Clinical, microbiological and genetics findings of a family with Aggressive Periodontitis from Maceio
Achados clínicos, genéticos e microbiológicos de uma família com Periodontite Agressiva em Maceió
Sogumo, Patrícia Mayumi; Cavalcante, Lícia Bezerra; Finoti, Lívia Sertori; Spolidório, Denise Madalena Palomari; Carlos Jr, Amaro Carlos Júnior; Lipinski-Figueiredo, Eneida; Pires, Juliana Rico; Scarel-Caminaga, Raquel Mantuaneli
Rev. odontol. UNESP, vol.39, n6, p.323-331, 2010
Abstract
The present study reports clinical, microbiological and genetic findings in members of a family with Aggressive Periodontitis (AgP) from Maceió - AL, Brazil. After periodontal exams in fourteen members of the family, DNA was obtained from epithelial buccal cells and microbiological samples were collected from subgingival plaque to detect five species of periodontopathogens by Polymerase Chain Reaction (PCR). PCR-RFLP (Restriction Fragment Length Polymorphism) was used to investigate human polymorphisms in interleukin genes (IL4, IL10). Six members of the family showed Generalized AgP and eight were considered unaffected by the AgP. There was no association of alleles, genotypes and haplotypes in the IL10 and IL4 genes with the AgP in the studied family. Treponema denticola (T.d.) was the prevalent pathogen, followed by the Tannerella forsythia (T.f.). There was correlation between clinical findings (clinical attachment loss, bleeding on probing and probing depth) with the presence of T.d., while T.f. was correlated with bleeding on probing. In conclusion, although the investigated polimorphisms were not associated with the susceptibility to AgP, the presence of periodontopathogens is related to worse periodontal clinical parameters.
Keywords
Periodontitis, microbiology, genetics, cytokines
Resumo
O presente estudo relata achados clínicos, genéticos e microbiológicos de indivíduos de uma família com periodontite agressiva (PA) residente em Maceió - AL, Brasil. Quatorze membros da família foram submetidos a exames clínicos periodontais, coleta de células da mucosa oral para extração de DNA e coleta de fluido subgengival para detecção de cinco espécies de periodontopatógenos por meio da PCR (Reação em Cadeia da Polimerase). Polimorfismos nos genes Interleucina 4 e 10 (IL4 e IL10) foram investigados em cada indivíduo por meio da PCR-RFLP (Polimorfismo por Comprimento de Fragmento de Restrição). Seis membros da família apresentaram PA generalizada e oito foram considerados não afetados pela PA. Não houve associação de alelos, genótipos e haplótipos nos genes IL10 e IL4 com a presença de PA na família estudada. Treponema denticola (T.d.) foi o patógeno prevalente, seguido por Tannerella forsythia (T.f.). Houve correlação dos parâmetros clínicos investigados (perda de inserção clínica, sangramento à sondagem e profundidade de sondagem) com a presença de T.d., enquanto que para T.f. houve associação deste com o sangramento à sondagem. Conclui-se que, apesar de os polimorfismos investigados não terem relação com a suscetibilidade à PA, a presença de periodontopatógenos está associada a piores índices clínicos periodontais.
Palavras-chave
Periodontite, microbiologia, genética, citocinas
References
1. Llorente MA, Griffiths GS. Periodontal status among relatives of aggressive periodontitis patients and reliability of family history report. J Clin Periodontol. 2006; 33: 121-5.
2. Hart AC. Genetic considerations of risk in human periodontal disease. Curr Opin Periodontol. 1994; 3: 3-11.
3. Loos BG, John RP, Laine ML. Identification of genetic risk factors for periodontitis and possible mechanisms of action. J Clin Periodontol. 2005; 32: 159-79.
4. Socransky SS, Haffajee AD. Periodontal microbial ecology. Periodontol 2000. 2005; 38: 135-87.
5. Lindhe J, Karring T, Lang NP, editors. Clinical periodontology and implant dentistry. 3rd ed. Copenhagen: Munksgaard; 1997. p. 227-57.
6. Loesche WJ, Grossman NS. Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment. Clin Microbiol Rev. 2001; 1: 727-52.
7. Michalowicz BS, Diehl SR, Gunsolley JC, Sparks BS, Brooks CN, Koertge TE, et al. Evidence of a substantial genetic basis for risk of adult periodontitis. J Periodontol. 2000; 71: 1699-701.
8. Bartova J, Krátka-Opatrná Z, Procházkova J, Krejsa O, Dusková J, Mrklas L. Th1 and Th2 cytokine profile in patients with early-onset periodontitis and their healthy siblings. Mediators Inflamm. 2000; 9: 115-20.
9. Manhart SS, Reinhart RA, Payne JB, Seymour GJ, Gemmell E, Dyer JK, et al. Gingival cell IL-2 and IL-4 in early-onset periodontitis. J Periodontol. 1994; 65: 807-13.
10. Stern DL. Evolutionary biology. The problem of variation. Nature. 2000; 408: 529-31.
11. Hobbs K, Negri J, Klinnert M., Rosenwasser LJ, Borish, L. Interleukin-10 and Transforming Growth Factor-β promoter polymorphisms in Allergies and Asthma. Am J Resp Crit Car Med. 1998; 158: 1958-62.
12. Holla LI, Fassmann A, Augustin P, Halabala T, Znojil V, Vanek J. The association of interleukin-4 haplotypes with chronic periodontitis in a Czech population. J Periodontol. 2008; 79: 1927-33.
13. Turner DM, Williams DM, Sankaran D, Lazarus M, Sinnot PJ, Hutchinson L. An investigation of polymorphisms in the interleukin-10 gene promoter. Eur J Immunogenet. 1997; 24: 1-8.
14. Lazarus M, Hajeer AH, Turner D, Sinnot P, Worthington J, Ollier WER, et al. Genetic variation in the interleukin- 10 gene promoter and systemic lupus erythematosus. J Rheumatol. 1997; 24: 2314-7.
15. Scarel-Caminaga RM, Trevilatto PC, Souza AP, Brito Jr, RB, Camargo LEA, Line SRP. Interleukin 10 gene promoter polymorphisms are associated with chronic periodontitis. J Clin Periodontol. 2004; 31: 443-8.
16. Tenório Neto JF, Pavão RJLP, Carlos Junior A. Periodontite Agressiva: análise clínica de suscetibilidade à doença. Periodontia. 2006; 16: 47‑51.
17. AAP – American Academy of Periodontology. Periodontal Diseases in children and adolescents. J Periodontol. 2003. 74: 1696-704.
18. Trevilatto PC, Line SR. Use of buccal epithelial cells for PCR amplification of large DNA fragments. J Forensic Odontostomatol. 2000; 18: 6-9.
19. Lowe PR, Galley HF. A novel PCR-RFLP assay for the detection of single nucleotide polymorphism at position –1082 in the human IL-10 gene promoter. Eur J Immunogenet. 2001; 28: 563-4.
20. Anovazzi G, Kim YJ, Viana AC, Curtis KMC, Orrico SRP, Cirelli JA, Scarel-Caminaga RM. Polymorphisms and Haplotypes in the Interleukin-4 gene are associated with chronic periodontitis in a brazilian population. J Periodontol. 2010; 81: 392-402.
21. Newbrun, E. Indices to measure gingival bleeding. J Periodontol. 1996; 67: 555-61.
22. Scarel-Caminaga RM, Trevilatto PC, Souza AP, Brito Jr, RB, Line SRP. Investigation of IL4 gene polymorphism in individual with different levels of chronic periodontitis in a Brazilian population. J Clin Periodontol. 2003; 30: 341-5.
23. Pontes CC, Gonzales JR, Novaes AB Jr, Taba Júnior M, Grisi MF, Michel J, et al. Interleukin-4 gene polymorphism and its relation to periodontal disease in a Brazilian population of African heritage. J Dent. 2004; 32: 241-6.
24. Gonzáles JR, Mann M, Stelzig J, Bodeker RH, Meyle J. Single-nucleotide polymorphisms in the IL-4 and IL-13 prommoter region in aggressive periodontitis. J Clin Periodontol. 2007; 34: 473-9.
25. Gonzáles JR, Michel J, Diete A, Herrmann JM, Bodeker RH, Meyle J. Analysis of genetic polymorphism at the interleukin-10 loci in aggressive and chronic periodontitis. J Clin Periodontol. 2002; 29: 816-22.
26. Yamazaki K, Tabeta K, Nakajima T, Ohsawa Y, Ueki K, Itoh H, et al. Interleukin-10 gene promoter polymorphism in Japanese patients with adult and early-onset periodontitis. J Clin Periodontol. 2001; 28: 828-32.
27. Reichert S, Machulla HKG, Klapproth J, Zimmermann U, Reichert Y, Gläser CH, et al. The interleukin-10 promoter haplotype ATA is a putative risk factor for aggressive periodontitis. J Periodontol Res. 2008; 43: 40-7.
28. Rivieri GR, Smith KS, Carranza NJr, Tzagaroulaki E, Kay SL, Dock M. Subgingival distribuition os Treponema denticola, Treponema socranskii, and pathogen-related oral spirochetes: prevalence and relationship to periodontal status of sampled sites. J Periodontol. 1995; 66: 829-37.
29. Simonson LG, Goodman CH, Bial JJ, Morton HE. Quantitative relationship os Treponema denticola to severity of periodontal disease. Infect Immun. 1988; 56: 726-8.
30. Takeuchi Y, Umeda M, Sakamoto M, Benno Y, Huang Y, Ishikawa I. Treponema socranskii, Ttreponema denticola and Porphyromonas gingivalis are associated with severith od periodontal tissue destrucion. J Periodontol. 2001; 72: 1354-63.
31. Corteli Jr, Cortelli SC, Jordan SF, Haraszthy VI, Zambon JJ. Prevalence of periodontal pathogens in Brazilians with aggressive or chronic Periodontitis. J Clin Periodontol. 2005; 32: 860-6.
32. Scarel-Caminaga RM, Pires JR, Sogumo PM, Salmon CR, Peres RCR, Spolidório DMP. A familial case of Aggressive Periodontitis: clinical, microbiological and genetic findings. Rev Odontol UNESP. 2009; 38: 175-83.
33. Zambon JJ, Christersson LA, Slots J. Actinobacillus actinomycetemcomitans in human periodontal disease. Prevalence in patient groups and distribution of biotypes and serotypes within families. J Periodontol. 1983; 54: 707-11.
34. Rosalem Jr W, de Souza RC, de Andrade AFB, Colombo APV. Analysis of leukotoxin gene types of Actinobacillus actinomycetemcomitans in Brazilians with aggressive periodontitis. Braz J Microbiol. 2006; 7: 127-34.
35. Trevilatto PC, Tramontina VA, Machado MAN, Gonçalves RB, Sallum AW, Line SRP. Clinical, genetic and microbiological findings in a Brazilian family with aggressive periodontitis. J Clin Periodontol. 2002; 29: 233-9.
36. Haffajee AD, Cugini M, Dibart S, Smith C, Kent Jr RL, Socransky SS. Clinical and microbiological features of subjects with adult periodontitis who responded poorly to scaling and root planning. J Clin Periodontol. 1997; 24: 767-76.
37. Papapanou PN, Baelum V, Luan WM, Madianos PN, Chen X, Fejerskov O, et al. Subgingival microbiota in adult Chinese: prevalence and relation to periodontal disease progression. J Periodontol. 1997; 68: 651-66.
38. Pabón MC, Ospina DPR, Guzmán DMI, Rojas LMO, Arroyave SIT. Detection of Treponema denticola in saliva obtained from patients with various periodontal conditions. Clin Oral Invest. 2008; 12: 73-81.
39. Yano-Higuchi K, Takamatsu N, He T, Umeda M, Ishikawa I. Prevalence of bacterioides forsythus, porphyromonas gingivalis and actinobacillus actinomycetemcomitans in subgigival microflora of Japanese patients with adult and rapidly progressive periodontitis. J Clin Periodontol. 2000; 27: 597-602.
40. Noguchi E, Nukaga-Nishio Y, Jian Z, Yokuchi Y, Kamioka M, Yamakawa-Kobayashi K, Hamaguchi H, Matsui A, Shibasaki M, Arinami T. Haplotypes of the 5’ region of the IL-4 gene SNPs in the intergene sequence between the IL-4 and IL-13 genes are associated with atopic asthma. Hum Immunol. 2001; 62: 1251-7.
41. Suzuki I, Yamaguchi E, Hizawa N, Itoh A, Kawakami Y. A new polymorphism in the 5’ flanking region of the human interleukin (IL)-4 gene. Immunogenetics 1999; 49: 738-9.
42. Michel J, Gonzáles JR, Wunderlich D, Herrmann JM, Meyle J. Interlekin-4 polymorphisms in early-onset periodontitis. J Clin Periodontol. 2001; 28: 483-8.
43. Ashimoto A, Chen, C, Bakker I, Slots J. Polymerase chain reaction 8 putative periodontal pathogens in subgingival plaque of gingivitis and advanced periodontitis lesions. Oral Microbiol Immunol. 1996; 11: 266-73.
44. Benkirane RR, Guillot E, Mouton C. Immunonagnetic PCR and DNA probe for detection and identification of Porphyromonas gingivalis. J Clin Microbiol. 1995; 33: 2908-12.
45. Guillot E, Mouton C. PCR-DNA probe assays for identification and detection of Prevotella intermedia sensu strictu and Prevotella nigrescens. J Clin Microbiol. 1997; 35: 1876-82.
46. Haraszthy VI, Hariharan G, Tinoco EM, Cortelli JR, Lally ET, Davis E, et al. Evidence for the role of highly leukotoxic Actinobacillus actinomycetemcomitans in the pathogenesis of localized juvenile and other forms of early-onset periodontitis. J Periodontal. 2000; 71: 912‑22.
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