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Morholt2012

Methanobrevibacter oralis is a potentially pathogenic archaea associated with the periodontal disease periodontitis. M. oralis has been found in the subgingival crevices and plaque biofilms of many people who are suffering from chronic periodontal disease[3-6,10-13]. To date, no archaea have been definitively identified as pathogenic to humans [3,4]. Periodontal diseases such as gingivitis and periodontitis have been identified as a polymicrobial disease states [1,9,12]. It is important to note that no specific microbe or polymicrobes have been identified as causative pathogens for periodontal diseases [1,3,9]. However, recent studies have gathered significant data that identifies M. oralis present only in patients exhibiting all stages (gingivitis to severe periodontitis) periodontal disease [6,10,12].

Periodontal or gum diseases involve many different advancing stages from mild called gingivitis to severe gum inflammation called periodontitis. People with gingivitis have swollen gums that are tender and often red [1,9]. If left untreated, gingivitis will advance to early and moderate periodontitis, noted by bleeding gums and subgingival pockets of 3-4mm [1,9]. If left untreated, moderate periodontitis will develop into severe periodontitis, which is characterized by further gum recession where subgingival pockets are as deep as 6mm or more [1,9]. Bone loss is also begins at this stage and teeth may become loose [1,9]. Finally, if the disease progresses, advanced periodontitis will develop which can ultimately lead to significant maxillary and/or mandibular bone decay, and may result in the loss of teeth [1,9]. For all stages of periodontal diseases, gingival sensitivity, inflammation (caused by adaptive immune response of the release of cytokines [14]), bleeding and depth of subgingival pockets is sufficient evidence for clinical diagnosis [1,9]. X-rays [1,9] and even subcultures may be taken from plaque biofilms and subgingival pockets to determine the microbes present [9].

Fig. 1. Photographic progression of periodontal diseases. Website December 5, 2012. http://www.zila.com/16/STATISTICS%20%26%20FACTS/

Primarily, gram-positive anaerobic bacterium including Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus, Aggreatibacter actinomycetemcomitans, Fusobacterium nucleatum, Capnocytophaga species, and Campylobacter rectus have been identified to be associated with periodontal disease [9]. Recent studies acknowledge that archaea have been found to be present in people who have periodontal disease however, the role and contribution of these prokaryotes to the disease is not yet known [3]. Referring to Fig. 2, we can clearly see that methanogenic archaea, are present only in subjects who are expressing all stages (gingivitis to
Fig. 2: This visual below is reflective of data compiled from Vianna, M. E., Conrads, G., Gomes, B. P. F. A., & Horz, H. P. (April 2006). Identification and quantification of archaea involved in primary endodontic infections. Journal of Clinical Microbiology, 44(4), 1274-1282. Note how methanogenic archaea, of which M. oralis is a member, have only been found in patients that are currently suffering from periodontitis.

severe) of periodontal disease [12]. Data from a study conducted by Lepp et al. (Fig 3.) also informs us that M. oralis and other methanogenic archaea population size increases as the severity of periodontal disease advances [6]. Researchers developed an archaea specific SSU rDNA 5 nuclease assay to evaluate the relationship between the abundance of archaea and periodontal disease severity. Due to the fact that archaeal SSU rDNA was not discovered in any of the 31 samples of the control group, findings are statistically significant (P = 1.0) [6]. Furthermore, archaeal SSU rDNA was found to be present in 36% of periodontitis patients [6]. The dental pulp (found in root canals) and the apex of a tooths root canal are typically devoid of microorganisms and sterile in healthy subjects [7,8]. Infections are caused by the polymicrobes listed above that overcome innate host defense mechanisms [7,8]. Generally the virulence mechanism is these bacterias and methanogenic archaea such as M. oralis is related to their life cycle and proliferation occurring within the
Fig. 3. Relative quantity of archea through various conditions of oral health. Lepp, P. W., Brinig, M. M., Ouverney, C. C., Palm, K., Armitage, G. C., & Relman, D. A. (2004). Methanogenic archaea and human periodontal disease. Proceedings of the National A cademy of Sciences of the United States of A merica, 101(16), 6176-6181. doi:10.1073/pnas.0308766101

biofilm plaque [2,4,5,11-13]. Evidence has been reported, in a study conducted by Vianna et al., that methanogenic archaea and M. oralis act as pathogens due to their ability to infest normally closed and sterile anatomical structures of teeth and contribute to these polymicrobial infections (i.e. endodontic infections and apical periodontitis) [11]. Vianna et al. findings include statistically significant data (5 out of 20 subjects with endodontic infections accounts for P = .25 = 25%) that methanogenic archaea and M. oralis are present in endodontic infections [11]. This studies finding are the strongest yet (to the best of this authors knowledge) in identifying archaea as disease causing pathogens to humans.

The good news is periodontitis is preventable and can in some stages be treatable. In fact, most stages of periodontal diseases can be treated and cured [9]. Sometimes gum damage can be reversed, however once bone has been lost, it will not regrow [1,9]. The important thing to understand is that periodontal diseases are not a communicable disease that can be transmitted from one person to another [9]. Maintaining oral health as well as prevention and treatment of all stages of periodontal diseases include the removal of these polymicrobes and plaque by brushing teeth twice a day, preferably with a fluoride toothpaste, daily flossing, and regular check-ups with professional cleanings by dental hygienists and dentists [2,8]. It is important as healthcare providers to encourage our patients to practice good oral health. Educating our patients about proper brushing (toothbrush is at a 45 angle to gums) and flossing technique will offer them the best chance to prevent gingivitis and/or periodontitis [2]. As one can imagine, the treatment of periodontitis can be quite extensive. Typically, initial treatments begin with the removal of plaque, calculus and stain in a process called scaling [2,9]. This procedure is similar to the scaling performed during a routine hygienist appointment. Root planning, which is the scaling of tooths root is often performed as well [2,9]. Special care must be exerted throughout this scaling process because roots are made of cementum, which is softer than enamel [9]. These procedures are often successful and subgingival pockets are reduced to 1mm [9]. However, it should be noted that it is quite common for biofilms to not be fully removed. Consequentially, M. oralis and other bacteria can quickly multiply and their numbers and biofilm return to pre-scaling quantities [9]. Periodontal flap debridement is often necessary to perform when conducting scaling and root planning. In an effort to expose the targeted areas for scaling and root planning this surgical procedure includes the cutting away of the gingival areas that are surrounding the planned treatment area [9]. Soft tissue grafts is another treatment measure that can be beneficial not only as a way to provide support for teeth, but is also is effective cosmetically. This surgical procedure involves taking gum tissue from another part of the oral cavity, usually the palate and attaching it to the gums that are affected with periodontitis [9]. Gingivectomy may also be performed. This is considered a minor surgery where the infected gum areas are simply cut off [9]. Finally, antibiotics are administered in an effort to prevent the return of bacteria [9].

Anyone who does not practice good oral health care (twice daily brushing, daily flossing, and regular teeth cleanings and check-ups from dental hygienists and dentists) is at risk for developing periodontal diseases. The CDC also cites smoking, stress, heredity, diabetes, and

hormonal changes (making pregnant females particularly vulnerable) as risk factors that make people susceptible to developing periodontal diseases [20]. Periodontal diseases affect more than 80 percent of adults in the U.S. population [21]. As of 2012, WHO has reported that 15% to 20% of adults (age 35-44 years) worldwide have severe periodontitis [15]. Statistics regarding the number of cases diagnosed in our local population of Utah were not available to the author at the time of this publication. While WHO in 2004 did not attribute any deaths worldwide due to periodontal diseases [16], many studies have been conducted that related poor oral health and periodontal diseases to be potentially systemic and related to overall health [17-19]. Trends in periodontal disease incidence are difficult to with confidence report due to the nature of the objectivity involved in diagnosing the progression of a patient through the various stages of periodontitis [1,9]. However, through the efforts of organizations like WHO, CDC, and the ADA as well as health care providers, we can experience a decline in periodontal diseases.
References 1. Armitage, G. C. (2003). Diagnosis of periodontal diseases. Journal of periodontology, 74(8), 1237. 2. Collins, F. (2006). Biofilm formation, identification, and removal. Dental CE Digest, 1-8. 3. Dridi, B., Raoult, D., & Drancourt, M. (2011). Archaea as emerging organisms in complex human microbiomes. A naerobe, 17(2), 56-63. doi:10.1016/j.anaerobe.2011.03.001 4. Horz, H., Conrads,G. (2011). Methanogenic archaea and oral infections - ways to unravel the black box. Journal of Oral Microbiology, 3(0) 5. Horz, H., Seyfarth, I., & Conrads, G. (2012). McrA and 16S rRNA gene analysis suggests a novel lineage of archaea phylogenetically affiliated with thermoplasmatales in human subgingival plaque. A naerobe, 18(3), 373-377. doi:10.1016/j.anaerobe.2012.04.006 6. Lepp, P. W., Brinig, M. M., Ouverney, C. C., Palm, K., Armitage, G. C., & Relman, D. A. (2004). Methanogenic archaea and human periodontal disease. Proceedings of the National A cademy of Sciences of the United States of A merica, 101(16), 6176-6181. doi:10.1073/pnas.0308766101 7. Love, R. M., & Jenkinson, H. F. (2002). Invasion of dentinal tubules by oral bacteria. Critical Reviews in Oral Biology & Medicine, 13(2), 171-183. 8. Nair, P. N. R. (2004). Pathogenesis of apical periodontitis and the causes of endodontic failures. Critical Reviews in Oral Biology & Medicine, 15(6), 348-381. 9. Kothari, S. (2012). Periodontal Chip: An adjunct to conventional surgical treatment. International Journal of Drug Research and Technology. Int. J. Drug Res. Tech, 2(6), 411-421. 10. Vianna, M. E., Conrads, G., Gomes, B. P. F. A., & Horz, H. P. (2009). T-RFLP-basedmcrA gene analysis of methanogenic archaea in association with oral infections and evidence of a novel methanobrevibacter phylotype. Oral Microbiology & Immunology, 24(5), 417-422. doi:10.1111/j.1399-302X.2009.00539.x 11. Vianna, M. E., Conrads, G., Gomes, B. P. F. A., & Horz, H. P. (April 2006). Identification and quantification of archaea involved in primary endodontic infections. Journal of Clinical Microbiology, 44(4), 1274-1282. doi:10.1128/JCM.44.4.1274-1282.2006 12. Vianna, M. E., Holtgraewe, S., Seyfarth, I., Conrads, G., & Horz, H. P. (May 15, 2008). Quantitative analysis of three hydrogenotrophic microbial groups, methanogenic archaea, sulfate-reducing bacteria, and acetogenic bacteria, within plaque biofilms associated with human periodontal disease. Journal of Bacteriology, 190(10), 3779-3785. doi:10.1128/JB.01861-07 13. Yamabe, K., Maeda, H., Kokeguchi, S., Soga, Y., Meguro, M., Naruishi, K., et al. (2010). Antigenic group II chaperonin in methanobrevibacter oralis may cross-react with human chaperonin CCT. Molecular Oral Microbiology, 25(2), 112-122. doi:10.1111/j.2041-1014.2009.00548.x 14. de Oliveira, R. R., Schwartz-Filho, H. O., Novaes Jr, A. B., Garlet, G. P., de Souza, R. F., Taba Jr, M., ... & Ribeiro, F. J. (2009). Antimicrobial photodynamic therapy in the non-surgical treatment of aggressive periodontitis: cytokine profile in gingival crevicular fluid, preliminary results. Journal of periodontology, 80(1), 98-105. 15. World Health Organization Oral health Fact sheet N318 April 2012. Website December 3, 2012. http://www.who.int/mediacentre/factsheets/fs318/en/ 16. World Health Organization The global burden of disease: 2004 update. 2004. Website December 3, 2012. http://www.who.int/entity/healthinfo/global_burden_disease/GBD_report_2004update_full.pdf. 17. Joshipura, K. J., Rimm, E. B., Douglass, C. W., Trichopoulos, D., Ascherio, A., & Willett, W. C. (1996). Poor oral health and coronary heart disease. Journal of dental research, 75(9), 1631-1636. 18. Williams, R. C., Barnett, A. H., Claffey, N., Davis, M., Gadsby, R., Kellett, M., ... & Thackray, S. (2008). 18. The potential impact of periodontal disease on general health: a consensus view. Current Medical Research and Opinion, 24(6), 1635-1643. 19. Williams, R. C., Barnett, A. H., Claffey, N., Davis, M., Gadsby, R., Kellett, M., ... & Thackray, S. (2008). The potential impact of periodontal disease on general health: a consensus view. Current Medical Research and Opinion, 24(6), 1635-1643. 20. Center for Disease Control. Website December 3, 2012. http://www.cdc.gov/oralhealth/topics/periodontal_disease.htm 21. Photographic progression of periodontal diseases. Website December 5, 2012. http://www.zila.com/16/STATISTICS%20%26%20FACTS/

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