ACID TOLERANCE RESPONCE OF CARIOGENIC MICROORGANISMS AND MALOLACTIC FERMENTATION

Yıl 2017, Cilt: 20 Sayı: 2, 132 - 144, 31.08.2017

Erol Keskin Serdar Bağlar

https://doi.org/10.7126/cumudj.345960

Öz

Dental caries is an infectious disease which
occurs by the metabolism of bacteria acids released to dental enviroment which
results hard tissue resolutions. Becouse of the oxygen-free structures of
mature plaques complex and deep layers,cariojenic bacteries which have the
ability of fermentation come forward. Strong acids like lactic acid, formic
acid and pürivat deminish ph of the plaque and the acidty of the plaque causes
demineralization of enamel during caries evolution. Existed plaque
acidification is not only causes losing minerals from enamel but also threats
microorganisms living in the biofilm of the plaque. So most of the
microorganisms can’t survive under the ph value of 2.5. The ability of bacteria
to survive in this acidic environment depends on the acid tolerance responses
they have. Protection against acidity is possible by the production of
glicoses,lactic acid and ATP(Adenosine triphosphate) by bacteries. Malolactic
fermentation is the most important system that provides these productions in acidic
environment. In order to better understand the
anti-caries treatment protocols used in current preventive dental practice, the
role of bacteria in the fermentation process needs to be known. İn this review
we examined: chemical reactions of fermentation, which acids has been occured
by the result of these reactions, ph changes in dental plaque, acidojenic and
aciduric properties of bacteries which realise fermentation, how can
microorganisms survive in acidic environment, what are the advantages propable
inhibition of acid tolerance responces for guest. So we tried to attract
attention to the anti-cariojenic strategies such as flour, chitosan, α-mangostin and gene studies which are used
in the inhibition of acid tolerance systems of bacteria.

Anahtar Kelimeler

Acidojenic&acidüric, dental plaque, fermentation, glycolyse, S.mutans

Karyojen Mikroorganizmaların Asit Tolerans Yetenekleri ve Malolaktik Fermantasyon

Öz

Diş çürüğü
karyojen bakterilerin metabolizmaları sonucu ortama saldıkları asitler
nedeniyle diş sert dokularında mineral çözünmesi sonucu oluşan bir çeşit
enfeksiyon hastalığıdır. Olgunlaşmış plağın komplike ve derin tabakalardaki
oksijensiz yapıdan dolayı çürük oluşumunda fermantasyon yapabilme yeteneği olan
bakteriler ön plana çıkmaktadır. Fermantasyon sonucu açığa çıkan laktik asit,
formik asit ve pirüvik asit gibi güçlü asitler, plak pH’sını düşürür ve oluşan
plak asiditesi çürük gelişimi süresince minenin demineralizasyonuna yol açar.  Oluşan plak asidifikasyonu sadece
minenin mineral kaybına neden olmakla kalmaz aynı zamanda plak biyofilminin
içerisinde yaşayan mikroorganizmalar için de tehlike oluşturur. Yani çoğu
mikroorganizmalar, ölümcül pH değerleri olan pH 2.5 ve altında hayatlarını
sürdüremezler. Bakterilerin bu asidik ortamda hayatta kalabilmeleri, sahip
oldukları asit tolerans cevaplarına bağlıdır. Bakterilerin bu asiditeye karşı
koyması glikoliz, laktik asit üretimi ve ATP(Adenozin trifosfat) üretimi
sayesinde olur. Malolaktik fermantasyon ise asidik ortamda bu üretimleri
sağlayan en önemli sistemdir. Güncel koruyucu diş hekimliği uygulamalarında
kullanılan çürük önleyici tedavi protokollerinin daha iyi anlaşılması için
bakterilerin fermantasyon sürecindeki rollerinin bilinmesi gerekmektedir. Bu
derlemede fermantasyon sürecinin kimyasal tepkimelerini, bu tepkimeler sonucu
hangi asitlerin oluştuğunu, dental plaktaki pH değişikliklerini, fermantasyonu
gerçekleştiren bakterilerin asidojenik&asidürik özelliklerini ve özellikle
oluşan asidik ortamda mikroorganizmaların hayatlarını nasıl sürdürebildiklerini
ayrıca asit tolerans cevabının muhtemel inhibisyonunun konak için ne tür
avantajlar oluşturabileceği incelenmiştir. Böylece bakterilerin asit tolerans
sistemlerinin inhibisyonunda kullanılan flor, çitosan, α-mangostin ve gen çalışmaları gibi antikaryojenik stratejilere
dikkat çekilmeye çalışılmıştır.

Anahtar Kelimeler

Asidürik&asidojenik, dental plak, fermantasyon, glikoliz, S. mutans

Kaynakça

• 1. Hamada S & Slade HD. Biology, immunology, and cariogenicity of Streptococcus mutans. Microbiol Rev 1980;44:331–384.
• 2. Harper DS & Loesche WJ. Growth and acid tolerance of human dental plaque bacteria. Arch Oral Biol 1984;10, 843–848.
• 3. Loesche WJ. Role of Streptococcus mutans in human dental decay. Microbiol Rev 1986;50:353–380.
• 4. Van Ruyven FO, Lingstrom P, Van Houte J & Kent R. Relationship among mutans streptococci, ‘‘low-pH’’ bacteria, and iodophilic polysaccharide-producing bacteria in dental plaque and early enamel caries in humans. J Dent Res 2000;79:778–784.
• 5. Belli WA, Marquis RE. Adaptation of Streptococcus mutans and Enterococcus hirae to acid stress in continuous culture. Appl Environ Microbiol 1991;57(4):1134–1138.
• 6. Svensater G, Larsson UB, Greif ECG, Cvitkovitch DG, Hamilton IR. Acid tolerance response and survival by oral bacteria. Oral Microbiol Immunol 1997;12:266-273.
• 7. Hamilton IR, Svensater G. Acid-regulated proteins induced by Streptococcus mutans and other oral bacteria during acid shock. Oral Microbiol Immunol 1998;13:292-300.
• 8. Costerton JW, Cheng KJ, Geesey GG, Ladd TI, Nickel NC. Bacterial bioflms in nature and disease. Annu Rev Microbiol 987;41:435-464.
• 9. Carr FJ, Chill D, Maida N. “The lactic acid bacteria: A literature survey”. Critical Rewievs in Microbiology 2002;28: 281-370
• 10. Walsh LJ. Dental plaque fermentation and its role in caries risk assessment. International Dentistry South Afria (Australasian Edition) 2006;1:3, 4-13.
• 11. Vratsanos SM, Mandel ID. Comparative plaque acidogenesis of caries-resistant vs. caries-susceptible adults. J Dent Res 1982;61:465-468.
• 12. Coogan MM, Motlekar HB. Salivary and plaque acids in caries active and caries free subjects. J Dent Assoc S Afr 1996;51:823-827.
• 13. De Soet JJ, Nyvad B, Kilian M. Strain–Related Acid Production by Oral Streptococci. Caries research 2000;34:(6), 486-490.
• 14. Hojo S, Komatsu M, Okuda R, Takahashi N, Yamada T. Acid profiles and pH of carious dentin in active and arrested lesions. Journal of dental research 1994;73(12): 1853-1857.
• 15. Bender GR, Sutton SV, Marquis RE. Acid tolerance, proton permeabilities, and membrane ATPases of oral streptococci. Infect Immun 1986;53:331–338.
• 16. Bowden GH, Hamilton IR. Survival of oral bacteria. Crit Rev Oral Biol Med 1998;9: 54-85.
• 17. Lemme A, Sztajer H, Wagner-Döbler I. Characterization of mleR, a positive regulator of malolactic fermentation and part of the acid tolerance response in Streptococcus mutans. BMC microbiology 2010;10:1,1.
• 18. Hamilton IR, Buckley ND. Adaptation by Streptococcus mutans to acid tolerance. Oral Microbiol Immunol 1991; 6: 65–71.
• 19. Neilands J, Sutherland D, Resin A, Wejse PL, Chávez de Paz LE. Chitosan nanoparticles affect the acid tolerance response in adhered cells of Streptococcus mutans. Caries research 2011;45:6, 501-505.
• 20. Welin-Neilands J, Svensäter G. Acid tolerance of biofilm cells of Streptococcus mutans. Applied and environmental microbiology 2007;73:17, 5633-5638.
• 21. Len AC, Harty DW, Jacques NA. Proteome analysis of Streptococcus mutans metabolic phenotype during acid tolerance. Microbiology 2004;150:1353-1366.
• 22. Wen ZT, Suntharaligham P, Cvitkovitch DG, Burne RA. Trigger factor in Streptococcus mutans is involved in stress tolerance, competence development, and biofilm formation. Infection and immunity (2005;73(1):219-225.
• 23. Lemos JA, Abranches J, Burne RA. Responses of cariogenic streptococci to environmental stresses. Curr Issues Mol Biol 2005;7:95–107.
• 24. Fozo EM, Quivey RG Jr. The fabM gene product of Streptococcus mutans is responsible for the synthesis of monounsaturated fatty acids and is necessary for survival at low pH. Journal of bacteriology 2004;186:4152–4158.
• 25. Sturr MG, Marquis RE. Comparative acid tolerances and inhibitor sensitivities of isolated F-ATPases of oral lactic acid bacteria. Appl. Environ. Microbiol 1992;58: 2287-2291.
• 26. Iwami Y, Abbe K, Takahashi-Abbe S, Yamada T. Acid production by streptococci growing at low pH in a chemostat under anaerobic conditions. Oral Microbiol Immunol 1992;7: 304–308.
• 27. Vadeboncoeur C, St Martin S, Brochu D, Hamilton IR. Effect of growth rate and pH on intracellular levels and activities of the components of the phosphoenolpyruvate: sugar phosphotransferase system in Streptococcus mutans Ingbritt. Infect Immun 1991;59: 900–906.
• 28. Quivey RG, Jr Faustoferri RC, Clancy KA, Marquis RE. Acid adaptation in Streptococcus mutans UA159 alleviates sensitization to environmental stress due to RecA deficiency. FEMS Microbiol Lett 1995:126, 257-261.
• 29. Hanna MN, Ferguson RJ, Li YH, Cvitkovitch DG. uvrA is an acid-inducible gene involved in the adaptive response to low pH in Streptococcus mutans. J. Bacteriol 2001;183: 5964-5973
• 30. Sheng J, Marquis RE. Enhanced acid resistance of oral streptococci at lethal pH values associated with acid-tolerant catabolism and with ATP synthase activity. FEMS microbiology letters 2006;262:93– 98.
• 31. Bender GR, Marquis RE. Membrane ATPases and acid tolerance of Actinomyces viscosus and Lactobacillus casei. Appl Environ Microbiol 1987;53:2124-2128.
• 32. Casiano-Colón AIDA, Marquis RE. Role of the arginine deiminase system in protecting oral bacteria and an enzymatic basis for acid tolerance. Applied and Environmental Microbiology 1988; 54(6): 1318-1324.
• 33. Burne RA, Marquis RE. Alkali production by oral bacteria and protection against dental caries. FEMS Microbiol Lett 2000;193:1.6
• 34. Nascimento MM, Gordan VV, Garvan CW, Browngardt CM, Burne RA. Correlations of oral bacterial arginine and urea catabolism with caries experience. Oral Microbiol Immunol 2009;24(2): 89-95.
• 35. Griswold AR, Jameson-Lee M, Burne RA. Regulation and physiologic significance of the agmatine deiminase system of Streptococcus mutans UA159. J. Bacteriol. 2006; 188(3):834–841
• 36. Sheng J, Marquis RE. Malolactic fermentation by Streptococcus mutans. FEMS Microbiol Lett 2007;272: 196–201.
• 37. Sheng J, Baldeck JD, Nguyen PT, Quivey RG, Marquis RE. Alkali production associated with malolactic fermentation by oral streptococci and protection against acid, oxidative, or starvation damage.Canadian journal of microbiology 2010;56(7): 539-547.
• 38. Ajdić D, McShan WM, McLaughlin RE, Savić G, Chang J, Carson MB, et al. Genome sequence of Streptococcus mutans UA159, a cariogenic dental pathogen. Proceedings of the National Academy of Sciences 2002;99(22): 14434-14439.
• 39. Kanapka JA, Hamilton IR. Fluoride inhibition of enolase activity in vivo and its relationship to the inhibition of glucose-6-P formation in the oral microbe, Streptococcus salivarius. Arch. Biochem. Biophys 1971;144: 596–602.
• 40. Matsui R, Cvitkovitch D. Acid tolerance mechanisms utilized by Streptococcus mutans. Future microbiology, 2010;5(3): 403-417.
• 41. Hasona A, Crowley PJ, Levesque CM, Mair RW, Cvitkovitch DG, Bleiweis AS, Brady LJ. Streptococcal viability and diminished stress tolerance in mutants lacking the signal recognition particle pathway or YidC2. Proceedings of the National Academy of Sciences of the United States of America 2005;102(48):17466-17471.
• 42. Hasona A, Zuobi-Hasona K, Crowley PJ, Abranches J, Ruelf MA, Bleiweis AS, et al. Membrane composition changes and physiological adaptation by Streptococcus mutans signal recognition particle pathway mutants. Journal of bacteriology 2007; 189(4):1219-1230.
• 43. Dunning DW, McCall LW, Powell WF Jr, Arscott WT, McConocha EM, McClurg CJ, Goodman SD, Spatafora GA. SloR modulation of the Streptococcus mutans acid tolerance response involves the GcrR response regulator as an essential intermediary. Microbiology 2008;154:1132–1143.
• 44. Rolerson E, Swick A, Newlon L, Palmer C, Pan Y, Keeshan B, Spatafora G. The SloR/Dlg metalloregulator modulates Streptococcus mutans virulence gene expression. Journal of bacteriology 2006;188:5033–5044.
• 45. Nguyen PT, Marquis RE. Antimicrobial actions of α-mangostin against oral streptococci. Canadian journal of microbiology 2011;57(3):217-225.
• 46. Duarte S, Gregoire S, Singh AP, Vorsa N, Schaich K, Bowen WH, Koo H. Inhibitory effects of cranberry polyphenols on formation and acidogenicity of Streptococcus mutans biofilms. FEMS Microbiology Letters 2006;257(1):50-56.
• 47. Len AC, Harty DW, Jacques NA. Stress responsive proteins are upregulated in Streptococcus mutans during acid tolerance. Microbiology 2004;150:1339- 1351.
• 48. Lemos JA, Chen YY, Burne RA. Genetic and physiologic analysis of the groE operon and role of the HrcA repressor in stress gene regulation and acid tolerance in Streptococcus mutans. J. Bacteriol. 2001;183:6074-6084.