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The Role for Specific Bacteria for Both Periodontal Disease and Systemic Inflammation

The Role for Specific Bacteria for Both Periodontal Disease and Systemic Inflammation

Our understanding of the role that specific microbes play in chronic inflammatory periodontitis has changed.1,2,3,4,5

Not long ago, most believed that all perio infections were basically the same. Thus, all perio infections were treated basically with the same goal in mind. Today, the evidence is clear: Periodontal infections are not the same infections from one person to another. 6,7,8,9,10,11,12,13  The specificity of very specific microbes and their concentration or dose helps us to understand the differences in diseases, the risk of disease progression, how we plan to treat the disease, and the potential negative systemic influence.

We should also know that the same microbes that are causative for chronic periodontal infections may also increase risk for heart disease and potentially all inflammatory diseases.

Dr. Anne Haffajee stated in her article in 1994, “The ultimate risk factor for any disease is the causative agent of that disease.” While a very simple sentence, it is profoundly correct. People do not develop bacterial infections without very specific bacteria and, typically, at different concentration than found in healthy people. Specific bacteria and concentration matter both in periodontal disease and also in systemic inflammation.

Virulence or pathogenic potential is important to understand.4,5   Different periodontopathogenic microbes have different virulence potential. One person with 4mm pockets may have a very different risk for disease progression than another person with the same degree of pocket depths. The most significant difference is often the type and concentration of specific periodontopathogenic bacteria.  One person may do well with a “prophy” and home care instructions while another may do poorly. 14Starting with the potential microbial differences of these two patients may help dramatically how the clinician treats each disease somewhat differently.

The same bacteria that are responsible for causation for chronic inflammatory perio infections are also seen as risk factors for implant infections both as causative organisms as well as potential risk for future bone loss. 15,16, 17  Thus, it makes good clinical “sense” to know when patients are at risk prior to implant surgery and when the earliest of signs of mucositis or implantitis occurs.

We should know the pathogenic potential of microbes found within different periodontal infections is different based on type and concentration. 4   The pathogenic potential of the bacteria themselves can cause such an immune response in subjects to cause the anatomical changes associated with these infections. There tends to be a “tipping point” of dose that is reached based on cumulative inflammatory burden which includes bacteria, genetics and a host of modifying factors.

Interestingly, the medical research also suggests the connection to chronic inflammatory periodontal infections and arterial disease.18,19

Recently, we are observing studies of the same microbes that are causative for perio infections to examine the risk for vascular injury and/or disease.  While clinical signs of periodontal disease have been traditionally used to review the potential risk for vascular disease, today, there is a movement toward looking more closely at the microbes of periodontal disease as risk for vascular injury, atherosclerosis, heart disease and stroke. I will only mention only two medical reviews to show this significant movement within medicine.

Article #1:

Periodontal Microbiota and Carotid Intima-Media Thickness: The Oral Infections and Vascular Disease Epidemiology Study (INVEST); Desvarieux. ,M., et. al., Circulation, 2005, February 8; 111(5): 576.

  • The investigators examined the relationship between periodontal microbiota and subclinical atherosclerosis.
  • Included and examined 657 dentate subjects: No history of stroke or myocardial infarction
  • All analyses adjusted for age, race/ethnicity, gender, education, BMI, smoking, diabetes, SBP, LDL, HDL


Microbes tested for association with periodontal infections and health related

(1) etiologically linked with periodontal diseases or frequently encountered in pathological periodontal conditions (Porphyromonas gingivalisTannerella forsythensisActinobacillus actinomyce-temcomitans, and Treponema denticola;

(2) putatively associated with periodontal disease (Prevotella intermediaFusobacterium nucleatum,Micromonas micros , Campylobacter rectus, and Eikenella corrodens; and

(3) primarily associated with healthy periodontal conditions (Veillonella parvula and Actinomyces naeslundii.

3 separate analyses of mean carotid artery intima-media thickness (IMT) regressed on tertiles of

  •  (1) burden of all bacteria: groups 1,2 & 3
  • (2) burden of causative bacteria: groups 1 & 2
  • (3) relative predominance of causative bacteria:  group 1 (P.g., A.a., T.f., T.d.)


  • Overall periodontal bacterial burden was related to carotid IMT. (1.2,3)
  • This relationship was specific to causative bacterial burden and the dominance of etiologic bacteria ; group 3: A.a., P.g., T.f. T.d.
  • Adjusted mean IMT values across tertiles of etiologic bacterial dominance were 0.84, 0.85, and 0.88 (P=0.002).
  • Similarly, WBC values increased across tertiles of etiologic bacterial burden from 5.57 to 6.09 cell x 109/L (P=0.01)


  • The magnitude of carotid IMT changes reported is in keeping with values that have been deemed significant in prior observational and interventional studies.
  • The Etude du Vieillssement Arteriel (EVA) reported that a cross-sectional difference of 0.03 mm in carotid IMT was associated with a 15-mm Hg increase in systolic blood pressure.
  • The cross-sectional difference of 0.04 mm in carotid IMT thickness was equivalent to a 10-year age difference in subjects without bulbar plaque.
  • In progression studies, Hodis et al reported that a 0.03-mm increase in carotid IMT is associated with a 2.3-increased relative risk for nonfatal myocardial infaction or coronary death.
  • The present finding of a 0.03-0.04-mm mean difference between the highest and lowest tertiles of bacterial burden/dominance appears to fall within the range of clinically relevant differences.
  • Data provides evidence of a direct relationship between periodontal microbiology and subclinical atherosclerosis
  • This relationship exists independent of C-reactive protein.

Article #2:

Periodontal bacteria and hypertension: the oral infections and vascular disease epidemiology study (INVEST); M Desvarieux, RT Demmer, DR Jacobs ; Journal of Hypertension 2010, 28: 1413-1421

  • Objective: To investigate the relationship between periodontal microbiota and hypertension
  • Bacterial species tested: Causal & Putative groups
    • Aggregatibacter actinomycetemcomitans (A.a.)
    • Porphyromonas gingivalis (P.g.)
    • Tannerella forsythia (T.f.)
    • Treponema denticola (T.d.)


  • Fusobacterium nucleatum (F.n.)
  • Prevotella intermedia (P.i.)
  • Campylobacter rectus (C.r.)
  • Parvimonas micra (P.m.)
  • Eikenella corrodens (E.c.)

653 subjects: No history of stroke, myocardial infaction

  • Adjusted for age, race, sex, education, BMI, smoking, diabetes, LDL, HDL

BP and hypertension each regressed on the level of bacteria


  •  Etiologic (causal) bacterial burden positively associated with both BP and prevalent hypertension
  • Comparing highest and lowest tertiles of etiologic bacterial burden
  • SBP was 9 mmHg higher
  • DBP was 5 mmHg higher (P for linear trend <0.001 in each case)


  • Our data provide evidence of a direct relationship between the levels of these subgingival periodontal bacteria (Aa, Pg, Tf, Td) and both SBP and DBP as well as hypertension prevalence.
  • Etiologic bacterial burden is positively associated with both BP and prevalent hypertension

Even this month, we have learned more about the pathogenic potential of these microbes due to their invasive characteristics. The ability for these organisms to invade gingival tissues as well as endothelial tissues is helping in our understanding of both the local potential for disease as well as the systemic potential for disease. We will address the issue of invasion within another article.


  1. Mariano Sanz, Arie Jan van Winkelhoff, Group 1 Seventh European Workshop; Periodontal infections: understanding  the complexity-Consensus of  the Seventh European Workshop on Periodontology; J Clin Periodontol 2011; 38 (Suppl.11): 3-6
  2. Van Winkelhoff, Winkel; Microbiological diagnostics in periodontics: biological significance and clinical validity: Periodontol 2000, Vol. 39, 2005, 40­52
  3. Socransky, Haffajee, Cugini; Microbial complexes in subgingival plaque; J Clin Periodontol Vol. 25, 134­144; 1998;
  4. Teles, Haffajee, Socransky; Microbiological goals of periodontal therapy;; Periodontol 2000, Vol 42, 2006, 180­218
  5. Socransky, Haffajee; Microbial etiological agents of destructive periodontal disease: Periodontol 2000, Vol. 5; 1994, 78-­111
  6. Control of oral biofilms: Thomas F. Flemmig, Thomas E. Beikler; Periodontology 2000, Vol. 55, 2011, 9-15
  7. Dental plaque biofilms: communities, conflict and control: Philip D. Marsh, Annette Moter, Deirdre A. Devine; Periodontology 2000, Vol. 55, 2011, 16-35
  8. Profiling of subgingival plaque biofilm microflora from periodontally healthy subjects and from subjects with periodontitis using quantitative real-time PCR: Abiko Y, Sato T, Mayanagi G, Takahashi N; J Periodont Res 2010; 45: 389-395
  9. Microbiological goals of periodontal therapy; Teles, Haffajee, Socransky; Periodontol 2000, Vol. 42, 2006, 180­218
  10. Microbial etiological agents of destructive periodontal disease: Periodontol 2000, Vol. 5; 1994, 78­111: Socransky, et al
  11. The  effect of periodontal therapy on the composition of the subgingival microbiota; Haffajee, Teles, Socransky Periodontol 2000, Vol. 42, 2006, 219-258
  12. Microbial Etiology of Periodontal Disease: Mini Review. Medicine and Biology Vol. 15, 2008, 1-6
  13. Beikler, et al., Specific  Antibiotics in the Treatment of Periodontitis-A Proposed Strategy; J Periodontology, Jan. 2004, Vol 75, #1, 169-175
  14. Perio-Implant Infection: Etiology, Diagnosis and Treatment; Frank Schwarz, Jΰrgen Becker; Quintessence Publishing Co. Ltd.
  15. Rethinking Periodontal Inflammation; J Periodont. August 2008 (Supplement) 1577-91; Offenbacher, Barros, Beck
  16. Periodontal disease as a risk for dental implant failure over time: A long-term historical cohort Source; Liran Levin, Ronen Ofec, Yoav Grossmann, Rachel Anner;  2 JUN 2011; J Clin Perio Vol. 38, Isssue 8, 732-737; August 2011
  17. A follow-up study of peri-implantitis cases after treatment; Georgios Charalampakis,  Per Rabe, Åsa Leonhardt, Gunnar Dahlén1Article first published online:, J of Clin Periodont;  Sept.2011;38(9):864-71
  18. The American Journal of Cardiology and The Journal of Periodontology, July 2009 ; 80: 1021-1032; Vincent E. Friedewald, Kenneth S. Kornman, James D. Beck, Robert Genco, Allison Goldfine, Peter Libby, Steven Offenbacher, Paul M. Ridker, Thomas E. Van Dyke, William C. Roberts
  19. Periodontology 2000, Vol. 55, 2011, 87-103; Oral biofilm-associated diseases: trends and implications for quality of life, systemic health and expenditures; Thomas Beikler, Thomas F. Flemmig