You must be signed in to read the rest of this article.
Registration on CDEWorld is free. You may also login to CDEWorld with your DentalAegis.com account.
Caries and periodontal disease were minor concerns for early hominids.1 In the late Neolithic Period, grain cultivation and the consequent rise in carbohydrate ingestion resulted in a considerable increase in both diseases. It wasn’t until the mid-19th century Industrial Revolution, however, that efficient procurement and refinement of sugars and grains resulted in enormous increases in consumption of these fermentable carbohydrates. Substantial alteration in oral environments ensued, causing the eruption of epidemic levels of caries and periodontal disease that, in many parts of the world, still continues today.2 This major dietary change moved the nascent dental profession from surgical treatments by mostly apprenticeship-trained barber-surgeons toward a more scientific education in university-affiliated dental schools. By the latter part of the 19th century, Willoughby Miller3 and GV Black4 began investigating bacteria as the causes of both decay and periodontal disease. Black recognized the need for vigorous tooth brushing and developed his classic cavity preparation designs into “self-cleansing” areas,4 and JM Riggs of Connecticut published his treatise on oral hygiene, regular “scraping” of the roots along with co-treatments of, interestingly, myrrh as an antibacterial.5
In 1676, van Leeuwenhoek scraped “scruff” from his teeth, examined it under one of his first microscopes, and saw strange “animalcules” scurrying about. A bit more than 200 years later, Black4 renamed the “scruff” plaque. Plaque has become more fully understood today as a biofilm: complex colonies of differing forms of microscopic life living together within a sticky film.6
Biofilms are extraordinarily complex multispecies aggregations of bacteria, fungi, and occasionally admixed viruses that “stick” to any wet surface and/or to each other within a self-produced “gluey” polysaccharide-polymeric matrix . These multispecies communities of sheets and clumps make up approximately 50% of the world’s overall biomass.6 Within humans, 97% of DNA is biofilm in origin; only 3% is actually human.7
Biofilms, like all living things, are crafted by their environments.8 Most environments result in primarily commensal or mutualistic biofilm organizations. Though many biofilms are health encouraging, others can become dysbiotic and pathogenic.9 Dysbiotic biofilms in the oral cavity often result from changes in local nutritional and/or overall host metabolic environments.
Cooperation or pathogenicity occurs through a communication processes called quorum sensing.10 Quorum sensing is like voting. Intraspecies-specific, hormone-like “votes” are produced by individual bacteria within a colony to let others know how strong the colony has become through reproduction. Once a certain quorum vote is reached, the genomic functions and/or structure of the species changes, becoming more organized and more flexible. Additionally, all bacterial species possess a second, chemically different interspecies voting system. Interspecies votes tell other species they may be in an environment to become allies—or stronger allies—with others. Such “alliances” cooperate to modify the composition of the biofilm for good or ill. It is only within the past 30 years that recognition of how complex environmental stressors existing within and around human beings can change harmless or beneficial oral biofilms into pathogenic entities that can cause caries and chronic periodontal disease.9 It is estimated that 70% to 80% of chronic diseases are the result of pathogenic biofilms.11
Healthy oral cavity biofilms live in slightly acidic to neutral pH environments (ie, between ~6.5 and 7.0).12 However, consuming high levels of fermentable carbohydrates, sugars in any form, and sticky, highly refined flours leads to acidic metabolic byproducts from acidophilic bacteria that considerably lower this “normal” pH. Thus the biofilm’s acidophilic bacterial populations continue to increase in the ever-intensifying acidic environment through intra- and interspecies quorum sensing. As an example, quorum sensing may facilitate their strategic reposition within the biofilm for better metabolic cooperation or nutrition. The combined acid byproducts of this interspecies cooperation further lower pH and dysbiotic, pathogenic biofilms form, ultimately causing dental caries.9
Another major cause of increased salivary acidity is reduction in the amount of saliva. The resulting xerostomia, or “dry mouth,” means a proportional decrease in salivary buffering proteins, thereby increasing acid levels. Autoimmune diseases, many chronic diseases and conditions, and many medications—both prescribed and over the counter (OTC)—are the major causes of xerostomia.13 This environmental change benefits population increases of acidophilic bacteria at the expense of more neutral pH-tolerating species.
Periodontal Disease Development
The first description of periodontal disease was made in 1757 in France by Etienne Bourdet, when he linked bone loss, gingival inflammation, and loosening teeth with the deepening of the periodontal sulcus.14 Various treatments have been advocated to control periodontal disease, but only recently has its complex genesis become clearer by understanding biofilm interactions with each other and their host environments.15 This information provided the basis for therapies and treatments to manage dysbiotic environments, as opposed to surgical interventions that attempt only to eliminate periodontal disease’s signs and symptoms.
The Role of Subgingival Biofilms
Subgingival biofilm formation is exceptionally complex. Many bacterial species form biofilms adhering to tooth and tissue pellicles and some to each other, but some other biofilm bacteria cannot attach to others or to pellicles. They may, however, coaggregate with bacteria that can attach to pellicles or other species through quorum sensing. Coaggregation is analogous to bridging, such as in a situation where two people who cannot hold hands with each other can “bridge” via a third person who holds hands with both.16
As undisrupted, mostly aerobic, supragingival plaque colonies grow in amount and density, internal biofilm pH increases in the slightly oxygen-depleted depths, allowing formation of facultative anaerobic micro-colonies. Multiple-species supragingival biofilms can generate tissue-irritating metabolites, many of which are tissue toxic, and cause gingivitis. With undisrupted biofilms, inflammatory gingival swelling deepens the periodontal sulcus and a more oxygen-depleted environment forms in its depths.
Facultative aerobes within the supragingival biofilm bridge with other facultative aerobes, forming more anaerobic periodontal pockets, and they then coaggregate with increasing types of obligate anaerobes. Subgingival dysbiotic biofilms are developed and the host inflammatory response goes into high gear, producing the mix of immune proteins, dead epithelial cells, and other proteomic materials upon which increasingly pathogenic anaerobic bacterial colonies feed. A more chemically basic, more anaerobic, and higher-temperature playing field continues to develop where the most aggressive periodontal pathogens are better able to gain dominance. Accelerating inflammation and host response lead subgingival pathogenic biofilms to continually destroy the periodontium.16
Pathogenicity only occurs as a result of dysbiotic biofilms.12 A myriad of oral environmental changes encourage dysbiotic biofilm formation: xerostomia, diet, social habits, inadequate hygiene, and/or host chronic diseases, to name only a few. Risk identification and evaluation provide information on which well-researched risk management strategies will be developed to positively change the course of caries and periodontal disease.
Risk assessment begins with medical, dental, social, and family histories to uncover past and present systemic risks for oral environmental biofilms. Intraoral and radiographic evaluations help identify present and past conditions or diseases. Together, these data help uncover the environmental stressors that have created and will continue to create caries and periodontal disease.
Both history and examination data for decay and periodontal disease should be recorded within specifically constructed forms to allow for more efficient risk assessment and diagnosis. Such forms facilitate risk management and treatment plans to manage dysbiotic biofilms and their damaging results. They can be created for the particular needs of each practice by using the following information.
CaMBRA, Caries Management By Risk Assessment, is a widely used and well-understood tool for risk assessment and management of dental caries.17 Table 118-20 shows modified CaMBRA risk factors13 arranged from low to extreme. Periodontal disease risk factors are presented in Table 2.19-21
Determining risk levels for caries and periodontal disease is not formulaic but should be determined by the experience and knowledge of the dentist and/or hygienist, preferably in consultation with each other.22 The following can serve as a helpful guide in determining risk level, however:
• Low/moderate risk—patients with none of the high-risk factors
• High risk—one or more risks in this category
• Extreme risk—one or more risks in this category
Caries Risk Management
A summary of caries management techniques by risk level is presented in Table 3. The main products and strategies are explained in more detail below.
Encouraging Plaque Control
Historically, one of the major tools for risk management of caries has been plaque control. Many products and techniques for plaque control exist, but demonstration and personalization of technique is as important as the devices or products used. The techniques a patient feels most comfortable with should be continually encouraged or modified at all visits. Positive behavioral reinforcement from all clinical staff members is very important.
Products that assist with plaque control include electronic brushes, whether rotating or sonic; water irrigation devices; and interdental plaque control products such as floss and flossing aids and other interdental floss disruption devices deemed appropriate by professional staff.
Modifying Tooth Surface Chemistry
Calcium and phosphate ion interchange between tooth structure and saliva constantly occurs, but within highly acidic saliva, ionic movement is greater from tooth structure into saliva than in the opposite direction. Effective formulations of fluoride and calcium phosphate varnishes and toothpastes will remineralize tooth surfaces and, in doing so, also create a microsurface of more acid-resistant fluorapatite. Fluorapatite surfaces have lower surface energies, making bacterial attachment more difficult.23
The combination of fluoride/calcium phosphate toothpastes and varnishes is a highly effective strategy for changing both tooth surface and oral environment in managing caries risk.24 Products for enhancing tooth surfaces against acid dissolution include fluoride/calcium phosphate varnishes, fluoride/calcium phosphate toothpastes, and calcium phosphate pastes and rinses.
Xerostomia is very difficult to manage. There are more than 600 medications that result in various levels of xerostomia.13 Many medications causing dry mouth are not within the control of the dentist to change, as many are prescribed by other health care professionals. Communication with other health care professionals with suggestions to change medications or initiate health-producing strategies to eliminate medications is strongly recommended. Patients also self-prescribe OTC medications that cause dry mouth. Communication with patients about OTC medications is very important and will often cause them to change their strategies for managing problems for which they have self-medicated. In addition, xerostomia can also be a common side effect of many chronic conditions or disorders.
No current oral products can easily change or modify xerostomia as a caries risk. However, there are some products available that contain calcium, phosphate, and pH-buffering ingredients that may play a role in the reduction of caries risk. They would, however, be most likely beneficial adjunctively in extreme xerostomic/extreme caries risk cases only based on product chemical interaction potential, cost, and patient compliance issues.
Altering Acidogenic Biofilm Development
Developing a more neutral salivary pH may be achieved through dietary changes that reduce easily fermentable sticky foods and sugars. As stated before, this is a difficult change to make. It requires a structured plan for dietary counseling that is beyond the scope of this article. However, urging patients to modify their diet is exceptionally helpful.
Strategies for reducing acidic saliva include using a baking soda rinse multiple times daily, especially after any food consumption, and brushing with baking soda combined with fluoride/calcium phosphate toothpastes.
Sealants and Class V restorations are effective in caries management both for children and adults, especially in patients who have deep pits and fissures,25 but they should be done only after remineralization has been initiated through the use of fluoride varnishes and toothpastes.
Periodontal Disease Risk Management
Risk reduction of periodontal disease should include strategies to restore biofilms to commensalism or preferably mutualism. As with caries, many risk factors for periodontal disease are difficult to change or cannot be changed. A summary of strategies is presented in Table 4.
Diagnosis of Active Disease
The first step in treatment of periodontal disease is to diagnose the problem, possibly using bacterial testing. Subgingival biofilm sampling for testing of pathogens should be performed at initial examination if the diagnosis of active periodontal disease is made. However, if signs or symptoms of infection continue to be present, testing also may be done following home care instruction review, or during re-evaluation following scaling/root planing, surgical treatments, or other treatments or therapies.26 Performing microbial testing through an oral microbiology lab is especially helpful in the identification of specific periodontal disease–causing bacteria and their susceptibility and/or resistance to certain antibiotics to help determine antibiotic options for their control.27
Plaque control in periodontal disease uses essentially the same techniques as for caries, with the strongly advised addition of an oral irrigator to access pockets at any depth but especially at 4.0 mm or greater. Removing supragingival plaque does not mean subgingival plaque is disrupted or removed. Evidence suggests that subgingival irrigation is a very worthwhile tool for achieving control of subgingival biofilms.28
Nonsurgical Periodontal Therapy
Antimicrobial agents in the form of rinses, irrigations, or locally placed antibiotics should perhaps be avoided as they might actually result in dysbiosis of a biofilm or in antibiotic resistance. In addition, pathogenic bacteria may become integrated into periodontal or granulation tissue or attached to root surfaces in the form of persister cells (cells that become dormant until advantageous environmental conditions return for reproduction).29
Interestingly, in Europe and South Asia, the treatment of aggressive periodontitis has for many years involved combinations of systemic antibiotics, mainly metronidazole and amoxicillin. The combination of antibiotic therapy with intra-pocket debridement has been shown to be more successful than conventional periodontal surgery, scaling and root planing alone, local antibiotic therapy alone, or systemic antibiotic combinations alone.26 Better success with combined systemic antibiotics and intra-pocket debridement/scaling and root planing therapy may in part be the result of reducing the chance that pathogenic persister cells reach reproduction levels.
Because many biofilms are host mutualistic and necessary for healthy function, it is critical to respect and not destroy all microbes in the interest of treating any particular diseases. If antibiotics are prescribed for periodontal therapy, an added twice a day probiotic supplemental regimen, either OTC or prescribed, is very strongly suggested during the antibiotic therapy.30 Probiotics for treatment and prevention of periodontal disease and caries are currently being studied.31
Risk assessment/management in biofilm control in caries and periodontal disease is an excellent approach to manage and treat both diseases. Risk levels and management strategies developed during consultation by both dentist and hygienist is very strongly advised. Continual patient communication on risks and their management enhances treatment and therapy outcomes and may encourage a positive and continuing referral base.13 A great amount of research over many years has substantiated the effectiveness of conservative therapies and treatments in managing dysbiotic and pathogenic biofilms that cause caries and periodontal disease.
1. Grine FE, Gwinnett AJ, Oaks JH. Early hominid dental pathology: interproximal caries in 1.5 million-year-old Paranthropus robustus from Swartkrans. Arch Oral Biol. 1990;35(5):381-386.
2. Adler CJ, Dobney K, Weyrich LS, et al. Sequencing ancient calcified dental plaque shows changes in oral microbiota with dietary shifts of the Neolithic and Industrial revolutions. Nat Genet. 2013;45(4):450-455.
3. Miller WD. The Micro-Organisms of the Human Mouth: The Local and General Diseases which Are Caused by Them. Philadelphia, PA: The S.S. White Dental Mfg. Co. 1890.
4. Black GV. Susceptibility and immunity in dental caries. Dent Cosmos. 1899;41:826-830.
5. Riggs J. Suppurative inflammation of the gums and absorption of the gums and alveolar process. Penn J Dent Sci. 1876;3:99.
6. Hall-Stoodley L, Costerton JW, Stoodley P. Bacterial biofilms: from the natural environment to infectious diseases. Nat Rev Microbiol. 2004;2(2):95-108.
7. Yang X, Xie L, Li Y, Wei C. More than 9,000,000 unique genes in human gut bacterial community: estimating gene numbers inside a human body. PLoS One. 2009;29;4(6):e6074.
8. Donlan RM. Biofilms: microbial life on surfaces. Emerg Infect Dis. 2002;8(9):881-890.
9. Sbordone L, Bortolaia C. Oral microbial biofilms and plaque-related diseases: microbial communities and their role in the shift from oral health to disease. Clin Oral Investig. 2003;7(4):181-188.
10. Mahajan A, Singh B, Kashyap D, et al. Interspecies communication and periodontal disease. ScientificWorldJournal. 2013;765434. doi: 10.1155/2013/765434.
11. Marsh PD. Are dental diseases examples of ecological catastrophes? Microbiology. 2003;149(pt 2):279-294.
12. Aframian DJ, Davidowitz T, Benoliel R. The distribution of oral mucosal pH values in healthy saliva secretors. Oral Dis. 2006;12(4):420-423.
13. Roberts DR, Maragliano PM, Chapman RJ. Put the plan into action: how to implement a successful and efficient caries management program. Dimensions of Dental Hygiene. 2011;9(6):70-73.
14. Garant PR. The contributions of Etienne Bourdet (1722-1789) to the diagnosis and treatment of periodontal disease. Bull Hist Dent. 1993;41(2):69-72.
15. Zijnge V, van Leeuwen MB, Degener JE, et al. Oral biofilm architecture on natural teeth. PLoS One. 2010;5(2):e9321.
16. Hojo K, Nagaoka S, Ohshima T, Maeda N. Bacterial interactions in dental biofilm development. J Dent Res. 2009;88(11):982-990.
17. Cheng J, Chaffee BW, Cheng NF, et al. Understanding treatment effect mechanisms of the CAMBRA randomized trial in reducing caries increment. J Dent Res. 2015;94(1):44-51.
18. Lukacs JR, Largaespada LL. Explaining sex differences in dental caries prevalence: saliva, hormones, and “life-history” etiologies. Am J Hum Biol. 2006;18(4):540-555.
19. Genco RJ, Ho AW, Kopman J, et al. Models to evaluate the role of stress in periodontal disease. Ann Periodontol. 1998;3(1):288-302.
20. Smith PC, Cáceres M, Martínez C, et al. Gingival Wound Healing: An Essential Response Disturbed by Aging? J Dent Res. 2015;94(3):395-402.
21. Thomson WM, Poulton R, Broadbent JM, et al. Cannabis smoking and periodontal disease among young adults. JAMA. 2008;299(5):525-531.
22. Macey R, Glenny A, Walsh T, et al. The efficacy of screening for common dental diseases by hygiene-therapists: a diagnostic test accuracy study. J Dent Res. 2015;94(3 suppl):70S-8S.
23. Hay DI, Moreno EC. Differential adsorption and chemical affinities of proteins for apatitic surfaces. J Dent Res.1979;58(spec issue B):930-942.
24. Marinho VC. Cochrane reviews of randomized trials of fluoride therapies for preventing dental caries. Eur Arch Paediatr Dent. 2009;10(3):183-191.
25. Ahovuo-Saloranta A, Forss H, Walsh T, et al. Sealants for preventing dental decay in the permanent teeth. Cochrane Database Syst Rev. 2013;3:CD001830. doi: 10.1002/14651858.CD001830.pub4.
26. Keestra JA, Grosjean I, Coucke W, et al. Non-surgical periodontal therapy with systemic antibiotics in patients with untreated aggressive periodontitis: a systematic review and meta-analysis [published online ahead of print December 18 2014]. J Periodontal Res. doi: 10.1111/jre.12252.
27. Rams TE, Degener JE, van Winkelhoff AJ. Antibiotic resistance in human chronic periodontitis microbiota. J Periodontol. 2014;85(1):160-169.
28. Sharma NC, Lyle DM, Qaqish JG, Schuller R. Comparison of two power interdental cleaning devices on the reduction of gingivitis. J Clin Dent. 2012;23(1):22-26.
29. Landini P, Antoniani D, Burgess JG, Nijland R. Molecular mechanisms of compounds affecting bacterial biofilm formation and dispersal. Appl Microbiol Biotechnol. 2010;86(3):813-823.
30. Dang Y, Reinhardt JD, Zhou X, Zhang G. The effect of probiotics supplementation on Helicobacter pylori eradication rates and side effects during eradication therapy: a meta-analysis. PLoS One. 2014;9(11):e111030.
31. Yao SG, Fine JB. Probiotics for bacterial disease treatment in the oral environment. Compend Contin Educ Dent. 2014;35(9):658-663.