高糖水平下牙周组织的形态与免疫特征

doi:10.13591/j.cnki.kqyx.2023.02.011

摘要/Abstract

摘要：

糖尿病可增加牙周炎的发病风险和严重程度,可能与该状态下的牙周组织免疫特征改变有关。本文就高糖状态引发的牙周组织形态结构改变、局部免疫细胞变化及其调控机制等方面,对糖尿病患者牙周组织的形态及免疫特征进行综述。

Abstract:

Diabetes mellitus can increase the risk and severity of periodontitis and may be associated with changes in the immune characteristics of periodontal tissues. In this paper, the morphological and immune characteristics of periodontal tissues in diabetic patients were reviewed in terms of the changes of morphology, structure and local immune cells in periodontal tissues caused by hyperglycemia and their regulatory mechanisms.

Key words: hyperglycemia, periodontitis, immune cell, mechanism

中图分类号:

R781.4

孙乐章,王琪. 高糖水平下牙周组织的形态与免疫特征[J]. 口腔医学, 2023, 43(2): 153-158.

SUN Yuezhang,WANG Qi. Morphological and immune characteristics of periodontal tissues under hyperglycemia[J]. Stomatology, 2023, 43(2): 153-158.

参考文献 52

[1]	郑旭, 甘姗灵, 郭竹玲. 牙周基础治疗调节2型糖尿病患者代谢的研究进展[J]. 口腔医学, 2019, 39(2):183-187.
[2]	Catanzaro OL, Andornino A, Brasquet N, et al. The effect of gingival aging in diabetic and non-diabetic status: An experimental study[J]. Acta Odontol Latinoam, 2018, 31(1):32-37. pmid: 30056464
[3]	Dağ A, Fırat ET, Uysal E, et al. Morphological changes caused by streptozotocin-induced diabetes in the healthy gingiva of rats[J]. Exp Clin Endocrinol Diabetes, 2016, 124(3):167-172. doi: 10.1055/s-00000017
[4]	Kominato H, Takeda K, Mizutani K, et al. Metformin accelerates wound healing by Akt phosphorylation of gingival fibroblasts in insulin-resistant prediabetes mice[J]. J Periodontol, 2022, 93(2):256-268.
[5]	Chen H, Feng ZH, Li LY, et al. microRNA-9 rescues hyperglycemia-induced endothelial cell dysfunction and promotes arteriogenesis through downregulating Notch1 signaling[J]. Mol Cell Biochem, 2021, 476(7):2777-2789. doi: 10.1007/s11010-021-04075-8 pmid: 33721156
[6]	Ashour A, Xue MZ, Al-Motawa M, et al. Glycolytic overload-driven dysfunction of periodontal ligament fibroblasts in high glucose concentration, corrected by glyoxalase 1 inducer[J]. BMJ Open Diabetes Res Care, 2020, 8(2):e001458. doi: 10.1136/bmjdrc-2020-001458
[7]	Zheng J, Chen S, Albiero ML, et al. Diabetes activates periodontal ligament fibroblasts via NF-κB in vivo[J]. J Dent Res, 2018, 97(5):580-588. doi: 10.1177/0022034518755697 pmid: 29439598
[8]	Toker H, BalciYuce H, LektemurAlpan A, et al. Morphometric and histopathological evaluation of the effect of grape seed proanthocyanidin on alveolar bone loss in experimental diabetes and periodontitis[J]. J Periodontal Res, 2018, 53(3):478-486. doi: 10.1111/jre.12536 pmid: 29446089
[9]	Shen YX, Guo SJ, Chen GQ, et al. Hyperglycemia induces osteoclastogenesis and bone destruction through the activation of Ca²⁺/calmodulin-dependent protein kinase Ⅱ[J]. Calcif TissueInt, 2019, 104(4):390-401.
[10]	Huang J, Xiao Y, Zheng PL, et al. Distinct neutrophil counts and functions in newly diagnosed type 1 diabetes, latent autoimmune diabetes in adults, and type 2 diabetes[J]. Diabetes Metab Res Rev, 2019, 35(1):e3064. doi: 10.1002/dmrr.v35.1
[11]	Insuela DBR, Ferrero MR, Gonçalves-de-Albuquerque CF, et al. Glucagon reduces neutrophil migration and increases susceptibility to Sepsis in diabetic mice[J]. Front Immunol, 2021, 12: 633540. doi: 10.3389/fimmu.2021.633540
[12]	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
[13]	Manosudprasit A, Kantarci A, Hasturk H, et al. Spontaneous PMN apoptosis in type 2 diabetes and the impact of periodontitis[J]. J Leukoc Biol, 2017, 102(6):1431-1440. doi: 10.1189/jlb.4A0416-209RR
[14]	Checchi V, Maravic T, Bellini P, et al. The role of matrix metalloproteinases in periodontal disease[J]. Int J Environ Res Public Health, 2020, 17(14):4923. doi: 10.3390/ijerph17144923
[15]	Zhang B, Yang Y, Yi JR, et al. Hyperglycemia modulates M1/M2 macrophage polarization via reactive oxygen species overproduction in ligature-induced periodontitis[J]. J Periodontal Res, 2021, 56(5):991-1005. doi: 10.1111/jre.v56.5
[16]	杨亚楠, 于时卉, 闫香珍, 等. 牙龈卟啉单胞菌对db/db小鼠骨髓来源巨噬细胞极化作用的初步探究[J]. 口腔医学, 2020, 40(1):13-16.
[17]	Zhuang Z, Yoshizawa-Smith S, Glowacki A, et al. Induction of M2 macrophages prevents bone loss in murine periodontitis models[J]. J Dent Res, 2019, 98(2):200-208. doi: 10.1177/0022034518805984 pmid: 30392438
[18]	Zhang P, Wang Q, Nie L, et al. Hyperglycemia-induced inflamm-aging accelerates gingival senescence via NLRC4 phosphorylation[J]. J Biol Chem, 2019, 294(49):18807-18819. doi: 10.1074/jbc.RA119.010648 pmid: 31676687
[19]	Lew JH, Naruishi K, Kajiura Y, et al. High glucose-mediated cytokine regulation in gingival fibroblasts and THP-1 macrophage: A possible mechanism of severe periodontitis with diabetes[J]. Cell Physiol Biochem, 2018, 50(3):973-986. doi: 10.1159/000494481
[20]	Zhao PF, Yue ZQ, Nie L, et al. Hyperglycaemia-associated macrophage pyroptosis accelerates periodontal inflamm-aging[J]. J Clin Periodontol, 2021, 48(10):1379-1392. doi: 10.1111/jcpe.v48.10
[21]	Shen ZS, Kuang SH, Zhang M, et al. Inhibition of CCL2 by bindarit alleviates diabetes-associated periodontitis by suppressing inflammatory monocyte infiltration and altering macrophage properties[J]. Cell Mol Immunol, 2021, 18(9):2224-2235. doi: 10.1038/s41423-020-0500-1
[22]	Ahmad R, Kochumon S, Chandy B, et al. TNF-α drives the CCL4 expression in human monocyticcells: Involvement of the SAPK/JNK and NF-κB signaling pathways[J]. Cell Physiol Biochem, 2019, 52(4):908-921. doi: 10.33594/000000000
[23]	Flynn MC, Kraakman MJ, Tikellis C, et al. Transient intermittent hyperglycemia accelerates atherosclerosis by promoting myelopoiesis[J]. Circ Res, 2020, 127(7):877-892. doi: 10.1161/CIRCRESAHA.120.316653 pmid: 32564710
[24]	Jagannathan R, Lavu V, Rao SR. Comparison of the proportion of non-classic (CD14⁺ CD16⁺) monocytes/macrophages in peripheral blood and gingiva of healthy individuals and patients with chronic periodontitis[J]. J Periodontol, 2014, 85(6):852-858. doi: 10.1902/jop.2013.120658 pmid: 24001047
[25]	刘利思, 杨婷, 叶展鸿, 等. S100钙结合蛋白A8在人慢性牙周炎牙龈组织巨噬细胞中表达的研究[J]. 口腔医学, 2020, 40(6):486-490, 495.
[26]	Song L, Dong G, Guo L, et al. The function of dendritic cells in modulating the host response[J]. Mol Oral Microbiol, 2018, 33(1):13-21. doi: 10.1111/omi.12195 pmid: 28845602
[27]	Kim JH, Park K, Lee SB, et al. Relationship between natural killer cell activity and glucose control in patients with type 2 diabetes and prediabetes[J]. J Diabetes Investig, 2019, 10(5):1223-1228. doi: 10.1111/jdi.v10.5
[28]	Fernø J, Strand K, Mellgren G, et al. Natural killer cells as sensors of adipose tissue stress[J]. Trends Endocrinol Metab, 2020, 31(1):3-12. doi: 10.1016/j.tem.2019.08.011
[29]	Theoharides TC, Stewart JM, Tsilioni I. Tolerability and benefit of a tetramethoxyluteolin-containing skin lotion[J]. Int J Immunopathol Pharmacol, 2017, 30(2):146-151. doi: 10.1177/0394632017707610 pmid: 28480804
[30]	Belkina AC, Azer M, Lee JJ, et al. Single-cell analysis of the periodontal immune niche in type 2 diabetes[J]. J Dent Res, 2020, 99(7):855-862. doi: 10.1177/0022034520912188 pmid: 32186942
[31]	Huang Z, Pei XY, Graves DT. The interrelationship between diabetes, IL-17 and bone loss[J]. Curr Osteoporos Rep, 2020, 18(1):23-31. doi: 10.1007/s11914-020-00559-6 pmid: 32002770
[32]	Chen XT, Chen LL, Tan JY, et al. Th17 and Th1 lymphocytes are correlated with chronic periodontitis[J]. ImmunolInvest, 2016, 45(3):243-254.
[33]	Polak D, Shapira L. An update on the evidence for pathogenic mechanisms that may link periodontitis and diabetes[J]. J Clin Periodontol, 2018, 45(2):150-166. doi: 10.1111/jcpe.12803 pmid: 29280184
[34]	Drumond MHF, Puhl LE, Duarte PM, et al. Preliminary findings on the possible role of B-lymphocyte Stimulator (BLyS) on diabetes-related periodontitis[J]. Braz Oral Res, 2020, 34: e038. doi: 10.1590/1807-3107bor-2020.vol34.0038 pmid: 32374812
[35]	Zhang P, Lu BY, Zhu R, et al. Hyperglycemia accelerates inflammaging in the gingival epithelium through inflammasomes activation[J]. J Periodontal Res, 2021, 56(4):667-678. doi: 10.1111/jre.12863 pmid: 33650689
[36]	Zhang R, Liang QY, Kang WY, et al. Metformin facilitates the proliferation, migration, and osteogenic differentiation of periodontal ligament stem cells in vitro[J]. Cell Biol Int, 2019, 99: 2019.
[37]	Monteiro MM, Lima CR, Gomes CC, et al. Lowered expression of microRNAs 221 and 222 mediate apoptosis induced by high glucose in human periodontal ligament cells[J]. Cell Biochem Biophys, 2020, 78(3):391-398. doi: 10.1007/s12013-020-00932-3 pmid: 32681442
[38]	Sudhakara P, Gupta A, Bhardwaj A, et al. Oral dysbiotic communities and their implications in systemic diseases[J]. Dent J (Basel), 2018, 6(2):10.
[39]	Graves DT, Ding ZJ, Yang YM. The impact of diabetes on periodontal diseases[J]. Periodontol 2000, 2020, 82(1):214-224. doi: 10.1111/prd.v82.1
[40]	Teissier T, Boulanger E, Cox LS. Interconnections between inflammageing and immunosenescence during ageing[J]. Cells, 2022, 11(3):359. doi: 10.3390/cells11030359
[41]	Zuo L, Prather ER, Stetskiv M, et al. Inflammaging and oxidative stress in human diseases: From molecular mechanisms to novel treatments[J]. Int J MolSci, 2019, 20(18):4472.
[42]	Wang Q, Nie L, Zhao PF, et al. Diabetes fuels periodontal lesions via GLUT1-driven macrophage inflammaging[J]. Int J Oral Sci, 2021, 13(1):11. doi: 10.1038/s41368-021-00116-6
[43]	Öngöz Dede F, Bozkurt Doğan Ş, Ballı U, et al. The effect of initial periodontal treatment on plasma, gingival crevicular fluid and salivary levels of 8-hydroxy-deoxyguanosine in obesity[J]. Arch Oral Biol, 2016, 62:80-85. doi: 10.1016/j.archoralbio.2015.11.014 pmid: 26655951
[44]	Xia SJ, Zhang XY, Zheng SB, et al. An update on inflamm-aging: Mechanisms, prevention, and treatment[J]. J Immunol Res, 2016, 2016: 8426874.
[45]	Huang X, Kuang SH, Shen ZS, et al. High glucose disrupts autophagy lysosomal pathway in gingival epithelial cells via ATP6V0C[J]. J Periodontol, 2020, 91(5):705-714. doi: 10.1002/JPER.19-0262 pmid: 31471894
[46]	Sun T, Yan Z, Cai J, et al. Effects of mechanical vibration on cell morphology, proliferation, apoptosis, and cytokine expression/secretion in osteocyte-like MLO-Y4 cells exposed to high glucose[J]. Cell Biol Int, 2019: 2019.
[47]	Goes P, Dutra C, Lösser L, et al. Loss of dkk-1 in osteocytes mitigates alveolar bone loss in mice with periodontitis[J]. Front Immunol, 2019, 10: 2924. doi: 10.3389/fimmu.2019.02924 pmid: 31921182
[48]	Ferioli M, Zauli G, Maiorano P, et al. Role of physical exercise in the regulation of epigenetic mechanisms in inflammation, cancer, neurodegenerative diseases, and aging process[J]. J Cell Physiol, 2019, 234(9):14852-14864. doi: 10.1002/jcp.v234.9
[49]	Liu Z, Chen T, Sun WH, et al. DNA demethylation rescues the impaired osteogenic differentiation ability of human periodontal ligament stem cells in high glucose[J]. Sci Rep, 2016, 6: 27447. doi: 10.1038/srep27447 pmid: 27273319
[50]	Fanucchi S, Domínguez-Andrés J, Joosten LAB, et al. The intersection of epigenetics and metabolism in trained immunity[J]. Immunity, 2021, 54(1):32-43. doi: 10.1016/j.immuni.2020.10.011 pmid: 33220235
[51]	Čugalj Kern B, TrebušakPodkrajšek K, Kovač J, et al. The role of epigenetic modifications in late complications in type 1 diabetes[J]. Genes, 2022, 13(4):705. doi: 10.3390/genes13040705
[52]	Radović N, NikolićJakoba N, Petrović N, et al. microRNA-146a and microRNA-155 as novel crevicular fluid biomarkers for periodontitis in non-diabetic and type 2 diabetic patients[J]. J Clin Periodontol, 2018, 45(6):663-671. doi: 10.1111/jcpe.12888 pmid: 29517812