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了解牙髓炎症:从信号到结构。

Understanding dental pulp inflammation: from signaling to structure.

机构信息

Department of Conservative Dentistry and Periodontology, University Hospital Regensburg, Regensburg, Germany.

Medical Department 3, Rheumatology and Immunology, University Hospital Erlangen, Erlangen, Germany.

出版信息

Front Immunol. 2024 Oct 29;15:1474466. doi: 10.3389/fimmu.2024.1474466. eCollection 2024.

DOI:10.3389/fimmu.2024.1474466
PMID:39534600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11554472/
Abstract

The pulp is a unique tissue within each tooth that is susceptible to painful inflammation, known as pulpitis, triggered by microbial invasion from carious lesions or trauma that affect many individuals. The host response involves complex immunological processes for pathogen defense and dentin apposition at the site of infection. The interplay of signaling between the immune and non-immune cells via cytokines, chemokines, neuropeptides, proteases, and reactive nitrogen and oxygen species leads to tissue reactions and structural changes in the pulp that escalate beyond a certain threshold to irreversible tissue damage. If left untreated, the inflammation, which is initially localized, can progress to pulpal necrosis, requiring root canal treatment and adversely affecting the prognosis of the tooth. To preserve pulp vitality and dental health, a deeper understanding of the molecular and cellular mechanisms of pulpitis is imperative. In particular, elucidating the links between signaling pathways, clinical symptoms, and spatiotemporal spread is essential to develop novel therapeutic strategies and push the boundaries of vital pulp therapy.

摘要

牙髓是每个牙齿内独特的组织,易受到疼痛性炎症的影响,这种炎症被称为牙髓炎,由龋病或创伤引起的微生物入侵引发,影响许多人。宿主反应涉及到针对病原体防御和感染部位牙本质形成的复杂免疫过程。免疫和非免疫细胞之间通过细胞因子、趋化因子、神经肽、蛋白酶、活性氮和氧物种进行信号传递的相互作用导致牙髓组织反应和结构变化,如果超过一定阈值,则会发展为不可逆的组织损伤。如果不进行治疗,最初局限的炎症可能进展为牙髓坏死,需要根管治疗,从而对牙齿的预后产生不利影响。为了保持牙髓活力和牙齿健康,必须更深入地了解牙髓炎的分子和细胞机制。特别是,阐明信号通路、临床症状和时空传播之间的联系对于开发新的治疗策略和推动牙髓治疗的发展至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/9a65e75f6a9d/fimmu-15-1474466-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/d1d106a58724/fimmu-15-1474466-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/cb89a6924cb8/fimmu-15-1474466-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/1755b1a73161/fimmu-15-1474466-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/cda8d5ebe51c/fimmu-15-1474466-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/df0b793bc254/fimmu-15-1474466-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/8a6f0f83d140/fimmu-15-1474466-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/04b637823209/fimmu-15-1474466-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/9a65e75f6a9d/fimmu-15-1474466-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/d1d106a58724/fimmu-15-1474466-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/cb89a6924cb8/fimmu-15-1474466-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/1755b1a73161/fimmu-15-1474466-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/cda8d5ebe51c/fimmu-15-1474466-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/df0b793bc254/fimmu-15-1474466-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/8a6f0f83d140/fimmu-15-1474466-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/04b637823209/fimmu-15-1474466-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0cab/11554472/9a65e75f6a9d/fimmu-15-1474466-g008.jpg

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