牙周炎氧化应激水平与铁代谢的研究进展

doi:10.13591/j.cnki.kqyx.2023.06.013

摘要/Abstract

摘要：

牙周炎被认为是牙周致病菌导致的牙周破坏性疾病,通过破坏牙周组织,最终导致牙齿丧失。铁作为人体中重要的微量元素之一,参与机体的各项生理活动。铁代谢平衡是维持正常生理功能的重要组成部分,其代谢异常与多种疾病相关。铁稳态失调会促使活性氧(reactive oxygen species,ROS)水平增高,破坏氧化与抗氧化防御系统之间的平衡,从而导致氧化应激,进一步破坏牙周组织,增加牙周炎的发病率。多项研究表明,铁代谢异常与牙周炎的发生发展存在一定关系,影响牙周炎的病程进展及预后情况。该文将就牙周炎中ROS导致氧化应激与铁代谢机制的研究进展展开综述,从铁代谢方向为牙周炎防治提供新思路。

关键词: 牙周炎, 活性氧, 氧化应激, 铁代谢

Abstract:

Periodontitis is considered to be a destructive periodontal disease caused by periodontal pathogens, which eventually leads to tooth loss through the destruction of periodontal tissue. As one of the important trace elements in human body, iron participates in various physiological activities of the body. Iron metabolism balance is an important part in maintaining the physiological function and its metabolic abnormality is associated with various diseases. Dysregulation of iron homeostasis can promote the increase of reactive oxygen species(ROS) level and destroy the balance between oxidative and antioxidant defense systems, thus leading to oxidative stress, further damaging the periodontal tissue and increasing the incidence of periodontitis. Several studies have shown that there is a certain relationship between abnormal iron metabolism and the occurrence and development of periodontitis, which affects the course and prognosis of periodontitis. This article reviews the research progress of ROS-induced oxidative stress and the mechanism of iron metabolism in periodontitis, and provides new ideas for the prevention and treatment of periodontitis from the direction of iron metabolism.

Key words: periodontitis, reactive oxygen species, oxidative stress, iron metabolism

中图分类号:

R781.42

田士霖, 陈晓涛. 牙周炎氧化应激水平与铁代谢的研究进展[J]. 口腔医学, 2023, 43(6): 552-555.

TIAN Shilin, CHEN Xiaotao. Research progress of oxidative stress level and iron metabolism in periodontitis[J]. Stomatology, 2023, 43(6): 552-555.

参考文献 46

[1]	Richards D. Review finds that severe periodontitis affects 11% of the world population[J]. Evid Based Dent, 2014, 15(3):70-71. doi: 10.1038/sj.ebd.6401037 pmid: 25343387
[2]	Yu N, van Dyke TE. Periodontitis: A host mediated disruption of microbial homeostasis[J]. Curr Oral Health Rep, 2020, 7(1):3-11. doi: 10.1007/s40496-020-00256-4
[3]	Sczepanik FSC, Grossi ML, Casati M, et al. Periodontitis is an inflammatory disease of oxidative stress: We should treat it that way[J]. Periodontol 2000, 2020, 84(1):45-68. doi: 10.1111/prd.v84.1
[4]	Martinez-Herrera M, López-Domènech S, Silvestre FJ, et al. Chronic periodontitis impairs polymorphonuclear leucocyte-endothelium cell interactions and oxidative stress in humans[J]. J Clin Periodontol, 2018, 45(12):1429-1439. doi: 10.1111/jcpe.13027 pmid: 30362144
[5]	Zeidán-Chuliá F, Yilmaz D, Häkkinen L, et al. Matrix metalloproteinase-7 in periodontitis with type 2 diabetes mellitus[J]. J Periodontal Res, 2018, 53(5):916-923. doi: 10.1111/jre.12583 pmid: 29974476
[6]	Stockwell BR, Jiang XJ. The chemistry and biology of ferroptosis[J]. Cell Chem Biol, 2020, 27(4):365-375. doi: S2451-9456(20)30110-0 pmid: 32294465
[7]	Liang DG, Deng L, Jiang XJ. A new checkpoint against ferroptosis[J]. Cell Res, 2020, 30(1):3-4. doi: 10.1038/s41422-019-0258-0 pmid: 31772274
[8]	Stockwell BR, Angeli JPF, Bayir H, et al. Ferroptosis: A regulated cell death Nexus linking metabolism, redox biology, and disease[J]. Cell, 2017, 171(2):273-285. doi: S0092-8674(17)31070-X pmid: 28985560
[9]	Baltacıoğlu E, KehribarMA, Yuva P, et al. Total oxidant status and bone resorption biomarkers in serum and gingival crevicular fluid of patients with periodontitis[J]. JPeriodontol, 2014, 85(2):317-326.
[10]	Marinho HS, Real C, Cyrne L, et al. Hydrogen peroxide sensing, signaling and regulation of transcription factors[J]. Redox Biol, 2014, 2: 535-562. doi: 10.1016/j.redox.2014.02.006 pmid: 24634836
[11]	Kawai T, Matsuyama T, Hosokawa Y, et al. B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease[J]. Am J Pathol, 2006, 169(3):987-998. pmid: 16936272
[12]	Ray PD, Huang BW, Tsuji Y. Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling[J]. Cell Signal, 2012, 24(5):981-990. doi: 10.1016/j.cellsig.2012.01.008 pmid: 22286106
[13]	Bullon P, Newman HN, Battino M. Obesity, diabetes mellitus, atherosclerosis and chronic periodontitis: A shared pathology via oxidative stress and mitochondrial dysfunction?[J]. Periodontol 2000, 2014, 64(1):139-153. doi: 10.1111/prd.2013.64.issue-1
[14]	Sack MN, Fyhrquist FY, Saijonmaa OJ, et al. Basic biology of oxidative stress and the cardiovascular system: Part 1 of a 3-part series[J]. J Am Coll Cardiol, 2017, 70(2):196-211. doi: 10.1016/j.jacc.2017.05.034
[15]	Sadasivam N, KimYJ, Radhakrishnan K, et al. Oxidative stress, genomic integrity, and liver diseases[J]. Molecules, 2022, 27(10):3159. doi: 10.3390/molecules27103159
[16]	Miyasaki KT. The neutrophil: Mechanisms of controlling periodo-ntal bacteria[J]. J Periodontol, 1991, 62(12):761-774. pmid: 1765939
[17]	Wang YF, Wu YN, Li T, et al. Iron metabolism and brain development in premature infants[J]. Front Physiol, 2019, 10: 463. doi: 10.3389/fphys.2019.00463 pmid: 31105583
[18]	Kawabata H. The mechanisms of systemic iron homeostasis and etiology, diagnosis, and treatment of hereditary hemochromatosis[J]. Int J Hematol, 2018, 107(1):31-43. doi: 10.1007/s12185-017-2365-3 pmid: 29134618
[19]	Muckenthaler MU, Rivella S, Hentze MW, et al. A red carpet for iron metabolism[J]. Cell, 2017, 168(3):344-361. doi: S0092-8674(16)31750-0 pmid: 28129536
[20]	Hou J, Yamada S, Kajikawa T, et al. Iron plays a key role in the cytodifferentiation of human periodontal ligament cells[J]. J Periodontal Res, 2014, 49(2):260-267. doi: 10.1111/jre.12103 pmid: 23710667
[21]	Messer JG, Cooney PT, Kipp DE. Iron Chelator deferoxamine alters iron-regulatory genes and proteins and suppresses osteoblast phenotype in fetal rat Calvaria cells[J]. Bone, 2010, 46(5):1408-1415. doi: 10.1016/j.bone.2010.01.376 pmid: 20102755
[22]	Kawabata T. Iron-induced oxidative stress in human diseases[J]. Cells, 2022, 11(14):2152. doi: 10.3390/cells11142152
[23]	Torti SV, Torti FM. CD63 orchestrates ferritin export[J]. Blood, 2021, 138(16):1387-1389. doi: 10.1182/blood.2021013181 pmid: 34673951
[24]	Toyokuni S, Kong YY, Zheng H, et al. Double-edged sword role of iron-loaded ferritin in extracellular vesicles[J]. J Cancer Prev, 2021, 26(4):244-249. doi: 10.15430/JCP.2021.26.4.244 pmid: 35047450
[25]	Gao GF, Li J, Zhang YT, et al. Cellular iron metabolism and regulation[J]. Adv Exp Med Biol, 2019, 1173:21-32. doi: 10.1007/978-981-13-9589-5_2 pmid: 31456203
[26]	Drakesmith H, Nemeth E, Ganz T. Ironing out ferroportin[J]. Cell Metab, 2015, 22(5):777-787. doi: 10.1016/j.cmet.2015.09.006 pmid: 26437604
[27]	Boshuizen M, Binnekade JM, Nota B, et al. Potential of parameters of iron metabolism for the diagnosis of Anemia of inflammation in the critically ill[J]. Transfus Med Hemother, 2020, 47(1):61-67. doi: 10.1159/000497123
[28]	Boyer E le Gall-David S, Martin B, et al. Increased transferrin saturation is associated with subgingival microbiota dysbiosis and severe periodontitis in genetic haemochromatosis[J]. Sci Rep, 2018, 8(1):15532. doi: 10.1038/s41598-018-33813-0 pmid: 30341355
[29]	Yauger YJ, Bermudez S, Moritz KE, et al. Iron accentuated reactive oxygen species release by NADPH oxidase in activated microglia contributes to oxidative stress in vitro[J]. J Neuroinflamma-tion, 2019, 16(1):41.
[30]	Nairz M, Theurl I, SwirskiFK, et al. “Pumping iron”-how macrophages handle iron at the systemic, microenvironmental, and cellular levels[J]. Pflugers Arch, 2017, 469(3/4):397-418. doi: 10.1007/s00424-017-1944-8
[31]	胡银平, 李立卓, 王金霞, 等. 运动防治2型糖尿病的铁调控机制研究进展[J]. 现代预防医学, 2015, 42(17):3236-3238, 3257.
[32]	Lin H, WangYF, Lai HQ, et al. Iron(Ⅱ)-polypyridyl complexes inhibit the growth of glioblastoma tumor and enhance TRAIL-induced cell apoptosis[J]. Chem Asian J, 2018, 13(18):2730-2738. doi: 10.1002/asia.v13.18
[33]	Sp N, Kang DY, Jo ES, et al. Iron metabolism as a potential mechanism for inducing TRAIL-mediated extrinsic apoptosis using methylsulfonylmethane in embryonic cancer stem cells[J]. Cells, 2021, 10(11):2847. doi: 10.3390/cells10112847
[34]	Poprac P, Jomova K, Simunkova M, et al. Targeting free radicals in oxidative stress-related human diseases[J]. Trends Pharmacol Sci, 2017, 38(7):592-607. doi: S0165-6147(17)30097-4 pmid: 28551354
[35]	Valko M, Leibfritz D, Moncol J, et al. Free radicals and antioxidants in normal physiological functions and human disease[J]. Int J Biochem Cell Biol, 2007, 39(1):44-84. doi: 10.1016/j.biocel.2006.07.001
[36]	Byrne DP, Potempa J, Olczak T, et al. Evidence of mutualism between two periodontal pathogens: Co-operative haem acquisition by the HmuY haemophore of Porphyromonas gingivalis and the cysteine protease interpain A (InpA) of Prevotella intermedia[J]. Mol Oral Microbiol, 2013, 28(3):219-229. doi: 10.1111/omi.12018 pmid: 23336115
[37]	Guan SM, Nagata H, Shizukuishi S, et al. Degradation of human hemoglobin by Prevotella intermedia[J]. Anaerobe, 2006, 12(5/6):279-282. doi: 10.1016/j.anaerobe.2006.09.001
[38]	Lewis JP. Metal uptake in host-pathogen interactions: Role of iron in Porphyromonas gingivalis interactions with host organisms[J]. Periodontol 2000, 2010, 52(1):94-116.
[39]	Cen WJ, Feng Y, Li SS, et al. Iron overload induces G1 phase arrest and autophagy in murine preosteoblast cells[J]. J Cell Physiol, 2018, 233(9):6779-6789. doi: 10.1002/jcp.v233.9
[40]	Mukherjee S. The role of crevicular fluid iron in periodontal disease[J]. J Periodontol, 1985, 56(< W>11 Suppl):22-27. doi: 10.1902/jop.1985.56.11s.22
[41]	Zhang YC, Zhai WJ, Zhao MF, et al. Effects of iron overload on the bone marrow microenvironment in mice[J]. PLoS One, 2015, 10(3):e0120219. doi: 10.1371/journal.pone.0120219
[42]	Tsay J, Yang ZW, Ross FP, et al. Bone loss caused by iron overload in a murine model: Importance of oxidative stress[J]. Blood, 2010, 116(14):2582-2589. doi: 10.1182/blood-2009-12-260083 pmid: 20554970
[43]	Jing XZ, Du T, Chen K, et al. Icariin protects against iron overload-induced bone loss via suppressing oxidative stress[J]. J Cell Physiol, 2019, 234(7):10123-10137. doi: 10.1002/jcp.27678 pmid: 30387158
[44]	Bonilla DA, Moreno Y, Petro JL, et al. A bioinformatics-assisted review on iron metabolism and immune system to identify potential biomarkers of exercise stress-induced immunosuppression[J]. Biomedicines, 2022, 10(3):724. doi: 10.3390/biomedicines10030724
[45]	陈辰, 蒋敬庭. 铁死亡机制及在肿瘤中的应用进展[J]. 中华实验外科杂志, 2019, 36(11):2110-2114.
[46]	Forciniti S, Greco L, Grizzi F, et al. Iron metabolism in cancer progression[J]. Int J Mol Sci, 2020, 21(6):2257. doi: 10.3390/ijms21062257