medigraphic.com
ISSN 2007-4360 (Impreso)
Asociación Mexicana de Periodontología, Colegio de Periodoncistas A.C

2017, Número 2-3

<< Anterior Siguiente >>

Rev Mex Periodontol 2017; 8 (2-3)


Polimorfismo -308 G›A del gen TNF-α y su papel en la periodontitis

Görnemann CN, Gómez SJR, Fuentes-Lerma MG, Gallegos Arreola MP, Mariaud Schmidt RP

Idioma: Español
Referencias bibliográficas: 50
Paginas: 54-59
Archivo PDF: 287.35 Kb.


RESUMEN

La periodontitis es una enfermedad inflamatoria que se distingue por la presencia de pérdida de inserción y hueso como resultado de las interacciones entre las especies microbianas subgingivales específicas y el huésped susceptible. Esta interacción conduce a la liberación de mediadores inflamatorios como las citocinas proinflamatorias, que intervienen en la destrucción del tejido con la intención de controlar a los microorganismos presentes en el surco gingival. El factor de necrosis tumoral alfa (TNF- α) pertenece a este grupo de citocinas, por lo que su presencia podría representar un factor de riesgo en el mantenimiento y progresión de la enfermedad periodontal. Se ha descrito que la heterogeneidad alélica en los genes de las citocinas y los factores que regulan su expresión pueden influir en las manifestaciones clínicas y progresión de la enfermedad periodontal. Diversos estudios han demostrado que los polimorfismos ubicados en el promotor del gen de TNF- α tienen un aumento significativo en su actividad transcripcional. A pesar de que el polimorfismo -308 G›A se encuentra en el promotor de dicho gen y hay un cambio de un alelo G por un alelo A, los cambios funcionales a causa del polimorfismo no son claros. Se han realizado diversos estudios en diferentes poblaciones del mundo en los que se han encontrado resultados controversiales respecto a la asociación de dicho polimorfismo con la enfermedad periodontal. Los polimorfismos de TNF- α pueden aparecer con patrones alélicos variables en distintas poblaciones. El uso de las técnicas moleculares y su aplicación diagnóstica en el área odontológica, particularmente en la enfermedad periodontal, ha permitido integrar más conocimientos sobre esta y su evolución; explorar estas herramientas nos permitirá dilucidar si en nuestra población existe o no asociación del polimorfismo -308G›A del gen TNF- α con la progresión o severidad de dicha enfermedad.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Kornman KS, Page RC, Tonetti MS. The host response to the microbial challenge in periodontitis: assembling the players. Periodontol 2000. 1997; 14: 33-53.

  2. Kornman KS. Mapping the pathogenesis of periodontitis: a new look. J Periodontol. 2008; 79 (8 Suppl): 1560-1568.

  3. Newman MG, Takei HH, Carranza FA. Periodontología clínica. 12.ª ed. Canadá: Elsevier; 2015.

  4. Graves DT, Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J Periodontol 2003; 74 (3): 391-401.

  5. Zucali JR, Elfenbein GJ, Barth KC, Dinarello CA. Effects of human interleukin 1 and human tumor necrosis factor on human T lymphocyte colony formation. J Clin Invest. 1987; 80 (3): 772-777.

  6. Page RC, Kornman KS. The pathogenesis of human periodontitis: an introduction. Periodontol 2000. 1997; 14: 9-11.

  7. Graves DT. The potential role of chemokines and inflammatory cytokines in periodontal disease progression. Clin Infect Dis. 1999; 28 (3): 482-490.

  8. Silva MJ, Sousa LM, Lara VP, Cardoso FP, Junior GM, Totola AH et al. The role of iNOS and PHOX in periapical bone resorption. J Dent Res. 2011; 90 (4): 495-500.

  9. Tai H, Endo M, Shimada Y, Gou E, Orima K, Kobayashi T et al. Association of interleukin-1 receptor antagonist gene polymorphisms with early onset periodontitis in Japanese. J Clin Periodontol. 2002; 29 (10): 882-888.

  10. Yang W, Jia Y, Wu H. Four tumor necrosis factor alpha genes polymorphisms and periodontitis risk in a Chinese population. Hum Immunol. 2013; 74 (12): 1684-1687.

  11. Taubman MA, Kawai T, Han X. The new concept of periodontal disease pathogenesis requires new and novel therapeutic strategies. J Clin Periodontol. 2007; 34 (5): 367-369.

  12. Kanakdande V, Patil KP, Nayyar AS. Comparative evaluation of clinical, hematological and systemic inflammatory markers in smokers and non-smokers with chronic periodontitis. Contemp Clin Dent. 2015; 6 (3): 348-357.

  13. Madianos PN, Bobetsis YA, Kinane DF. Generation of inflammatory stimuli: how bacteria set up inflammatory responses in the gingiva. J Clin Periodontol. 2005; 32 (6): 57-71.

  14. Ohlrich EJ, Cullinan MP, Seymour GJ. The immunopathogenesis of periodontal disease. Aust Dent J. 2009; 54 (Suppl 1): S2-10.

  15. Boyle WJ, Simonet WS, Lacey DL. Osteoclast differentiation and activation. Nature. 2003; 423 (6937): 337-342.

  16. Cochran DL. Inflammation and bone loss in periodontal disease. J Periodontol. 2008; 79 (8 Suppl): 1569-1576.

  17. Wei S, Kitaura H, Zhou P, Ross FP, Teitelbaum SL. IL-1 mediates TNF-induced osteoclastogenesis. J Clin Invest. 2005; 115 (2): 282-290.

  18. Loos BG, John RP, Laine ML. Identification of genetic risk factors for periodontitis and possible mechanisms of action. J Clin Periodontol. 2005; 32 (Suppl 6): 159-179.

  19. Brenner DA, O’Hara M, Angel P, Chojkier M, Karin M. Prolonged activation of jun and collagenase genes by tumour necrosis factor-alpha. Nature. 1989; 337 (6208): 661-663.

  20. Graves DT, Oskoui M, Volejnikova S, Naguib G, Cai S, Desta T et al. Tumor necrosis factor modulates fibroblast apoptosis, PMN recruitment, and osteoclast formation in response to P. gingivalis infection. J Dent Res. 2001; 80 (10): 1875-1879.

  21. Correa FO, Gonçalves G, Figueredo CM, Bastos AS, Gustafsson A, Orrico SR. Effect of periodontal treatment on metabolic control, systemic inflammation and cytokines in patients with type 2 diabetes. J Clin Periodontol. 2010; 37 (1): 53-58.

  22. Sexton WM, Lin Y, Kryscio RJ, Dawson III DR, Ebersole JL, Miller CS. Salivary biomarkers of periodontal disease in response to treatment. J Clin Periodontol. 2011; 38 (5): 434-441.

  23. Kejriwal S, Bhandary R, Thomas B, Kumari S. Estimation of levels of salivary mucin, amylase and total protein in gingivitis and chronic periodontitis patients. J Clin Diagn Res. 2014; 8 (10): ZC56-60.

  24. Pennica, D, Nedwin GE, Hayflick JS, Seeburg PH, Derynck R, Palladino MA et al. Human tumour necrosis factor: precursor structure, expression and homology to lymphotoxin. Nature. 1984; 312: 724-729.

  25. Nedwin GE, Svedersky LP, Bringman TS, Palladino MA Jr, Goeddel DV. Effect of interleukin 2, interferon-gamma, and mitogens on the production of tumor necrosis factors alpha and beta. J Immunol. 1985; 135 (4): 2492-2497.

  26. Herrmann SM, Ricard S, Nicaud V, Mallet C, Arveiler D, Evans A et al. Polymorphisms of the tumour necrosis factor-alpha gene, coronary heart disease and obesity. Eur J Clin Invest. 1998; 28 (1): 59-66.

  27. Kroeger KM, Carville KS, Abraham LJ. The -308 tumor necrosis factor-alpha promoter polymorphism effects transcription. Mol Immunol. 1997; 34 (5): 391-399.

  28. Wilson AG, Symons JA, McDowell TL, McDevitt HO, Duff GW. Effects of a polymorphism in the human tumor necrosis factor alpha promoter on transcriptional activation. Proc Natl Acad Sci USA. 1997; 94 (7): 3195-3199.

  29. Elahi MM, Asotra K, Matata BM, Mastana SS. Tumor necrosis factor alpha -308 gene locus promoter polymorphism: An analysis of association with health and disease. Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease. 2009; 1792 (3): 163-172.

  30. Chen D, Liu JL, Liu Y, Zhu J, Wang SW. Lack of an association between -308G>A polymorphism of the TNF-alpha gene and liver cirrhosis risk based on a meta-analysis. Genet Mol Res. 2011; 10: 2765-2774.

  31. Matthews N. Anti-tumour cytotoxin produced by human monocytes: studies on its mode of action. Br J Cancer. 1983; 48 (3): 405-410.

  32. Skoog T, van’t Hooft FM, Kallin B, Jovinge S, Boquist S, Nilsson J et al. A common functional polymorphism (C>A substitution at position -863) in the promoter region of the tumour necrosis factor-alpha (TNF-alpha) gene associated with reduced circulating levels of TNF-alpha. Hum Mol Genet. 1999; 8: 1443-1449.

  33. Karthikeyan R, Peeran SW, Murugan M, Awidat K, Basheer O, Al Mugrabi MH. Single nucleotide polymorphisms and periodontitis. Dent Med Res. 2014; 2 (1): 3-7.

  34. Khosropanah H, Sarvestani EK, Mahmoodi A, Golshah M. Association of IL-8 (-251 A/T) gene polymorphism with clinical parameters and chronic periodontitis. J Dent (Tehran). 2013; 10 (4): 312-318.

  35. Ni XB, Jia C, Yu HD, Li YQ, Zeng XT, Leng WD. Comprehensive analysis of interleukin-8 gene polymorphisms and periodontitis susceptibility. Oncotarget. 2017; 8 (30): 48996-49004.

  36. Cereda C, Cova E, Diamanti L, Ceroni M, Gagliardi S. The role of TNF-alpha in ALS: New hypotheses for future therapeutic approaches. Amyotrophic-lateral-sclerosis. In Tech. 2012: 413-435.

  37. Guadagni F, Ferroni P, Palmirotta R, Portarena I, Formica V, Roselli M. Review TNF/VEGF cross-talk in chronic inflammation related cancer initiation and progression: an early target in anticancer therapeutic strategy. In Vivo. 2007; 21 (2): 147-161.

  38. Qing H, Guo-Guang L, Ying-Chao L, LeQian, Bo-Dong L. The tumor necrosis factor α -308 and -238 polymorphisms and risk of hepatocellular carcinoma for Asian populations: a meta-analysis. Curr Ther Res Clin Exp. 2014; (76): 70-75.

  39. Da Costa TA, Silva MJ, Alves PM, Chica JE, Barcelos EZ, Giani MA et al. Inflammation biomarkers of advanced disease in nongingival tissues of chronic periodontitis patients. Mediators Inflamm. 2015; 2015: 983782.

  40. Pociot F, D’Alfonso S, Compasso S, Scorza R, Richiardi PM. Functional analysis of a new polymorphism in the human TNF-alpha gene promoter. Scand J Immunol. 1995; 42 (4): 501-504.

  41. Özer Yücel Ö, Berker E, Mesci L, Eratalay K, Tepe E, Tezcan İ. Analysis of TNF-α (-308) polymorphism and gingival crevicular fluid TNF-α levels in aggressive and chronic periodontitis: a preliminary report. Cytokine. 2015; 72 (2): 173-177.

  42. Song GG, Choi SJ, Ji JD, Lee JH. Association between tumor necrosis factor-a promoter -308 A/G,-238 A/G, interleukin-6 -174 G/C and -572 G/C polymorphisms and periodontal disease: a meta-analysis. Mol Biol Rep. 2013; 40: 5191-5203.

  43. D’Aiuto F, Parkar M, Brett PM, Ready D, Tonetti MS. Gene polymorphisms in pro-inflammatory cytokines are associated with systemic inflammation in patients with severe periodontal infections. Cytokine. 2004; 28 (1): 29-34.

  44. Galbraith GM, Hendley TM, Sanders JJ, Palesch Y, Pandey JP. Polymorphic cytokine genotypes as markers of disease severity in adult periodontitis. J Clin Periodontol. 1999; 26 (11): 705-709.

  45. Ding C, Ji X, Chen X, Xu Y, Zhong L. TNF-α gene promoter polymorphisms contribute to periodontitis susceptibility: evidence from 46 studies. J Clin Periodontol. 2014; 41: 748-759.

  46. Wang S, Lewis CM Jr., Jakobsson M, Ramachandran S, Ray N, Bedoya G et al. Genetic variation and population structure in Native Americans. PLoS Genet. 2007; 3 (11): e185.

  47. Acuña AV, Flores DT, Kruit JK, Villareal MT, Arellano O, Hünemeier T et al. A functional ABCA1 gene variant is associated with low HDL-cholesterol levels and shows evidence of positive selection in Native Americans. Hum Mol Genet. 2010; 19 (14): 2877-2885.

  48. Williams AL, Jacobs SB, Moreno MH, Huerta CA, Churchhouse C, Márquez LC et al. Sequence variants in SLC16A11 are a common risk factor for type 2 diabetes in Mexico. Nature. 2014; 506: 97-101.

  49. Vázquez-Huerta DI, Alvarez-Rodríguez BA, Topete-Reyes JF, Muñoz-Valle JF, Parra-Michel R, Fuentes-Ramírez F et al. Tumor necrosis factor alpha -238 G/A and -308 G/A polymorphisms and soluble TNF-α levels in chronic kidney disease: correlation with clinical variables. Int J Clin Exp Med. 2014; 7 (8): 2111-2119.

  50. Moreno-Estrada A, Gignoux CR, Fernández-López JC, Zakharia F, Sikora M, Contreras AV et al. Human genetics. The genetics of Mexico recapitulates Native American substructure and affects biomedical traits. Science. 2014; 344 (6189): 1280-1285.




2020     |     www.medigraphic.com