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Minimizing Bacteremia in Periodontal Disease Treatment

Localized and systemically adverse effects of the host response to subgingival biofilm microbial “triggers” are critical concerns for clinical practitioners, only heightened by the prevalence of periodontal disease and the limitations of current treatment methods. Scaling and root planing (SRP) is the accepted gold standard in non-surgical treatment for gum disease. Its benefits are well known, but significant limitations occur with SRP, including an inability to remove all bacterial cells mechanically, resulting in biofilm regeneration that requires repetitive debridement procedures. The most important concern for anyone who takes oral-systemic relationships seriously is the risk of bacteremia associated with these debridement procedures.

Biofilms that induce diseases like periodontitis cause inflammation, resist clearance by host defenses, and resist systemic antibiotic therapy (1, 2). While physical removal of biofilms has developed as the gold standard in the treatment of virtually all biofilm infections, as it is in dentistry with SRP, it is impossible to eliminate all of the biofilm in a sulcus with SRP (3)and re-colonization can result (4,5).

Mechanical debridement, in fact, can stimulate biofilm regeneration. In one study mechanical removal of 50% of the initial biofilm resulted in a four-fold increase in biofilm development. A biofilm that is mechanically disturbed can thus increase its reproductive capabilities as a response. (6)

To improve the results in periodontal disease treatment, adjunctive antibiotic therapies are combined with mechanical debridement. Antibiotics, however, are most effective in killing individual planktonic cells and some of the peripheral, actively dividing elements in the biofilm; they have little impact on the dormant core enclosed in the protective slime matrix (7, 8).  In order for the adjunctive antibiotic therapies to work more effectively, the matrix has to be removed and the dormant core stimulated; however, when mechanical debridement removes the matrix and stirs up the core, rapid regeneration helps the biofilm returns to a protected, stable population stasis, for which additional SRP is often necessary in a cyclical fashion (9).  Thus, for most patients with chronic or aggressive periodontitis who have SRP performed every 3-6 months, the procedures may never adequately address the disease because of persistent biofilm regeneration.

Repetitive use of SRP increases the risks of bacteremia associated with mechanical debridement and scaling (10), 11).For most healthy adults bacteremia associated with periodontal debriding procedures does not present serious adverse inflammatory systemic effects; the host immune system is capable of managing these challenges.  But for the millions of immunocompromized individuals and adults with diabetes, cardiovascular disease, joint replacements and other inflammatory illnesses, an increase in the chronic systemic inflammatory burden may pose additional health risks (12). Given these potential adverse effects, a treatment modality that could avoid or reduce the possibility of bacteremia would be beneficial.

Recently new attention has been paid to peroxides usage as viable subgingival (13)and supragingival (14)antibiofilm chemotherapeutic agents. Aqueous ≤3% hydrogen peroxide is a known oral debriding agent and wound cleanser and has been used in dental medicine for decades (15, 16).One problem, of course, is the delivery and maintenance of peroxides in the sulcus. The sulcus is a unique space for chemotherapeutic treatment of chronic biofilm infections because it is accessible topically, but the problem of overcoming the flow of gingival crevicular fluid tends to limit chemical contact in the sulcus. The most effective topical administration of peroxides appears to be tray delivery of a gel formulation (17, 18, 19). If peroxides can be maintained in the sulcus for long enough to debride subgingival planktonic cells of the biofilm and significantly trim the healthy peripheral elements of biofilms, the agents may shift biofilm communities into a defensive mode-of-growth in which they cannot spread and are much less able to trigger inflammation.

And, in fact, studies on the Perio Protect Method® bear this out. When oxidizing agents are delivered into the sulcus and maintained there with a custom-formed prescription tray (Perio Tray®, Perio Protect, LLC) chemical debridement reduces the biofilm population and leads to decreased pocket depths, reductions in bleeding upon probing, and less tissue inflammation (20, 21, 22, 23, 24, 25).If the prescription tray delivery of medication is used before SRP, then the risks of bacteremia associated with mechanical debridement may also be reduced. For more information on the Perio Protect Method and the use of the customized, prescription tray delivery of medication into the sulcus as an adjunct to mechanical procedures, visit PerioProtect or click to emailsupport@perioprotect.com.


1. Schaudinn C, Gorur A, Keller D, Sedghizadeh P, Costerton W. Periodontitis An archetypical biofilm disease. JADA 2009;140(8):978-86.

2. Krayer J, Renata L, Kirkwood K. Non-surgical chemotherapeutic Treatment Strategies for the Management of Periodontal Diseases. Dent Clin N Am 2010(54):13-33.

3. Adriaens P, Adriaens L. Effects of nonsurgical periodontal therapy on hard and soft tissues. Periodontol 2000 2004;36:121-45.

4. Zijine V, Meijer H, Lie M, Tromp J, Degener J, Harmsen H, Abbas F. The recolonization hypothesis in a full-mouth or multiple-session treatment protocol: a blinded, randomized clinical trial. J Clin Periodontol. 2010;37(6): 518-25.

5. Resposo S, Tobler J, Alfant B, Gollwitzer J, Walker C, Shaddox L. Poster presentation: Differences between Biofilm Growth Before and After Periodontal Therapy. AADR 37th Annual Meeting. April 3, 2008. Abstract available online

6. Palmer, RJ, Caldwell DE.  J Micro Methods 1995;24(2):171-82 . A flowcell for the study of plaque removal and regrowth.

7. Tuomanen E. Cozens R, Tosch W et al.  The rate of killing of Escherichia coly by B lactam antibiotics is strictly proportional to the rate of bacterial growth.  J Gen Micriobio 1986;132, 1297-1304

8. Stewart, P.S., Theoretical aspects of antibiotic diffusion into microbial biofilms. Antimicrob. Agents Chemother 1996;40:2517-2522.

9. Schara R, Medvescek M, Skaleric U.  Periodontal disease and diabetes metabolic control: a full-mouth disinfection approach. J Int Acad Periodontol. 2006 Apr;8(2):61-6.

10. Lafaurie GI, Mayorga-Fayad I, Torres MF, Castillo DM, Aya MR, BaronA, Hurtado PA. Periodontopathic microorganisms in peripheric blood after scaling and root planing. J Clin Periodontol. 2007;34(10):873-9.

11. Morozumi T, Kubota T, Abe D, Shimizu T, Komatsu Y, Yoshie H. Effects of irrigation with an antiseptic and oral administration of azithromycin on bacteremia caused by scaling and root planing. J Periodontol. 2010;81(11):1555-63.

12. Fischer MA, Borgnakke WS, Taylor GW. Periodontal disease as a risk marker in coronary heart disease and chronic kidney disease. Curr Opin Nephrol Hypertens. 2010;19(6):519-26.

13. Schaudinn et al. Periodontitis An archetypical biofilm disease. JADA 2009;140(8):978-86.

14. Lazarchik DA, Haywood VB. Use of tray-applied 10 percent carbamide peroxide gels for improving oral health in patients with special-care needs. J Am Dent Asso. 2010;141(6):639-46.

15. 21 CFR Parts 201, 356, and 369. Federal Register, Vol 53. No. 17. Wednesday, January 27, 1988.

16. Marshall M, Cancro L, Fischman S. Hydrogen Peroxide. A review of its uses in dentistry.  J Periodontol. 1995;66(9):786-96.

17. Gusberti FA, Sampathkumar P, Siegrist BE, Lang NP. Microbiological and clinical effects of chlorhexidine digluconate and hydrogen peroxide mouthrinses on developing plaque and gingivitis. J Clin Periodontol. 1988;15(1):60-7.

18. Lazarchik DA, Haywood VB. Use of tray-applied 10 percent carbamide peroxide gels for improving oral health in patients with special-care needs. J Am Dent Asso. 2010;141(6):639-46.

19. Keller D, Costerton B, Schaudinn C. Poster presentation: SEM Results of Periopathogenic Control with the Perio Protect Method. IADR/AADR (March 21-24, 2007), Abstract available online: http://iadr.confex.com/iadr/2007orleans/techprogram/abstract_88428.htm

20. Schaudinn C, Gorur A, Sedghizadeh P, Costerton J, and Keller D. Manipulation of the microbial ecology of the periodontal pocket. World Dental 2010 Feb-March: 14-18.

21. Steele C, Keller D. Poster Presentation. C-reactive protein changes during Perio Protect treatment of periodontal disease. IADR/AADR (March 21-24, 2007). Abstract available on line: http://iadr.confex.com/iadr/2007orleans/techprogram/abstract_92806.htm

22. Keller D, Nguyen LT, Jobe LR, Sindelar BJ. Poster presentation: Preliminary Data on Periodontal Disease Treatment Using Topical Oxidizing Agents. AADR (March 3-6, 2010), Washington DC. Abstract available online: http://iadr.confex.com/iadr/2010dc/webprogram/Paper130185.html

23. Keller, D.C. Managing periodontal disease in a patient suffering from renal failure. Dentistry Today. 2008:27(7)144-47.

24. Schaudinn C, Gorur A, Sedghizadeh P, Costerton J, and Keller D. Manipulation of the microbial ecology of the periodontal pocket. World Dental 2010 Feb-March: 14-18.

25. Keller, D. How to manage oral biofilm using perio protect as a minimally invasive method for lasting oral health. DPR 2010;44(7):54-55.