国际口腔医学杂志 ›› 2023, Vol. 50 ›› Issue (5): 587-593.doi: 10.7518/gjkq.2023087

• 综述 • 上一篇    下一篇

牙周炎与帕金森病相关性的研究进展

龚美灵(),程兴群,吴红崑()   

  1. 口腔疾病防治全国重点实验室 国家口腔医学中心 国家口腔疾病临床医学研究中心四川大学华西口腔医院老年口腔科 成都 610041
  • 收稿日期:2022-12-20 修回日期:2023-05-27 出版日期:2023-09-01 发布日期:2023-09-01
  • 通讯作者: 吴红崑
  • 作者简介:龚美灵,硕士,Email:1139766106@qq.com
  • 基金资助:
    四川省海外留学人员科研项目(2021-29-1);四川大学华西口腔医院人才队伍建设项目(RCDWJS2021-16)

Research progress on the correlation between Parkinson’s disease and periodontitis

Gong Meiling(),Cheng Xingqun,Wu Hongkun.()   

  1. State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Dept. of Geriatric Dentistry, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2022-12-20 Revised:2023-05-27 Online:2023-09-01 Published:2023-09-01
  • Contact: Hongkun. Wu
  • Supported by:
    Science and Technology Program for Overseas Students in Sichuan Province(2021-29-1);Research Funding from West China Hospital of Stomatology Sichuan University(RCDWJS2021-16)

摘要:

帕金森病是一种多见于老年人的神经系统退行性疾病,慢性神经炎症与其病理生理密切相关。牙周炎作为一种常见的口腔慢性炎症性疾病,可引起局部甚至全身炎症,是众多全身疾病的危险因素,但与帕金森病的相关研究还比较缺乏。目前为止,尚无直接证据表明牙周炎在帕金森病的发病机制中起作用,但其可能通过多种途径引起神经炎症,从而影响帕金森病的发生。本文就近年来牙周炎与帕金森病相关的研究进展作一综述,为口腔与全身慢病共同防治提供理论依据。

关键词: 帕金森病, 牙周炎, 神经炎症, 神经退行性疾病, 慢病同治

Abstract:

Parkinson’s disease (PD) is a degenerative disease of nervous system that commonly occurs in the elderly. Chronic neuroinflammation is closely related to its pathophysiology. As one of the most common chronic inflammatory diseases, periodontitis can cause local and even systemic inflammation and is a risk factor for many systemic diseases. The correlation between PD and periodontitis is still unclear. Although no direct evidence confirms that periodontitis plays a role in the pathogenesis of PD, periodontitis may cause neuroinflammation through various ways and thus affect the occurrence of PD. This work reviews the research progress of PD and periodontitis to provide a theoretical basis for the prevention and treatment of oral and systemic chronic diseases.

Key words: Parkinson’s disease, periodontitis, neuroinflammation, neurodegenerative diseases, co-treatment of chronic diseases

中图分类号: 

  • R 781.4
1 刘疏影, 陈彪. 帕金森病流行现状[J]. 中国现代神经疾病杂志, 2016, 16(2): 98-101.
Liu SY, Chen P. Epidemiology of Parkinson’s di-sease[J]. Chin J Contemp Neurol Neurosurg, 2016, 16(2): 98-101.
2 Uppoor AS, Lohi HS, Nayak D. Periodontitis and Alzheimer’s disease: oral systemic link still on the rise[J]. Gerodontology, 2013, 30(3): 239-242.
3 Kamer AR, Craig RG, Dasanayake AP, et al. Inflammation and Alzheimer’s disease: possible role of periodontal diseases[J]. Alzheimers Dement, 2008, 4(4): 242-250.
4 Kaur T, Uppoor A, Naik D. Parkinson’s disease and periodontitis-the missing link? A review[J]. Gero-dontology, 2016, 33(4): 434-438.
5 Hashioka S, Inoue K, Miyaoka T, et al. The possible causal link of periodontitis to neuropsychiatric disorders: more than psychosocial mechanisms[J]. Int J Mol Sci, 2019, 20(15): 3723.
6 Pradeep AR, Singh SP, Martande SS, et al. Clinical evaluation of the periodontal health condition and oral health awareness in Parkinson’s disease patients[J]. Gerodontology, 2015, 32(2): 100-106.
7 Cicciù M, Risitano G, Lo Giudice G, et al. Periodontal health and caries prevalence evaluation in patients affected by Parkinson’s disease[J]. Parkinsons Dis, 2012, 2012: 541908.
8 Lyra P, Machado V, Proença L, et al. Parkinson’s di-sease, periodontitis and patient-related outcomes: a cross-sectional study[J]. Medicina (Kaunas), 2020, 56(8): 383.
9 García-de-la-Fuente AM, Fernández-Jiménez A, Lafuente-Ibáñez-de-Mendoza I, et al. Periodontal heal-th in a population with Parkinson’s disease in Spain: a cross-sectional study[J]. Med Oral Patol Oral Cir Bucal, 2023, 28(1): e32-e40.
10 John T, Vasanthy B, Madhavanpillai B, et al. Does Parkinsonism affect periodontal health? A cross-sectional study in a tertiary hospital[J]. J Indian Soc Periodontol, 2021, 25(6): 538-543.
11 Fleury V, Zekeridou A, Lazarevic V, et al. Oral dysbiosis and inflammation in Parkinson’s disease[J]. J Parkinsons Dis, 2021, 11(2): 619-631.
12 Martimbianco ALC, Prosdocimi FC, Anauate-Netto C, et al. Evidence-based recommendations for the oral health of patients with Parkinson’s disease[J]. Neurol Ther, 2021, 10(1): 391-400.
13 Nicholson JS, Landry KS. Oral dysbiosis and neurodegenerative diseases: correlations and potential causations[J]. Microorganisms, 2022, 10(7): 1326.
14 Rozas NS, Tribble GD, Jeter CB. Oral factors that impact the oral microbiota in Parkinson’s disease[J]. Microorganisms, 2021, 9(8): 1616.
15 Chen CK, Wu YT, Chang YC. Periodontal inflammatory disease is associated with the risk of Parkinson’s disease: a population-based retrospective mat-ched-cohort study[J]. PeerJ, 2017, 5: e3647.
16 Hsu YC, Chang CW, Lee HL, et al. Association between history of dental amalgam fillings and risk of Parkinson’s disease: a population-based retrospective cohort study in Taiwan[J]. PLoS One, 2016, 11(12): e0166552.
17 Liu TC, Sheu JJ, Lin HC, et al. Increased risk of Parkinsonism following chronic periodontitis: a retrospective cohort study[J]. Mov Disord, 2013, 28(9): 1307-1308.
18 Jeong E, Park JB, Park YG. Evaluation of the association between periodontitis and risk of Parkinson’s disease: a nationwide retrospective cohort study[J]. Sci Rep, 2021, 11(1): 16594.
19 Liu ZW, Roosaar A, Axéll T, et al. Tobacco use, oral health, and risk of Parkinson’s disease[J]. Am J Epidemiol, 2017, 185(7): 538-545.
20 Kannarkat GT, Boss JM, Tansey MG. The role of innate and adaptive immunity in Parkinson’s disease[J]. J Parkinsons Dis, 2013, 3(4): 493-514.
21 Ebersole JL, Cappelli D. Acute-phase reactants in infections and inflammatory diseases[J]. Periodontol 2000, 2000, 23(1): 19-49.
22 D’Mello C, Swain MG. Immune-to-brain communication pathways in inflammation-associated sickness and depression[J]. Curr Top Behav Neurosci, 2017, 31: 73-94.
23 Herrera AJ, Tomás-Camardiel M, Venero JL, et al. Inflammatory process as a determinant factor for the degeneration of substantia nigra dopaminergic neurons[J]. J Neural Transm (Vienna), 2005, 112(1): 111-119.
24 Herrera AJ, Castaño A, Venero JL, et al. The single intranigral injection of LPS as a new model for studying the selective effects of inflammatory reactions on dopaminergic system[J]. Neurobiol Dis, 2000, 7(4): 429-447.
25 Alvarenga MOP, Frazão DR, de Matos IG, et al. Is there any association between neurodegenerative diseases and periodontitis? A systematic review[J]. Front Aging Neurosci, 2021, 13: 651437.
26 Ledwon B, Miskiewicz A, Grabowska E, et al. The relationship between periodontal disease and motor impairment in the course of Parkinson’s disease[J]. Postepy Hig Med Dosw, 2020, 74: 340-347.
27 Kamer AR, Pirraglia E, Tsui W, et al. Periodontal disease associates with higher brain amyloid load in normal elderly[J]. Neurobiol Aging, 2015, 36(2): 627-633.
28 Perry VH. The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease[J]. Brain Behav Immun, 2004, 18(5): 407-413.
29 Frister A, Schmidt C, Schneble N, et al. Phosphoinositide 3-kinase γ affects LPS-induced disturbance of blood-brain barrier via lipid kinase-independent control of cAMP in microglial cells[J]. Neuromolecular Med, 2014, 16(4): 704-713.
30 Olsen I, Singhrao SK. Can oral infection be a risk factor for Alzheimer’s disease[J]. J Oral Microbiol, 2015, 7: 29143.
31 Gao HM, Jiang J, Wilson B, et al. Microglial activation-mediated delayed and progressive degeneration of rat nigral dopaminergic neurons: relevance to Parkinson’s disease[J]. J Neurochem, 2002, 81(6): 1285-1297.
32 Kim WG, Mohney RP, Wilson B, et al. Regional difference in susceptibility to lipopolysaccharide-induced neurotoxicity in the rat brain: role of micro-glia[J]. J Neurosci, 2000, 20(16): 6309-6316.
33 Olsen I, Kell DB, Pretorius E. Is Porphyromonas gingivalis involved in Parkinson’s disease[J]. Eur J Clin Microbiol Infect Dis, 2020, 39(11): 2013-2018.
34 Cunningham C, Wilcockson DC, Campion S, et al. Central and systemic endotoxin challenges exacerbate the local inflammatory response and increase neuronal death during chronic neurodegeneration[J]. J Neurosci, 2005, 25(40): 9275-9284.
35 McColl BW, Rothwell NJ, Allan SM. Systemic inflammatory stimulus potentiates the acute phase and CXC chemokine responses to experimental stroke and exacerbates brain damage via interleukin-1- and neutrophil-dependent mechanisms[J]. J Neurosci, 2007, 27(16): 4403-4412.
36 Liu Y, Wu Z, Nakanishi Y, et al. Infection of microglia with Porphyromonas gingivalis promotes cell migration and an inflammatory response through the gingipain-mediated activation of protease-activated receptor-2 in mice[J]. Sci Rep, 2017, 7(1): 11759.
37 Wu Z, Ni JJ, Liu YC, et al. Cathepsin B plays a critical role in inducing Alzheimer’s disease-like phenotypes following chronic systemic exposure to lipopolysaccharide from Porphyromonas gingivalis in mice[J]. Brain Behav Immun, 2017, 65: 350-361.
38 Liu YC, Wu Z, Zhang XW, et al. Leptomeningeal cells transduce peripheral macrophages inflammatory signal to microglia in reponse to Porphyromonas gingivalis LPS[J]. Mediators Inflamm, 2013, 2013: 407562.
39 Wu Z, Zhang J, Nakanishi H. Leptomeningeal cells activate microglia and astrocytes to induce IL-10 production by releasing pro-inflammatory cytokines during systemic inflammation[J]. J Neuroimmunol, 2005, 167(1/2): 90-98.
40 Lee H, James WS, Cowley SA. LRRK2 in periphe-ral and central nervous system innate immunity: its link to Parkinson’s disease[J]. Biochem Soc Trans, 2017, 45(1): 131-139.
41 Kozina E, Sadasivan S, Jiao Y, et al. Mutant LRRK2 mediates peripheral and central immune responses leading to neurodegeneration in vivo [J]. Brain, 2018, 141(6): 1753-1769.
42 Feng YK, Wu QL, Peng YW, et al. Oral P. gingivalis impairs gut permeability and mediates immune responses associated with neurodegeneration in LRRK2 R1441G mice[J]. J Neuroinflammation, 2020, 17(1): 347.
43 Kishimoto Y, Zhu WD, Hosoda W, et al. Chronic mild gut inflammation accelerates brain neuropathology and motor dysfunction in α-synuclein mutant mice[J]. Neuromolecular Med, 2019, 21(3): 239-249.
44 Kelly LP, Carvey PM, Keshavarzian A, et al. Progression of intestinal permeability changes and alpha-synuclein expression in a mouse model of Parkinson’s disease[J]. Mov Disord, 2014, 29(8): 999-1009.
45 Houser MC, Tansey MG. The gut-brain axis: is intestinal inflammation a silent driver of Parkinson’s disease pathogenesis[J]. NPJ Parkinsons Dis, 2017, 3: 3.
46 Daher JP. Interaction of LRRK2 and α-synuclein in Parkinson’s disease[J]. Adv Neurobiol, 2017, 14: 209-226.
47 Sun J, Zhang SS, Zhang X, et al. IL-17A is implica-ted in lipopolysaccharide-induced neuroinflammation and cognitive impairment in aged rats via microglial activation[J]. J Neuroinflammation, 2015, 12: 165.
48 Waisman A, Hauptmann J, Regen T. The role of IL-17 in CNS diseases[J]. Acta Neuropathol, 2015, 129(5): 625-637.
49 Liu Z, Qiu AW, Huang Y, et al. IL-17A exacerbates neuroinflammation and neurodegeneration by activating microglia in rodent models of Parkinson’s di-sease[J]. Brain Behav Immun, 2019, 81: 630-645.
50 Kebir H, Kreymborg K, Ifergan I, et al. Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation[J]. Nat Med, 2007, 13(10): 1173-1175.
51 Sharon G, Sampson TR, Geschwind DH, et al. The central nervous system and the gut microbiome[J]. Cell, 2016, 167(4): 915-932.
52 Braak H, Sastre M, Bohl JR, et al. Parkinson’s di-sease: lesions in dorsal horn layer Ⅰ, involvement of parasympathetic and sympathetic pre- and postganglionic neurons[J]. Acta Neuropathol, 2007, 113(4): 421-429.
53 Auffret M, Meuric V, Boyer E, et al. Oral health disorders in Parkinson’s disease: more than meets the eye[J]. J Parkinsons Dis, 2021, 11(4): 1507-1535.
54 Hajishengallis G, Chavakis T. Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities[J]. Nat Rev Immunol, 2021, 21(7): 426-440.
55 Kitamoto S, Nagao-Kitamoto H, Jiao Y, et al. The intermucosal connection between the mouth and gut in commensal pathobiont-driven colitis[J]. Cell, 2020, 182(2): 447-462.e14.
56 Li DC, Ren TZ, Li H, et al. Porphyromonas gingivalis: a key role in Parkinson’s disease with cognitive impairment[J]. Front Neurol, 2022, 13: 945523.
57 Chen CK, Huang JY, Wu YT, et al. Dental scaling decreases the risk of Parkinson’s disease: a nationwide population-based nested case-control study[J]. Int J Environ Res Public Health, 2018, 15(8): 1587.
58 Diederich NJ, Moore CG, Leurgans SE, et al. Parkinson disease with old-age onset: a comparative study with subjects with middle-age onset[J]. Arch Neurol, 2003, 60(4): 529-533.
59 Wong DF, Wagner HN Jr, Dannals RF, et al. Effects of age on dopamine and serotonin receptors measured by positron tomography in the living human brain[J]. Science, 1984, 226(4681): 1393-1396.
[1] 傅豫, 何薇, 黄兰. 铁死亡在口腔疾病中的研究进展[J]. 国际口腔医学杂志, 2024, 51(1): 36-44.
[2] 罗晓洁,王德续,陈晓涛. 基于生物信息学分析铁死亡调控基因与牙周炎的关系[J]. 国际口腔医学杂志, 2023, 50(6): 661-668.
[3] 黄元鸿,彭显,周学东. 骨碎补在治疗口腔骨相关疾病的研究进展[J]. 国际口腔医学杂志, 2023, 50(6): 679-685.
[4] 孙佳,韩烨,侯建霞. 白细胞介素-6-铁调素信号轴调控牙周炎相关性贫血致病机制的研究进展[J]. 国际口腔医学杂志, 2023, 50(3): 329-334.
[5] 刘体倩,梁星,刘蔚晴,李晓虹,朱睿. 咬合创伤在牙周炎发生发展中的作用及机制的研究进展[J]. 国际口腔医学杂志, 2023, 50(1): 19-24.
[6] 李琼,于维先. 白藜芦醇治疗牙周炎及其生物利用度的研究进展[J]. 国际口腔医学杂志, 2023, 50(1): 25-31.
[7] 黄伟琨,徐秋艳,周婷. 黄芩苷抑制脂多糖促巨噬细胞氧化应激损伤作用的研究[J]. 国际口腔医学杂志, 2022, 49(5): 521-528.
[8] 周剑鹏,谢旭东,赵蕾,王骏. 辅助性T细胞17及白细胞介素17在牙周炎中的作用及机制的研究进展[J]. 国际口腔医学杂志, 2022, 49(5): 586-592.
[9] 陈荟宇,白明茹,叶玲. 信号素3A与口腔常见病关系的研究进展[J]. 国际口腔医学杂志, 2022, 49(5): 593-599.
[10] 周佳佳,赵蕾,徐欣. 牙周炎相关基因多态性的研究进展[J]. 国际口腔医学杂志, 2022, 49(4): 432-440.
[11] 马玉,左玉,张鑫. 光动力疗法辅助治疗牙周炎治疗效果的Meta分析[J]. 国际口腔医学杂志, 2022, 49(3): 305-316.
[12] 钱素婷,丁玲敏,纪雅宁,林军. 微小RNA在牙周炎龈沟液中的表达差异及对牙周炎的调控机制[J]. 国际口腔医学杂志, 2022, 49(3): 349-355.
[13] 蒋端,申道南,赵蕾,吴亚菲. 内皮发育调节基因-1与牙周炎相关性的研究进展[J]. 国际口腔医学杂志, 2022, 49(2): 244-248.
[14] 白慧敏,张雨薇,孟姝,刘程程. 特异性促炎症消退介质在牙周炎中作用的研究进展[J]. 国际口腔医学杂志, 2022, 49(1): 85-93.
[15] 黄晓慧,祁本婷,杨洁,刘玉,孙卫斌. 机械性邻面菌斑控制措施对牙周非手术治疗效果影响的系统评价[J]. 国际口腔医学杂志, 2021, 48(6): 656-663.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
[1] 张京剧. 青年期至中年期颅面复合体变化的头影测量研究[J]. 国际口腔医学杂志, 1999, 26(06): .
[2] 刘玲. 镍铬合金中铍对可铸造性和陶瓷金属结合力的影响[J]. 国际口腔医学杂志, 1999, 26(06): .
[3] 王昆润. 在种植体上制作固定义齿以后下颌骨密度的动态变化[J]. 国际口腔医学杂志, 1999, 26(06): .
[4] 王昆润. 修补颌骨缺损的新型生物学相容材料[J]. 国际口腔医学杂志, 1999, 26(06): .
[5] 陆加梅. 不可复性关节盘移位患者术前张口度与关节镜术后疗效的相关性[J]. 国际口腔医学杂志, 1999, 26(06): .
[6] 王昆润. 重型颌面部炎症死亡和康复病例的实验室检查指标比较[J]. 国际口腔医学杂志, 1999, 26(06): .
[7] 王昆润. 二甲亚砜和双氯芬酸并用治疗根尖周炎[J]. 国际口腔医学杂志, 1999, 26(06): .
[8] 汤庆奋,王学侠. 17β-雌二醇对人类阴道和口腔颊粘膜的渗透性[J]. 国际口腔医学杂志, 1999, 26(06): .
[9] 王昆润. 咀嚼口香糖对牙周组织微循环的影响[J]. 国际口腔医学杂志, 1999, 26(06): .
[10] 宋红. 青少年牙周炎外周血分叶核粒细胞的趋化功能[J]. 国际口腔医学杂志, 1999, 26(06): .