Porphyromonas gingivalis: Infectious substances pathogen safety data sheet

Section I – Infectious agent

Name

Porphyromonas gingivalis

Agent type

Bacteria

Taxonomy

Family

Porphyromonadaceae

Genus

Porphyromonas

Species

Gingivalis

Synonym or cross-reference

Also known as Bacteroides gingivalis^{Footnote 1}. Formerly, Bacteroides melaninogenicus^{Footnote 2}.

Characteristics

Brief description

P. gingivalis are Gram-negative, non-motile coccobacilli that measure 0.5 µm by 1.0 to 3.0 µm^{Footnote 3}. They are obligate anaerobes favouring high humidity environments and requiring protoheme; as such, cells are often grown on blood agar at 37°C^{Footnote 3}^{Footnote 4}. Colonies initially appear light in colour, and after 4 to 8 days, turn deep red or black due to cellular accumulation of iron^{Footnote 4}^{Footnote 5}.

Properties

P. gingivalis has a variety of virulence determinants, including capsule, fimbriae, lipopolysaccharides (LPS), hemagglutinins, and proteinases (e.g., gingipains)^{Footnote 5}^{Footnote 6}^{Footnote 7}. The significant proteolytic activity of P. gingivalis aids in survival and growth in the host and is strongly implicated in disease progression^{Footnote 6}. Virulence varies among strains due to differences in invasive ability and proteolytic activities^{Footnote 8}^{Footnote 9}^{Footnote 10}.

Section II – Hazard identification

Pathogenicity and toxicity

P. gingivalis colonizes the gingival sulcus of the human oral cavity, but has been recovered from the tongue, tonsils, and saliva. P. gingivalis is found in 10 – 25% of periodontically healthy individuals, and in 69-79% of those with periodontal disease^{Footnote 11}^{Footnote 12}^{Footnote 13}. Presence of P. gingivalis is associated with initiation and progression of generalized aggressive periodontitis, which is considered a chronic condition that can persist for many years if left untreated^{Footnote 3}^{Footnote 5}^{Footnote 14}. Aggressive periodontitis is characterised by rapid attachment loss and bone destruction in individuals that are otherwise clinically healthy. Aggressive periodontitis is more likely to occur in younger age groups and was originally called early-onset periodontitis^{Footnote 15}. Severity of periodontal disease ranges from mild inflammation of the gums and supporting structures of teeth, to chronic tissue destruction that results in the formation of a periodontal pocket and ultimately, tooth loss^{Footnote 5}^{Footnote 6}. Other symptoms of periodontitis include bleeding gums and alveolar bone resorption^{Footnote 16}.

P. gingivalis has also been implicated in lung abscesses, aspiration pneumonia, and pulmonary infections^{Footnote 3}^{Footnote 17}. Studies suggest that P. gingivalis-associated periodontal disease represents a risk factor for cardiovascular disease and is associated with low birth weight deliveries^{Footnote 18}^{Footnote 19}^{Footnote 20}^{Footnote 21}. Colonization of P. gingivalis and periodontitis are associated with higher incidence of mortality in patients with orodigestive cancer^{Footnote 22}. P. gingivalis has been linked to other systemic diseases such as atherosclerosis, hypertension, adverse pregnancy outcomes, inflammatory bowel disease, diabetes mellitus, non-alcoholic fatty liver disease, rheumatoid arthritis, and Alzheimer's disease^{Footnote 16}^{Footnote 23}.

P. gingivalis is not known to cause disease in natural animal hosts, although experimentally infected animals can develop periodontal disease^{Footnote 24}^{Footnote 25}.

Epidemiology

Disease caused by P. gingivalis is maintained in human populations^{Footnote 24}. P. gingivalis is associated with severe (chronic) and aggressive periodontitis^{Footnote 26}. Severe periodontitis affects 5-20% of adults globally^{Footnote 27}^{Footnote 28}, while prevalence of aggressive periodontitis is 0.1-5%^{Footnote 26}^{Footnote 27}^{Footnote 29}. The incidence rate of severe periodontitis varies among countries from 251 to 1,428 new cases per 100,000 person-years^{Footnote 28}. Among adults 30 or older in the United States, populations with the highest prevalence of total periodontitis include men (50.2%), adults below the federal poverty level (60.4%), and current smokers (62.4%)^{Footnote 30}.

Diabetes, HIV and Down syndrome are associated with increased rates of periodontal disease^{Footnote 5}^{Footnote 31}^{Footnote 32}. Poor oral hygiene and aging are also factors which may predispose to P. gingivalis infection^{Footnote 33}.

Host range

Natural host(s)

Humans^{Footnote 24}.

Other host(s)

In an experimental setting, P. gingivalis can cause infection in various animals (e.g., rodents, rabbits, pigs, dogs, non-human primates)^{Footnote 34}^{Footnote 35}. Non-human primates orally challenged with P. gingivalis can develop periodontal disease^{Footnote 36}.

Infectious dose

Unknown.

Incubation period

Unknown.

Communicability

P. gingivalis can spread via saliva, direct mucosal contact and intimate contact, but transmission does not always result in colonization^{Footnote 37}^{Footnote 38}. Shared toothbrushes and eating utensils are possible vehicles of transmission^{Footnote 25}^{Footnote 39}^{Footnote 40}. Contact with a P. gingivalis-infected family member increases the risk of P. gingivalis colonization for other family members^{Footnote 40}.

Section III – Dissemination

Reservoir

Humans.

Zoonosis

None.

Vectors

None.

Section IV – Stability and viability

Drug susceptibility/resistance

P. gingivalis is generally susceptible to amoxicillin-clavulanate^{Footnote 41}^{Footnote 42}^{Footnote 43}, piperacillin-tazobactam^{Footnote 44}, cephaclor^{Footnote 41}, cephalosporins^{Footnote 44}, tetracycline and doxycycline^{Footnote 41}^{Footnote 43}, clindamycin^{Footnote 41}^{Footnote 43}, imipenem^{Footnote 44}, metronidazole^{Footnote 41}^{Footnote 44}, moxifloxacin^{Footnote 45}^{Footnote 46}, azithromycin^{Footnote 45}, and cefoxitin^{Footnote 45}.

Some P. gingivalis isolates are resistant to ciprofloxacin^{Footnote 43}, erythromycin^{Footnote 41}^{Footnote 43}, and azithromycin^{Footnote 41} as well as other antibiotics such as metronidazole (21.56%), amoxicillin (25.49%), and clindamycin (23.52%)^{Footnote 46}^{Footnote 47}. Over a 20 year period, in vitro resistance of P. gingivalis increased significantly to clindamycin (15 fold increase to 9.3% in patients) and amoxicillin (28 fold increase to 2.8% of patients)^{Footnote 46}^{Footnote 48}.

Susceptibility to disinfectants

Hypochlorous acid, sodium hypochlorite, 70% ethanol, and chlorhexidine are effective against P. gingivalis biofilm^{Footnote 49}. Treatment with ozonated water (2mg/L)^{Footnote 50}, nitric oxide^{Footnote 51}, povidone iodine solutions^{Footnote 50}, and quaternary ammonium compounds, such as cetylpyridinium chloride (0.05%)^{Footnote 52}, cause a significant reduction in viable P. gingivalis cells. Treatment with chlorine dioxide gas is effective against P. gingivalis cells grown on materials with smooth surfaces^{Footnote 53}.

Antiseptic mouth washes are effective at killing P. gingivalis within a biofilm^{Footnote 54}.

Physical inactivation

UV irradiation has a bactericidal effect on P. gingivalis cells^{Footnote 51}. Application of moist heat (121°C for 15 minutes) and dry heat (170°C for 1 hour) are generally effective at eliminating most bacteria^{Footnote 55}. Low-temperature Atmospheric Pressure Plasma has been shown to have a significant inactivation effect on P. gingivalis^{Footnote 56}. Photodynamic and photothermal therapy are also successful in significantly eradicating P. gingivalis^{Footnote 57}.

Survival outside host

Other oral pathogens survive for less than 8 hours outside the oral cavity^{Footnote 39}. Generally, bacterial persistence on inanimate surfaces depends on environmental conditions, such as relative humidity, temperature, biofilm, and surface type^{Footnote 58}.

Section V – First aid/medical

Surveillance

Diagnosis is accomplished through the monitoring of clinical symptoms. Oral specimens are cultured on selective agar containing colistin, bacitracin and nalidixic acid to inhibit growth of other bacteria commonly found in the oral cavity^{Footnote 59}. P. gingivalis can be identified using PCR-based or biochemical detection systems^{Footnote 60}^{Footnote 61}^{Footnote 62}.

Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook.

First aid/treatment

Infections can be treated with appropriate antibiotics and/or dental procedures, such as surface debridement, to remove plaque bacteria^{Footnote 63}.

Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which is developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the Canadian Biosafety Handbook.

Immunization

There is no vaccine currently available; however, vaccine development for P. gingivalis is an active area of research^{Footnote 63}.

Note: More information on the medical surveillance program can be found in the Canadian Biosafety Handbook and by consulting the Canadian Immunization Guide.

Prophylaxis

None.

Note: More information on prophylaxis as part of the medical surveillance program can be found in the Canadian Biosafety Handbook.

Section VI – Laboratory hazard

Laboratory-acquired infections

None reported to date.

Note: Please consult the Canadian Biosafety Standard and Canadian Biosafety Handbook for additional details on requirements for reporting exposure incidents. A Canadian biosafety guideline describing notification and reporting procedures is also available.

Sources/specimens

Saliva, dental plaque, cardiovascular specimens^{Footnote 64}^{Footnote 65}.

Primary hazards

Mucous membrane exposure and accidental parenteral inoculation.

Special hazards

None.

Section VII – Exposure controls/personal protection

Risk group classification

P. gingivalis is a Risk Group 2 human pathogen and a Risk Group 1 animal pathogen^{Footnote 66}.

Containment requirements

Containment Level 2 facilities, equipment, and operational practices as outlined in the Canadian Biosafety Standard are required for work involving infectious or potentially infectious materials, cultures, or animals.

Protective clothing

The applicable Containment Level 2 requirements for personal protective equipment and clothing outlined in the Canadian Biosafety Standard are to be followed. At minimum, it is recommended to use a labcoat and closed-toe cleanable shoes, gloves when direct skin contact with infected materials or animals is unavoidable, and eye protection where there is a known or potential risk of exposure to splashes.

A local risk assessment will identify the appropriate hand, foot, head, body, eye/face, and respiratory protection, and the personal protective equipment requirements for the containment zone and work activities must be documented.

Other precautions

A biological safety cabinet (BSC) or other primary containment devices to be used for activities with open vessels, based on the risks associated with the inherent characteristics of the regulated material, the potential to produce infectious aerosols or aerosolized toxins, the handling of high concentrations of regulated materials, or the handling of large volumes of regulated materials.

Use of needles and syringes are to be strictly limited. Bending, shearing, re-capping, or removing needles from syringes to be avoided, and if necessary, performed only as specified in standard operating procedures (SOPs). Additional precautions are required with work involving animals or large-scale activities.

Additional information

For diagnostic laboratories handling primary specimens that may contain P. gingivalis, the following resources may be consulted:

Section VIII – Handling and storage

Spills

Allow aerosols to settle. Wearing protective clothing, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time with disinfectant before clean up (Canadian Biosafety Handbook).

Disposal

All materials/substances that have come in contact with the regulated materials to be completely decontaminated before they are removed from the containment zone or standard operating procedures (SOPs) to be in place to safely and securely move or transport waste out of the containment zone to a designated decontamination area / third party. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the regulated material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (Canadian Biosafety Handbook).

Storage

The applicable Containment Level 2 requirements for storage outlined in the Canadian Biosafety Standard are to be followed. Primary containers of regulated materials removed from the containment zone to be labelled, leakproof, impact resistant, and kept either in locked storage equipment or within an area with limited access.

Section IX – Regulatory and other information

Canadian regulatory information

Controlled activities with P. gingivalis require a Pathogen and Toxin licence issued by the Public Health Agency of Canada.

The following is a non-exhaustive list of applicable designations, regulations, or legislations:

Last file update

February, 2024

Prepared by

Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

The scientific information, opinions, and recommendations contained in this Pathogen Safety Data Sheet have been developed based on or compiled from trusted sources available at the time of publication. Newly discovered hazards are frequent and this information may not be completely up to date. The Government of Canada accepts no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information.

Persons in Canada are responsible for complying with the relevant laws, including regulations, guidelines and standards applicable to the import, transport, and use of pathogens in Canada set by relevant regulatory authorities, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. The risk classification and related regulatory requirements referenced in this Pathogen Safety Data Sheet, such as those found in the Canadian Biosafety Standard, may be incomplete and are specific to the Canadian context. Other jurisdictions will have their own requirements.

References

Footnote 1

Catalogue of Life. 2015. Porphyromonas gingivalis.

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Footnote 2

Kuramitsu, H. K. 2003. Molecular genetic analysis of the virulence of oral bacterial pathogens: an historical perspective. Critical Reviews in Oral Biology & Medicine. 14:331-344.

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Footnote 3

Summanen, P., and S. M. Finegold. 2012. Genus I. Porphyromonas, p. 62. N. R. Krieg, J. T. Staley, D. R. Brown, B. P. Hedlund, B. J. Paster, N. L. Ward, W. Ludwig, and W. B. Whitman (eds.), Bergey's Manual of Systematic Bacteriology, Second ed., vol. 4. Springer.

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Footnote 4

Masuda, T., Y. Murakami, T. Noguchi, and F. Yoshimura. 2006. Effects of various growth conditions in a chemostat on expression of virulence factors in Porphyromonas gingivalis. Appl. Environ. Microbiol. 72:3458-3467.

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Footnote 5

Gibson, F. C., and C. A. Genco. 2006. The Genus Porphyromonas, p. 428. M. Dworkin, S. Falkow, E. Rosenberg, K. Schleifer, and E. Stackebrandt (eds.), The Prokaryotes: A Handbook on the Biology of Bacteria, Third ed., vol. 7. Springer.

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Footnote 6

Holt, S. C., and J. L. Ebersole. 2000. Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia: the "red complex", a prototype polybacterial pathogenic consortium in periodontitis. Periodontol. 2000. 38:72-122.

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Footnote 7

Bostanci, N., and G. N. Belibasakis. 2012. Porphyromonas gingivalis: an invasive and evasive opportunistic oral pathogen. FEMS Microbiol. Lett. 333:1-9.

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Footnote 8

Griffen, A. L., S. R. Lyons, M. R. Becker, M. L. Moeschberger, and E. J. Leys. 1999. Porphyromonas gingivalis Strain Variability and Periodontitis. J. Clin. Microbiol. 37:4028-4033.

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Footnote 9

Dorn, B. R., J. N. Burks, K. N. Seifert, and A. Progulske-Fox. 2000. Invasion of endothelial and epithelial cells by strains of Porphyromonas gingivalis. FEMS Microbiol. Lett. 187:139-144.

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Footnote 10

Baek, K. J., S. Ji, Y. C. Kim, and Y. Choi. 2015. Association of the invasion ability of Porphyromonas gingivalis with the severity of periodontitis. Virulence. 6:274-281.

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Footnote 11

Carrouel, F., S. Viennot, J. Santamaria, P. Veber, and D. Bourgeois. 2016. Quantitative Molecular Detection of 19 Major Pathogens in the Interdental Biofilm of Periodontally Healthy Young Adults. Front. Microbiol. 7:10.3389/fmicb.2016.00840.

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Footnote 12

Griffen, A. L., M. R. Becker, S. R. Lyons, M. L. Moeschberger, and E. J. Leys. 1998. Prevalence of Porphyromonas gingivalis and periodontal health status. J. Clin. Microbiol. 36:3239-3242.

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Footnote 13

van Winkelhoff, A. J., B. G. Loos, van der Reijden, W. A., and U. van der Velden. 2002. Porphyromonas gingivalis, Bacteroides forsythus and other putative periodontal pathogens in subjects with and without periodontal destruction. J Clin Periodontol. 29:1023.

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Footnote 14

How, K. Y., Song, K. P., and Chan, K. G. 2016. Porphyromonas gingivalis: An overview of periodontopathic pathogen below the gum line. Front Microbiol. 7:53.

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Footnote 15

Albandar, J. M. 2014. Aggressive periodontitis: case definition and diagnostic criteria. Periodontol. 2000. 65:13-26.

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Footnote 16

Li, C., Yu, R., and Ding, Y. 2022. Association between Porphyromonas Gingivalis and systemic diseases: Focus on T cells-mediated adaptive immunity. Front Cell Infect Microbiol. 12:1026457.

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Footnote 17

Benedyk, M., P. M. Mydel, N. Delaleu, K. Plaza, K. Gawron, A. Milewska, K. Maresz, J. Koziel, K. Pyrc, and J. Potempa. 2016. Gingipains: Critical Factors in the Development of Aspiration Pneumonia Caused by Porphyromonas gingivalis. J. Innate Immun. 8:185-198.

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Footnote 18

Tonetti, M. S., S. Jepsen, L. Jin, and J. Otomo-Corgel. 2017. Impact of the global burden of periodontal diseases on health, nutrition and wellbeing of mankind: A call for global action. J. Clin. Periodontol. 44:456-462.

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Footnote 19

Beck, J. D., S. Offenbacher, R. Williams, P. Gibbs, and R. Garcia. 1998. Periodontitis: a risk factor for coronary heart disease? Ann. Periodontol. 3:127-141.

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Footnote 20

Dasanayake, A. P., D. Boyd, P. N. Madianos, S. Offenbacher, and E. Hills. 2001. The association between Porphyromonas gingivalis-specific maternal serum IgG and low birth weight. J. Periodontol. 72:1491-1497.

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Footnote 21

Ali, T. B., and K. Z. Abidin. 2012. Relationship of periodontal disease to pre-term low birth weight infants in a selected population--a prospective study. Community Dent. Health. 29:100-105.

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Footnote 22

Ahn, J., S. Segers, and R. B. Hayes. 2012. Periodontal disease, Porphyromonas gingivalis serum antibody levels and orodigestive cancer mortality. Carcinogenesis. 33:1055-1058.

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Footnote 23

Olsen, I., Singhrao, S. K., and Potempa, J. 2018. Citrullination as a plausible link to periodontitis, rheumatoid arthritis, atherosclerosis and Alzheimer's disease. J Oral Microbiol. 10:1487742.

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Footnote 24

Genco, C. A., T. Van Dyke, and S. Amar. 1998. Animal models for Porphyromonas gingivalis-mediated periodontal disease. Trends Microbiol. 6:444-449.

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Footnote 25

Van Winkelhoff, A. J., and K. Boutaga. 2005. Transmission of periodontal bacteria and models of infection. J. Clin. Periodontol. 32 Suppl 6:16-27.

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Footnote 26

Rylev, M., and M. Kilian. 2008. Prevalence and distribution of principal periodontal pathogens worldwide. J. Clin. Periodontol. 35:346-361.

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Footnote 27

Petersen, P. E., D. Bourgeois, H. Ogawa, S. Estupinan-Day, and C. Ndiaye. 2005. The global burden of oral diseases and risks to oral health. Bull. World Health Organ. 83:661-669.

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Footnote 28

Kassebaum, N. J., E. Bernabe, M. Dahiya, B. Bhandari, C. J. Murray, and W. Marcenes. 2014. Global burden of severe periodontitis in 1990-2010: a systematic review and meta-regression. J. Dent. Res. 93:1045-1053.

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Footnote 29

Susin, C., A. N. Haas, and J. M. Albandar. 2014. Epidemiology and demographics of aggressive periodontitis. Periodontol. 2000. 65:27-45.

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Footnote 30

Eke, P. I., Thornton-Evans, G. O., Wei, L., Borgnakke, W. S., Dye, B. A., and Genco, R. J. 2018. Periodontitis in US Adults: National Health and Nutrition Examination Survey 2009-2014. J Am Dent Assoc. 149:576-588.e6.

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Footnote 31

Amano, A., J. Murakami, S. Akiyama, and I. Morisaki. 2008. Etiologic factors of early-onset periodontal disease in Down syndrome. Japanese Dental Science Review. 44:118-127.

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Footnote 32

Katz, P. P., M. R. Wirthlin Jr, S. M. Szpunar, J. V. Selby, S. J. Sepe, and J. A. Showstack. 1991. Epidemiology and prevention of periodontal disease in individuals with diabetes. Diabetes Care. 14:375-385.

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Footnote 33

Olsen, I., and Singhrao, S. K. 2019. Poor Oral Health and Its Neurological Consequences: Mechanisms of Porphyromonas gingivalis Involvement in Cognitive Dysfunction. Curr Oral Health Rep. 6:120–129.

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Footnote 34

Oz, H. S., and D. A. Puleo. 2011. Animal models for periodontal disease. J. Biomed. Biotechnol. 2011.

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Footnote 35

Polak, D., A. Wilensky, L. Shapira, A. Halabi, D. Goldstein, E. I. Weiss, and Y. Houri-Haddad. 2009. Mouse model of experiemental periodontitis induced by Porphyromonas gingivalis / Fusobacterium nucleatum infection: bone loss and host response. J. Clin. Periodontol. 36:406-410.

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Footnote 36

Holt, S. C., J. Ebersole, J. Felton, M. Brunsvold, and K. S. Kornman. 1988. Implantation of Bacteroides gingivalis in nonhuman primates initiates progression of periodontitis. Science. 239:55-57.

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Footnote 37

Asikainen, S., and C. Chen. 1999. Oral ecology and person-to-person transmission of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. Periodontol. 2000. 20:65-81.

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Footnote 38

Gibson, F. C., Genco, C. A. 2006. The Genus Porphyromonas. Dworkin, M., Falkow, S., Rosenberg, E., Schleifer, K. H., and Stackebrandt, E. (eds) The Prokaryotes. Springer, New York, NY.

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Footnote 39

Quirynen, M., M. de Soete, M. Pauwels, K. Goossens, W. Teughels, J. van Eldere, and D. van Steenberghe. 2001. Bacterial survival rate on tooth- and interdental brushes in relation to the use of toothpaste. J. Clin. Periodontol. 28:1106-1114.

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Footnote 40

Tuite-McDonnell, M., A. L. Griffen, M. L. Moeschberger, R. E. Dalton, P. A. Fuerst, and E. J. Leys. 1997. Concordance of Porphyromonas gingivalis colonization in families. J. Clin. Microbiol. 35:455-461.

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Footnote 41

Jacinto, R. C., B. P. Gomes, H. N. Shah, C. C. Ferraz, A. A. Zaia, and F. J. Souza-Filho. 2006. Incidence and antimicrobial susceptibility of Porphyromonas gingivalis isolated from mixed endodontic infections. Int. Endod. J. 39:62-70.

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Footnote 42

Japoni, A., A. Vasin, S. Noushadi, F. Kiany, S. Japoni, and A. Alborzi. 2011. Antibacterial susceptibility patterns of Porphyromonas gingivalis isolated from chronic periodontitis patients. Med. Oral Patol. Oral Cir. Bucal. 16:e1031-5.

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Footnote 43

Lakhssassi, N., N. Elhajoui, J. P. Lodter, J. L. Pineill, and M. Sixou. 2005. Antimicrobial susceptibility variation of 50 anaerobic periopathogens in aggressive periodontitis: an interindividual variability study. Oral Microbiol. Immunol. 20:244-252.

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Footnote 44

Sakamoto, M. 2014. The Family Porphyromonadaceae, p. 811. E. Rosenberg, E. F. DeLong, S. Lory, E. Stackebrandt, and F. Thompson (eds.), The Prokaryotes - Other Major Lineages of Bacteria and the Archaea. Springer.

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Footnote 45

Conrads, G., Klomp, T., Deng, D., Wenzler, J. S., Braun, A., and Abdelbary, M. M. H. 2021. The Antimicrobial Susceptibility of Porphyromonas gingivalis: Genetic Repertoire, Global Phenotype, and Review of the Literature. Antibiotics (Basel). 10:1438.

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Footnote 46

Ardila, C. M., and Bedoya-García, J. A. 2020. Antimicrobial resistance of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia in periodontitis patients. J Glob Antimicrob Resist. 22:215-218.

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Footnote 47

Carrol, D. H., Chassagne, F., Dettweiler, M., and Quave, C. L. 2020. Antibacterial activity of plant species used for oral health against Porphyromonas gingivalis. PLoS One. 15:e0239316.

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Footnote 48

Rams, T. E., Sautter, J. D., and van Winkelhoff, A. J. 2023. Emergence of Antibiotic-Resistant Porphyromonas gingivalis in United States Periodontitis Patients. Antibiotics (Basel). 12:1584

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Footnote 49

Chen, C., C. -. Chen, and S. -. DIng. 2016. Effectiveness of hypochlorous acid to reduce the biofilms on titanium alloy surfaces in vitro. Int. J. Mol. Sci. 17:1161.

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Footnote 50

Nakagawa, T., Y. Hosaka, K. Ishihara, T. Hiraishi, S. Sato, T. Ogawa, and K. Kamoi. 2006. The efficacy of povidone-iodine products against periodontopathic bacteria. Dermatology. 212 Suppl 1:109-111.

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Footnote 51

Takada, A., K. Matsushita, S. Horioka, Y. Furuichi, and Y. Sumi. 2017. Bactericidal effects of 310Â nm ultraviolet light-emitting diode irradiation on oral bacteria. BMC Oral Health. 17:10.1186/s12903-017-0382-5.

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Footnote 52

Sreenivasan, P. K., V. I. Haraszthy, and J. J. Zambon. 2013. Antimicrobial efficacy of 0.05% cetylpyridinium chloride mouthrinses. Lett. Appl. Microbiol. 56:14-20.

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Footnote 53

Kubota, R., S. Osato, I. Kuroyama, T. Ogawa, and S. Nakajima. 2005. Efficacy of Chlorine Dioxide Gas against Porphyromonas gingivalis. J Jap Soc Oral Implant. 18:222-228.

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Footnote 54

Bercy, P., and Lasserre, J. 2007. Susceptibility to various oral antiseptics of Porphyromonas gingivalis W83 within a biofilm. Adv Ther. 24:1181-91.

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Footnote 55

Hancock, C. O. 2013. Heat Sterilization, p. 277-293. A. P. Fraise, P. A. Lambert, and J. Y. Maillard (eds.), Russell, Hugo & Ayliffe's: Principles and Practice of Disinfection, Preservation and Sterilization, Fifth Edition. Wiley-Blackwell.

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Footnote 56

Mahasneh, A., Darby, M., Tolle, S., Hynes, W., Laroussi, M., and Karakas, E. 2011. Inactivation of Porphyromonas gingivalis by Low-Temperature Atmospheric Pressure Plasma. Plasma Medicine. 1:191-204.

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Footnote 57

Fekrazad, R., Khoei, F., Bahador, A., and Hakimiha, N. 2020. Comparison of different modes of photo-activated disinfection against Porphyromonas gingivalis: An in vitro study. Photodiagnosis Photodyn Ther. 32:101951.

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Footnote 58

Kramer, A., and O. Assadian. 2014. Survival of microorganisms on inanimate surfaces, p. 7. G. Borkow (ed.), Use of Biocidal Surfaces for Reduction of Healthcare Acquired Infections. Springer.

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Footnote 59

Hunt, D. E., J. V. Jones, and V. R. Dowell Jr. 1986. Selective medium for the isolation of Bacteroides gingivalis. J. Clin. Microbiol. 23:441-445.

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Footnote 60

Sakamoto, M., Y. Takeuchi, M. Umeda, I. Ishikawa, and Y. Benno. 2001. Rapid detection and quantification of five periodontopathic bacteria by real-time PCR. Microbiol. Immunol. 45:39-44.

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Footnote 61

Riggio, M. P., T. W. Macfarlane, D. Mackenzie, A. Lennon, A. J. Smith, and D. Kinane. 1996. Comparison of polymerase chain reaction and culture methods for detection of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in subgingival plaque samples. J. Periodontal. Res. 31:496-501.

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Footnote 62

Gerits, E., N. Verstraeten, and J. Michiels. 2017. New approaches to combat Porphyromonas gingivalis biofilms. J. Oral Microbiol. 9:1300366.

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Footnote 63

O'Brien-Simpson, N. M., J. A. Holden, J. C. Lenzo, Y. Tan, G. C. Brammar, K. A. Walsh, W. Singleton, R. K. Orth, N. Slakeski, K. J. Cross, I. B. Darby, D. Becher, T. Rowe, A. B. Morelli, A. Hammet, A. Nash, A. Brown, B. Ma, D. Vingadassalom, J. McCluskey, H. Kleanthous, and E. C. Reynolds. 2016. A therapeutic Porphyromonas gingivalis gingipain vaccine induces neutralising IgG1 antibodies that protect against experimental periodontitis. Npj Vaccines 1, 16022

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Footnote 64

Oliveira, F. A., C. P. Forte, P. G. Silva, C. B. Lopes, R. C. Montenegro, A. K. Santos, C. R. Sobrinho, M. R. Mota, F. B. Sousa, and A. P. Alves. 2015. Molecular Analysis of Oral Bacteria in Heart Valve of Patients With Cardiovascular Disease by Real-Time Polymerase Chain Reaction. Medicine (Baltimore). 94:e2067.

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Footnote 65

Nakano, K., H. Nemoto, R. Nomura, H. Inaba, H. Yoshioka, K. Taniguchi, A. Amano, and T. Ooshima. 2009. Detection of oral bacteria in cardiovascular specimens. Oral Microbiol. Immunol. 24:64-68.

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Footnote 66

Public Health Agency of Canada. 2015. Human Pathogens and Toxins Act (HPTA).

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Date modified:: 2025-02-05