之间复杂的相互作用对清楚了解牙本质牙髓复合体对细菌入侵的反应和变化提出了挑战。然而，它为基于特定机制的调节以促进组织修复和愈合的新型疗法和牙科生物材料的开发开辟了新的途径。
Purpose of the ReviewPresently, dental materials science is driven by the search for new and improved materials that can trigger specific reactions from the affected tissue to stimulate repair or regeneration while interacting with the oral environment to promote or maintain oral health. In parallel, evidence from the past decades has challenged the exclusive role of bacteria in dentin tissue degradation in caries, questioning our understanding of caries etiopathogenesis. The goal of this review is to recapitulate the current evidence on the host and bacterial contributions to degradation, inflammation, and repair of the dentin-pulp complex in caries.Recent FindingsContrasting findings attribute dentin breakdown to the activity of endogenous enzymes, such as matrix metalloproteinases (MMPs) and cathepsins, while the role of bacteria and their by-products in the destruction of dentin organic matrix and pulp inflammation has been for decades supported as an incontestable paradigm. Aiming to better understand the mechanisms involved in collagen degradation by host enzymes in caries, studies have showed that these proteinases are expressed in the mature dentin (i.e., after dentin formation) and become activated by the low pH in the acidic environment resulted by bacterial metabolism in caries. However, different host sources other than dentin-bound proteinases seem to also contribute to caries progression, such as saliva and pulp. Interestingly, studies evaluating pulp responses to bacteria invasion and inflammation in caries report higher levels of MMPs and cathepsins in inflamed tissue, but also showed MMP potential to resolve inflammation and stimulate wound healing. Notably, as reported for other tissues, MMPs exert dual roles in the dentin-pulp complex in caries, participating or regulating both degradative and reparative mechanisms.SummaryThe specific roles of host and bacteria and their by-products in caries progression have yet to be clarified. The complex interactions between inflammation and repair in caries pose challenges to a clear understanding of the dentin-pulp complex responses and changes to bacteria invasion. However, it opens new venues for the development of novel therapies and dental biomaterials based on the modulation of specific mechanisms to favor tissue repair and healing.