侵袭性牙周炎唾液诊断标记物的研究进展
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摘要
侵袭性牙周炎是好发于青年人群,以进展迅速、破坏严重为特征,伴有家族聚集性的一类牙周炎。唾液中生物标记物能实时反映口腔软组织和硬组织、口腔内微生物的状态,在侵袭性牙周炎的诊断中有运用潜力,并可监测其活动状态。同时,唾液诊断具有廉价、无创、简便、舒适等优点。因此,唾液中的生物标记物有助于侵袭性牙周炎的早期诊断、实时监测。本文对侵袭性牙周炎唾液诊断标记物的研究现状进行综述,以期为侵袭性牙周炎唾液诊断提供思路。
Aggressive periodontitis is a specific form of periodontal disease with a high rate of progression and patterns of tissue destruction. This infection mostly affects young individuals and exhibits familial aggregation. Given the ability of salivary biomarkers to indicate the condition of soft tissues, bones and microorganisms in oral, salivary biomarkers may possess the potential to diagnosis and monitor aggressive periodontitis. Obtaining saliva can be low cost, noninvasive,simple and comfortable. Salivary biomarkers can be applied to early diagnosis and real-time monitoring of aggressive periodontitis. In this review, we summarise the research progression on salivary markers for aggressive periodontitis diagnosis to provide new ideas for diagnosis of such infection.
Aggressive periodontitis is a specific form of periodontal disease with a high rate of progression and patterns of tissue destruction. This infection mostly affects young individuals and exhibits familial aggregation. Given the ability of salivary biomarkers to indicate the condition of soft tissues, bones and microorganisms in oral, salivary biomarkers may possess the potential to diagnosis and monitor aggressive periodontitis. Obtaining saliva can be low cost, noninvasive,simple and comfortable. Salivary biomarkers can be applied to early diagnosis and real-time monitoring of aggressive periodontitis. In this review, we summarise the research progression on salivary markers for aggressive periodontitis diagnosis to provide new ideas for diagnosis of such infection.
引文
[1] Albandar JM. Aggressive periodontitis:case definition and diagnostic criteria[J]. Periodontol 2000,2014, 65(1):13-26.
[2] Liu J, Duan Y. Saliva:a potential media for disease diagnostics and monitoring[J]. Oral Oncol, 2012, 48(7):569-577.
[3] Jaedicke KM, Preshaw PM, Taylor JJ. Salivary cytokines as biomarkers of periodontal diseases[J]. Periodontol 2000, 2016, 70(1):164-183.
[4] Smith M, Seymour GJ, Cullinan MP. Histopathological features of chronic and aggressive periodontitis[J]. Periodontol 2000, 2010, 53:45-54.
[5] Van der Velden U. What exactly distinguishes aggre-ssive from chronic periodontitis:is it mainly a difference in the degree of bacterial invasiveness[J].Periodontol 2000, 2017, 75(1):24-44.
[6] Taylor JJ. Protein biomarkers of periodontitis in saliva[J]. ISRN Inflamm, 2014, 2014:593151.
[7] Proctor GB. The physiology of salivary secretion[J].Periodontol 2000, 2016, 70(1):11-25.
[8] Hajishengallis G. Periodontitis:from microbial immune subversion to systemic inflammation[J]. Nat Rev Immunol,2015, 15(1):30-44.
[9] Yucel-Lindberg T, Bage T. Inflammatory mediators in the pathogenesis of periodontitis[J]. Expert Rev Mol Med, 2013, 15:e7.
[10] Trindade F, Oppenheim FG, Helmerhorst EJ, et al.Uncovering the molecular networks in periodontitis[J]. Proteomics Clin Appl, 2014, 8(9/10):748-761.
[11] Takahashi N. Oral microbiome metabolism:from"Who are they?"to"What are they doing?"[J]. J Dent Res, 2015,94(12):1628-1637.
[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]Gumus P,Nizam N, Nalbantsoy A, et al. Saliva and serum levels of pentraxin-3 and interleukin-1(3 in generalized aggressive or chronic periodontitis[J]. J Periodontol, 2014, 85(3):e40-e46.
[14] Elabdeen HR, Mustafa M, Szklenar M, et al. Ratio of pro-resolving and pro-inflammatory lipid mediator precursors as potential markers for aggressive periodontitis[J]. PLoS One, 2013, 8(8):e70838.
[15] Nunes LA, Mussavira S, Bindhu OS. Clinical and diagnostic utility of saliva as a non-invasive diagnostic fluid:a systematic review[J]. Biochem Med(Zagreb), 2015,25(2):177-192.
[16] Haririan H,Andrukhov 0, Bertl K,et al. Microbial analysis of subgingival plaque samples compared to that of whole saliva in patients with periodontitis[J].J Periodontol,2014, 85(6):819-828.
[17] Kononen E, Muller HP. Microbiology of aggressive periodontitis[J]. Periodontol 2000, 2014, 65(1):46-78.
[18]冯向辉,张立,孟焕新,等.牙周炎患者唾液中伴放杆线放线杆菌的检出状况分析[J].中华口腔医学杂志,2008, 43(7):402-405.Feng XH,Zhang L, Meng HX, et al. Prevalence of Actinobacillus actinomycetemcomitans in saliva of different types of periodontitis[J]. Chin J Stomatol,2008,43(7):402-405.
[19] Lopez R, Dahlen G, Retamales C, et al. Clustering of subgingival microbial species in adolescents with periodontitis[J]. Eur J Oral Sci, 2011, 119(2):141-150.
[20] Li Y, Feng X,Xu L, et al. Oral microbiome in Chinese patients with aggressive periodontitis and their family members[J]. J Clin Periodontol, 2015, 42(11):1015-1023.
[21] Saygun I, Nizam N, Keskiner I, et al. Salivary infectious agents and periodontal disease status[J]. J Periodont Res, 2011,46(2):235-239.
[22] 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.
[23] Ryder MI. Comparison of neutrophil functions in aggressive and chronic periodontitis[J]. Periodontol2000, 2010, 53:124-137.
[24] Acquier AB, De Couto Pita AK, Busch L, et al. Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis[J]. Redox Rep, 2017, 22(3):119-126.
[25] Baltacioglu E, Yuva P, Aydin G, et al. Lipid peroxidation levels and total oxidant/antioxidant status in serum and saliva from patients with chronic and aggressive periodontitis. Oxidative stress index:a new biomarker for periodontal disease[J]. J Periodontol, 2014, 85(10):1432-1441.
[26] Villa-Correa YA,Isaza-Guzman DM,Tobon-Arroyave SI. Influence of periodontal clinical status on salivary levels of glutathione reductase[J]. J Periodontol, 2016, 87(6):716-724.
[27] Zamora-Perez AL, Ortiz-Garcia YM, Lazalde-Ramos BP, et al. Increased micronuclei and nuclear abnormalities in buccal mucosa and oxidative damage in saliva from patients with chronic and aggressiveperiodontal diseases[J]. J Periodont Res, 2015, 50(1):28-36.
[28] Ghallab N, Hamdy E, Shaker O. Malondialdehyde,superoxide dismutase and melatonin levels in gingival crevicular fluid of aggressive and chronic periodontitis patients[J]. Aust Dent J, 2016, 61(1):53-61.
[29] Gümus P,Nizam N,Lappin DF,et al. Saliva and serum levels of B-cell activating factors and tumor necrosis factor-a in patients with periodontitis[J]. J Periodontol,2014, 85(2):270-280.
[30] Tobon-Arroyave SI, Jaramillo-Gonzalez PE, IsazaGuzman DM. Correlation between salivary IL-1βlevels and periodontal clinical status[J]. Arch Oral Biol, 2008, 53(4):346-352.
[31] Yue Y, Liu Q, Xu C, et al. Comparative evaluation of cytokines in gingival crevicular fluid and saliva of patients with aggressive periodontitis[J]. Int J Biol Markers, 2013,28(1):108-112.
[32] Nizam N, Gumus P, Pitkanen J, et al. Serum and salivary matrix metalloproteinases, neutrophil elastase, myeloperoxidase in patients with chronic or aggressive periodontitis[J]. Inflammation, 2014, 37(5):1771-1778.
[33]康军,沙月琴,陈智滨.不同牙周状况下唾液和龈沟液中弹性蛋白酶的含量[J].北京大学学报(医学版),2012,44(1):17-21.Kang J, Shan YQ, Chen ZB. Granulocyte elastase levels in saliva and gingival crevicular fluid of subjects with various periodontal conditions[J]. J Peking Univ(Health Sci),2012, 44(1):17-21.
[34] Aral CA, Koseoglu S, Saglam M, et al. Gingivalcrevicular fluid and salivary periostin levels in nonsmoker subjects with chronic and aggressive periodontitis:periostin levels in chronic and aggressive periodontitis[J]. Inflammation, 2016, 39(3):986-993.
[35] Hagewald S, Bernimoulin JP, K6ttgen E, et al.Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitis[J]. J Periodontal Res, 2002, 37(5):333-339.
[36] Fu Y, Korostoff JM, Fine DH, et al. Fey receptor genes as risk markers for localized aggressive periodontitis in African-Americans[J]. J Periodontol,2002, 73(5):517-523.
[37] Obayashi K. Salivary mental stress proteins[J]. Clin Chim Acta, 2013,425:196-201.
[38] Haririan H, Bertl K, Laky M, et al. Salivary and serum chromogranin A and a-amylase in periodontal health and disease[J]. J Periodontol, 2012, 83(10):1314-1321.
[39] Kamin HS, Kertes DA. Cortisol and DHEA in development and psychopathology[J]. Horm Behav,2017,89:69-85.
[40] Cakmak O, Tasdemir Z,Aral CA, et al. Gingival crevicular fluid and saliva stress hormone levels in patients with chronic and aggressive periodontitis[J].J Clin Periodontol, 2016, 43(12):1024-1031.
[41] Mestnik MJ, Feres M, Figueiredo LC, et al. The effects of adjunctive metronidazole plus amoxicillin in the treatment of generalized aggressive periodontitis:a 1-year double-blinded, placebo-controlled,randomized clinical trial[J]. J Clin Periodontol, 2012,39(10):955-961.
[2] Liu J, Duan Y. Saliva:a potential media for disease diagnostics and monitoring[J]. Oral Oncol, 2012, 48(7):569-577.
[3] Jaedicke KM, Preshaw PM, Taylor JJ. Salivary cytokines as biomarkers of periodontal diseases[J]. Periodontol 2000, 2016, 70(1):164-183.
[4] Smith M, Seymour GJ, Cullinan MP. Histopathological features of chronic and aggressive periodontitis[J]. Periodontol 2000, 2010, 53:45-54.
[5] Van der Velden U. What exactly distinguishes aggre-ssive from chronic periodontitis:is it mainly a difference in the degree of bacterial invasiveness[J].Periodontol 2000, 2017, 75(1):24-44.
[6] Taylor JJ. Protein biomarkers of periodontitis in saliva[J]. ISRN Inflamm, 2014, 2014:593151.
[7] Proctor GB. The physiology of salivary secretion[J].Periodontol 2000, 2016, 70(1):11-25.
[8] Hajishengallis G. Periodontitis:from microbial immune subversion to systemic inflammation[J]. Nat Rev Immunol,2015, 15(1):30-44.
[9] Yucel-Lindberg T, Bage T. Inflammatory mediators in the pathogenesis of periodontitis[J]. Expert Rev Mol Med, 2013, 15:e7.
[10] Trindade F, Oppenheim FG, Helmerhorst EJ, et al.Uncovering the molecular networks in periodontitis[J]. Proteomics Clin Appl, 2014, 8(9/10):748-761.
[11] Takahashi N. Oral microbiome metabolism:from"Who are they?"to"What are they doing?"[J]. J Dent Res, 2015,94(12):1628-1637.
[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]Gumus P,Nizam N, Nalbantsoy A, et al. Saliva and serum levels of pentraxin-3 and interleukin-1(3 in generalized aggressive or chronic periodontitis[J]. J Periodontol, 2014, 85(3):e40-e46.
[14] Elabdeen HR, Mustafa M, Szklenar M, et al. Ratio of pro-resolving and pro-inflammatory lipid mediator precursors as potential markers for aggressive periodontitis[J]. PLoS One, 2013, 8(8):e70838.
[15] Nunes LA, Mussavira S, Bindhu OS. Clinical and diagnostic utility of saliva as a non-invasive diagnostic fluid:a systematic review[J]. Biochem Med(Zagreb), 2015,25(2):177-192.
[16] Haririan H,Andrukhov 0, Bertl K,et al. Microbial analysis of subgingival plaque samples compared to that of whole saliva in patients with periodontitis[J].J Periodontol,2014, 85(6):819-828.
[17] Kononen E, Muller HP. Microbiology of aggressive periodontitis[J]. Periodontol 2000, 2014, 65(1):46-78.
[18]冯向辉,张立,孟焕新,等.牙周炎患者唾液中伴放杆线放线杆菌的检出状况分析[J].中华口腔医学杂志,2008, 43(7):402-405.Feng XH,Zhang L, Meng HX, et al. Prevalence of Actinobacillus actinomycetemcomitans in saliva of different types of periodontitis[J]. Chin J Stomatol,2008,43(7):402-405.
[19] Lopez R, Dahlen G, Retamales C, et al. Clustering of subgingival microbial species in adolescents with periodontitis[J]. Eur J Oral Sci, 2011, 119(2):141-150.
[20] Li Y, Feng X,Xu L, et al. Oral microbiome in Chinese patients with aggressive periodontitis and their family members[J]. J Clin Periodontol, 2015, 42(11):1015-1023.
[21] Saygun I, Nizam N, Keskiner I, et al. Salivary infectious agents and periodontal disease status[J]. J Periodont Res, 2011,46(2):235-239.
[22] 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.
[23] Ryder MI. Comparison of neutrophil functions in aggressive and chronic periodontitis[J]. Periodontol2000, 2010, 53:124-137.
[24] Acquier AB, De Couto Pita AK, Busch L, et al. Parameters of oxidative stress in saliva from patients with aggressive and chronic periodontitis[J]. Redox Rep, 2017, 22(3):119-126.
[25] Baltacioglu E, Yuva P, Aydin G, et al. Lipid peroxidation levels and total oxidant/antioxidant status in serum and saliva from patients with chronic and aggressive periodontitis. Oxidative stress index:a new biomarker for periodontal disease[J]. J Periodontol, 2014, 85(10):1432-1441.
[26] Villa-Correa YA,Isaza-Guzman DM,Tobon-Arroyave SI. Influence of periodontal clinical status on salivary levels of glutathione reductase[J]. J Periodontol, 2016, 87(6):716-724.
[27] Zamora-Perez AL, Ortiz-Garcia YM, Lazalde-Ramos BP, et al. Increased micronuclei and nuclear abnormalities in buccal mucosa and oxidative damage in saliva from patients with chronic and aggressiveperiodontal diseases[J]. J Periodont Res, 2015, 50(1):28-36.
[28] Ghallab N, Hamdy E, Shaker O. Malondialdehyde,superoxide dismutase and melatonin levels in gingival crevicular fluid of aggressive and chronic periodontitis patients[J]. Aust Dent J, 2016, 61(1):53-61.
[29] Gümus P,Nizam N,Lappin DF,et al. Saliva and serum levels of B-cell activating factors and tumor necrosis factor-a in patients with periodontitis[J]. J Periodontol,2014, 85(2):270-280.
[30] Tobon-Arroyave SI, Jaramillo-Gonzalez PE, IsazaGuzman DM. Correlation between salivary IL-1βlevels and periodontal clinical status[J]. Arch Oral Biol, 2008, 53(4):346-352.
[31] Yue Y, Liu Q, Xu C, et al. Comparative evaluation of cytokines in gingival crevicular fluid and saliva of patients with aggressive periodontitis[J]. Int J Biol Markers, 2013,28(1):108-112.
[32] Nizam N, Gumus P, Pitkanen J, et al. Serum and salivary matrix metalloproteinases, neutrophil elastase, myeloperoxidase in patients with chronic or aggressive periodontitis[J]. Inflammation, 2014, 37(5):1771-1778.
[33]康军,沙月琴,陈智滨.不同牙周状况下唾液和龈沟液中弹性蛋白酶的含量[J].北京大学学报(医学版),2012,44(1):17-21.Kang J, Shan YQ, Chen ZB. Granulocyte elastase levels in saliva and gingival crevicular fluid of subjects with various periodontal conditions[J]. J Peking Univ(Health Sci),2012, 44(1):17-21.
[34] Aral CA, Koseoglu S, Saglam M, et al. Gingivalcrevicular fluid and salivary periostin levels in nonsmoker subjects with chronic and aggressive periodontitis:periostin levels in chronic and aggressive periodontitis[J]. Inflammation, 2016, 39(3):986-993.
[35] Hagewald S, Bernimoulin JP, K6ttgen E, et al.Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitis[J]. J Periodontal Res, 2002, 37(5):333-339.
[36] Fu Y, Korostoff JM, Fine DH, et al. Fey receptor genes as risk markers for localized aggressive periodontitis in African-Americans[J]. J Periodontol,2002, 73(5):517-523.
[37] Obayashi K. Salivary mental stress proteins[J]. Clin Chim Acta, 2013,425:196-201.
[38] Haririan H, Bertl K, Laky M, et al. Salivary and serum chromogranin A and a-amylase in periodontal health and disease[J]. J Periodontol, 2012, 83(10):1314-1321.
[39] Kamin HS, Kertes DA. Cortisol and DHEA in development and psychopathology[J]. Horm Behav,2017,89:69-85.
[40] Cakmak O, Tasdemir Z,Aral CA, et al. Gingival crevicular fluid and saliva stress hormone levels in patients with chronic and aggressive periodontitis[J].J Clin Periodontol, 2016, 43(12):1024-1031.
[41] Mestnik MJ, Feres M, Figueiredo LC, et al. The effects of adjunctive metronidazole plus amoxicillin in the treatment of generalized aggressive periodontitis:a 1-year double-blinded, placebo-controlled,randomized clinical trial[J]. J Clin Periodontol, 2012,39(10):955-961.