牙周炎与活性氧致病机制的研究进展

Abstract
Figure/Table
References (40)
Related Citation (15)

Download: PDF (527 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Recent studies suggest that the direct and indirect participation of oxidative stress is also a key factor in the destruction of periodontal tissue. Reactive oxygen species (ROS) is a product of oxidative stress in the body. It has become a hot research topic in the pathogenesis of periodontitis in recent years. Physiological levels of ROS can participate in physiological activities such as homeostasis, signal transduction and apoptosis in cells as second messengers. Excessive ROS play a cytotoxic role, causing oxidative damage to proteins , lipids and DNA, interfering with cell growth and cell cycle progression , and induce gingival fibroblast apoptosis. These effects of ROS together cause irreversible and direct damage to the periodontal tissue. In addition, ROS can also indirectly cause serious damage to periodontal tissues by activating inflammatory factors, nuclear factor κB (NF-κB), c-Jun N-terminal kinases and autophagy. This article summarizes the relationship between the excessive production of ROS and its activated signal transduction pathway and periodontitis, so as to provide evidence for further exploration of the correlation between ROS and periodontitis.

Key words： Periodontitis Reactive oxygen species Inflammatory factors Nuclear factor-κB C-Jun N-terminal kinases Autophagy

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	FANG Hui LIU QI

Cite this article:

FANG Hui LIU QI. Research progress of pathogenic mechanism of periodontitis and active oxygen[J]. 中国医药导报, 2018, 15(5): 22-26.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2018/V15/I5/22

[1] Wells PG，Mccallum GP，Chen CS，et al. Oxidative stress in developmental origins of disease：teratogenesis，neurodevelopmental deficits，and cancer [J]. Toxicol Sci，2009，108（1）：4-18.
[2] Chang MC，Tsai YL，Chen YW，et al. Butyrate induces reactive oxygen species production and affects cell cycle progression in human gingival fibroblasts [J]. J Periodontal Res，2013，48（1）：66-73.
[3] Yu JY，Lee SY，Son YO，et al. Continuous presence of H2O2 induces mitochondrial-mediated， MAPK- and caspase-independent growth inhibition and cytotoxicity in human gingival fibroblasts [J]. Toxicol In Vitro，2012，26（4）：561-570.
[4] Filomeni G，De Zio D，Cecconi F. Oxidative stress and autophagy：the clash between damage and metabolic needs [J]. Cell Death Differ，2015，22（3）：377-388.
[5] Valko M， Jomova K， Rhodes CJ，et al. Redox- and non-redox-metal-induced formation of free radicals and their role in human disease [J]. Arch Toxicol，2016，90（1）：1-37.
[6] Netto LE，Antunes F. The Roles of Peroxiredoxin and Thioredoxin in Hydrogen Peroxide Sensing and in Signal Transduction [J]. Mol Cells，2016，39（1）：65-71.
[7] Sandalio LM，Romero-Puertas MC. Peroxisomes sense and respond to environmental cues by regulating ROS and RNS signalling networks [J]. Ann Bot，2015，116（4）：475-485.
[8] Nibali L，Donos N. Periodontitis and redox status: a review [J]. Curr Pharm Des，2013，19（15）：2687-2697.
[9] Patil VS，Patil VP，Gokhale N，et al. Chronic Periodontitis in Type 2 Diabetes Mellitus：Oxidative Stress as a Common Factor in Periodontal Tissue Injury [J]. J Clin Diagn Res，2016，10（4）：BC12-BC16.
[10] Palwankar P，Rana M，Arora K，et al. Evaluation of non-surgical therapy on glutathione levels in chronic periodontitis [J]. Eur J Dent，2015，9（3）：415-422.
[11] Zhang CZ，Cheng XQ，Li JY，et al. Saliva in the diagnosis of diseases [J]. Int J Oral Sci，2016，8（3）：133-137.
[12] Baser U，Gamsiz-isik H，Cifcibasi E，et al. Plasma and salivary total antioxidant capacity in healthy controls compared with aggressive and chronic periodontitis patients [J]. Saudi Med J，2015，36（7）：856-861.
[13] Punj A，Shenoy S，Kumari NS，et al. Estimation of Antioxidant Levels in Saliva and Serum of Chronic Periodontitis Patients with and without Ischemic Heart Disease [J]. Int J Dent，2017，2017（6）：1-9.
[14] Akhtar MJ，Ahamed M，Alhadlaq HA，et al. Mechanism of ROS scavenging and antioxidant signalling by redox metallic and fullerene nanomaterials：Potential implications in ROS associated degenerative disorders [J]. Biochim Biophys Acta，2017，1861（4）：802-813.
[15] Cavalla F，Osorio C，Paredes R，et al. Matrix metalloproteinases regulate extracellular levels of SDF-1/CXCL12，IL-6 and VEGF in hydrogen peroxide-stimulated human periodontal ligament fibroblasts [J]. Cytokine，2015，73（1）：114-121.
[16] Klotz LO，Sanchez-Ramos C，Prieto-Arroyo I，et al. Redox regulation of FoxO transcription factors [J]. Redox Biol，2015，6（2）：51-72.
[17] Levy M，Thaiss CA，Katz MN，et al. Inflammasomes and the microbiota--partners in the preservation of mucosal homeostasis [J]. Semin Immunopathol，2015，37（1）：39-46.
[18] Schroder K，Tschopp J. The inflammasomes [J]. Cell，2010， 140（6）：821-832.
[19] Huang X，Yang X，Ni J，et al. Hyperglucose contributes to periodontitis：involvement of the NLRP3 pathway by engaging the innate immunity of oral gingival epithelium [J]. J Periodontol，2015，86（2）：327-335.
[20] von Moltke JV，Ayres JS，Kofoed EM，et al. Recognition of bacteria by inflammasomes [J]. Annu Rev of Immunol，2013，31（31）：73-106.
[21] Park E，Na HS，Song YR，et al. Activation of NLRP3 and AIM2 inflammasomes by Porphyromonas gingivalis infection [J]. Infect Immun，2014，82（1）：112-123.
[22] Nikhil K，Sharan S，Roy P. A pterostilbene derivative suppresses osteoclastogenesis by regulating RANKL-mediated NFκB and MAPK signaling in RAW264.7 cells [J]. Pharmacol Rep，2015，67（6）：1264-1272.
[23] Ozcan E，Saygun NI，Ilikci R，et al. Increased visfatin expression is associated with nuclear factor-kappa B and phosphatidylinositol 3-kinase in periodontal inflammation [J]. Clin Oral Investig，2017，21（4）：1113-1121.
[24] Meyle J，Chapple I. Molecular aspects of the pathogenesis of periodontitis [J]. Periodontol，2015，69（1）：7-17.
[25] Czupkallo L，Rahnama M，Kielbowicz D et al. Bone metabolism and RANKL/RANK/OPG trail in periodontal disease [J]. Curr Issues in Pharm Med Sci，2016，29（4）：171-175.
[26] Ni XB，Jia C，Yu HD，et al. Comprehensive analysis of interleukin-8 gene polymorphisms and periodontitis susceptibility [J]. Oncotarget，2017，8（30）：48 996-49 004.
[27] Bauernfeind FG，Horvath G，Stutz A，et al. Cutting edge：NF-kappaB activating pattern recognition and cytokine receptors license NLRP3 inflammasome activation by regulating NLRP3 expression [J]. J Immunol，2009，183（2）：787-791.
[28] Yoshida K，Okamura H，Hiroshima Y，et al. PKR induces the expression of NLRP3 by regulating the NF-kappaB pathway in Porphyromonas gingivalis-infected osteoblasts [J]. Exp Cell Res，2017，354（1）：57-64.
[29] Kang SW，Park HJ，Ban JY，et al. Effect of nicotine on apoptosis in human gingival fibroblast [J]. Arch Oral Biol，2011，56（10）：1091-1097.
[30] Li X，Wang X，Zheng M，et al. Mitochondrial reactive oxygen species mediate the lipopolysaccharide-induced pro-inflammatory response in human gingival fibroblasts [J]. Exp Cell Res，2016，347（1）：212-221.
[31] Nakano H，Nakajima A，Sakonkomazawa S，et al. Reactive oxygen species mediate crosstalk between NF-kappaB and JNK [J]. Cell Death Differ，2006，13（5）：730-737.
[32] Filomeni G，De ZD，Cecconi F. Oxidative stress and autophagy：the clash between damage and metabolic needs [J]. Cell Death Differ，2015，22（3）：377-388.
[33] Tan YQ，Zhang J，Zhou G. Autophagy and its implication in human oral diseases [J]. Autophagy，2017，13（2）：225-236.
[34] Kim MS，Yun JW，Park JH，et al. Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts [J]. Int J Med Sci，2016，13（5）：357-364.
[35] Song B， Zhou T，Yang WL，et al. Programmed cell death in periodontitis：recent advances and future perspectives [J]. Oral Dis，2017，23（5）：609-619.
[36] Ebe N，Harayokoyama M，Iwasaki K，et al. Pocket epithelium in the pathological setting for HMGB1 release [J]. J Dent Res，2011，90（2）：235-240.
[37] An Y，Liu W，Xue P，et al. Increased autophagy is required to protect periodontal ligament stem cells from apoptosis in inflammatory microenvironment [J]. J Clin Periodontol，2016，43（7）：618-625.
[38] Rodrigues PH，Bëlanger M，Jr DW，et al. Porphyromonas gingivalis and the autophagic pathway：an innate immune interaction? [J]. Front Biosci，2008，13（4）：178-187.
[39] Cho TJ，Wee SW，Woo VH，et al. Porphyromonas gingivalis-induced autophagy suppresses cell proliferation through G1 arrest in oral cancer cells [J]. Arch Oral Biol，2014， 59（4）：370-378.
[40] Takeuchi H，Furuta N，Amano A. Cell entry and exit by periodontal pathogen via recycling pathway [J]. Commun Integr Biol，2011，4（5）：587-589.
[41] Takeuchi H，Furuta N，Morisaki I，et al. Exit of intracellular Porphyromonas gingivalis from gingival epithelial cells is mediated by endocytic recycling pathway [J]. Cell Microbiol，2011，13（5）：677-691.