October 2011, Volume 32, Issue 3
Published by AEGIS Communications
New Approaches in Disease Management
Samuel B. Low, DDS, MS, MEd
Due to advances in research, there is now a greater understanding of the etiologies and pathogenesis of dental diseases starting at the molecular level and ending with the entire human body. Such advances have led to the development of new or modified clinical techniques. Innovative and efficacious equipment and products for both in-office and at-home use provide a broad array of actions that produce better health outcomes. To fully benefit from these advances, it is important that clinicians acquire a deeper knowledge and evidence base upon which to guide the management of their patients. While clinicians should continue to emphasize the fundamentals of dental disease prevention and the return to a healthy state, they must also be receptive to well-controlled and rigorous studies suggesting a modification of therapeutic concepts in controlling oral disease and enhancing oral health.
There is no doubt that the two primary dental diseases—caries and periodontal disease—are major chronic diseases of the human body, which affect major elements of all populations.1 Dental caries brings the distinction of being the most prevalent of all non-communicable and chronic diseases worldwide. In their respective ways, both caries and periodontal diseases lead to infection and inflammation, pain, difficulty in mastication, and loss of self-esteem and quality of life. In addition to the physical and emotional costs are the billions of dollars spent each year on efforts to prevent or correct these unfortunate outcomes. As for periodontal disease, its bidirectional relationship to systemic diseases such as cardiovascular disease and diabetes has been widely demonstrated and established, with the common pathways of chronic inflammation being their shared mode of development.2
Promotion and Maintenance of Healthy Oral Ecosystem
The oral cavity has always been considered to be a complex architectural monolith joining the gastrointestinal tract, the urinogenital tract, and the skin in harboring hundreds of different microbial species in both aerobic and anaerobic environments.3 Until the early 1960s, the prevailing hypothesis about plaque was that it was “nonspecific” (ie, all plaque is harmful to health). The currently held “specific plaque” hypothesis maintains that certain combinations of specific microbial species jointly form a harmful environment among otherwise healthy bacteria. The current theory that the oral complex is a biofilm entity, rather than a plaque environment, calls for a change in approaches to disease management. Just as a physician would never attempt to sterilize the gastrointestinal tract, dental professionals should likewise avoid efforts to render the oral cavern sterile.
Along with this new concept regarding dental plaque and biofilm formation, the clinician is now being introduced to related products designed to modify the microbial ecology of the oral environment. Such products include probiotics and therapeutic anti-plaque agents that, instead of directly destroying microorganisms, change the environment to benefit the inhabitation of nonpathogenic flora. These concepts of replacement systems call for a change in mindset from a purely antimicrobial to microbial-health equilibrium, heralding a new age in disease management and the promotion of wellness.4 The use of a therapeutic anti-plaque rinse, for example, may decrease the timeliness of recolonization and biofilm maturation—especially after mechanical removal by in-office debridement or even patient-mechanical means. Likewise, introducing a nonpathogenic microflora via a probiotic agent after disruption of a biofilm can reduce the periodontal inflammatory response or cariogenic activity.
Achieving a level of “oral hygiene”—both mechanical and chemical—that is adequate for managing a disease process can be daunting, as it must become part of the daily regimen for the patient. Countless studies have attempted to establish best practice in reducing caries and gingivitis. However, it is compliance that continues to undermine ability of clinicians to manage their patients’ self-care. As demonstrated by low compliance ratios for flossing, it is clear that many patients gravitate away from the mechanical aspects of their oral health regimen. While adjunctive chemical agents in the form of anti-plaque rinses and chewing gums, and even probiotic lozenges, are considered to be mechanical in the fundamental methodology in controlling the plaque biofilm, they are generally more acceptable to patients and provide a means to overcome the compliance dilemma.
Management vs. Treatment Approach
While these new concepts about dental disease focus on disease management, rather than treatment, third-party payment methods require that dental care be delivered on a procedure-by-procedure basis. Therefore, dental care is primarily delivered on a tooth-by-tooth basis, instead of considering the oral cavity as a functioning entity of the entire system. Considering that the etiology of primary oral diseases is the complex plaque biofilms, managing these biofilms by establishing a nonpathogenic environment seems to be rational.
As the oral cavity cannot be made sterile, recolonization is inevitable, and periodontitis is a chronic inflammatory disease that—like diabetes and cardiovascular disease—requires ongoing management. This management should be accomplished by modifying the pathogenic microflora and then reestablishing a non-pathogenic ecosystem.
Level of Disease Management and Risk
Oral and body systems are not created equal. The pivotal factor in determining the level of disease management necessary for a given patient is the risk of that patient. Developing the appropriate balances between mechanical and chemical biofilm management systems for patients should be determined by their susceptibility and individual response to the microbial ecosystem. To determine an oral health management plan for a patient, the clinician must first categorize the risk, and then choose from among different modalities. Patients with low compliance to mechanical oral hygiene methods might be considered candidates for chemical rather than mechanical methods, but those with a high susceptibility to their respective dental disease should be strongly advised to combine both mechanical and chemical biofilm control, which can work together synergistically and adjunctively.
Relationship of Inflammation to Disease
Gingivitis may have previously been considered a “reversible” periodontal disease with thorough plaque removal leading to clinical resolution; evidence now demonstrates that the chronic inflammatory response to the plaque biofilm may establish “memory” in the gingival connective tissue. The hypothesis suggests that when the gingival crevicular site is exposed to a disease-inducing biofilm again, the memory enhances the inflammatory cascade, resulting in attachment loss and destructive periodontitis. This mechanism of action parallels those found in other chronic inflammatory diseases for which mediating factors include neutrophils and monocytes, increased oxidative burst, impaired phagocytosis and chemotaxis, increase of prostaglandins, tissue-necrosing factor, collagenase, and elastase.
Systems that reduce the pathogenic microflora within biofilm, but moreover have a direct anti-inflammatory effect—as with some oral probiotics—are likely to be advantageous in reducing the resulting destruction of gingival connective tissue.
War or Peace?
For many years, clinicians have been at war, seeking the outright destruction and removal of all plaque from the dentogingival borders and the death of plaque bacteria that persist after mechanical oral hygiene and adjunctive use of antimicrobial rinse agents. However, this objective has seldom been achieved due to either continuous microbial recolonization from sites elsewhere in the oral ecosystem or faultless mechanical oral hygiene regimens, or both. In view of the advances in clinical research that have led to a broader understanding of plaque biofilm and its complex role in the determination of health or inflammatory diseases, clinicians can take a more peaceful approach to living with the inevitable dental plaque. They can do this by tipping the balance in favor of a biofilm that does not mature into a pathogenic plaque due to its frequent mechanical disruption and the presence of probiotic organisms. Probiotic agents containing species such as Lactobacillus reuteri have the capability to establish and maintain healthy oral flora and biofilm ecosystems.4 Anti-plaque agents with anti-adhesive rather than microbiocidal mechanisms of action can provide a layer of protection on the tooth surface by inhibiting the original adhesion of the early colonizing microbes—the first and essential stage of biofilm development—and helping to disrupt the sticky matrix that holds the biofilm to the dental surfaces, thus enabling easier mechanical removal from the disease-prone areas of the dentogingival complex.5
These approaches to treatment and management of periodontal disease require additional clinical research; the results and clinical applications will be interesting to observe. Use of these new approaches in promoting a healthy oral ecosystem in patients’ treatment plans for improved oral health could provide many benefits to patients in their daily struggle to comply with necessary oral hygiene regimens.
1. FDI World Dental Federation. The Oral Health Atlas: Mapping a Neglected Global Health Issue. Brighton, UK: Myriad Editions; 2009.
2. Genco R, Williams R. Periodontal Disease and Overall Health: A Clinician’s Guide. Yardley, PA: Professional Audience Communications, Inc.; 2010.
3. Marsh PD. Are dental diseases examples of ecological catastrophes? Microbiology. 2003;149(2):279-294.
4. Thomas J. Prebiotics, probiotics and oral microbial wellness. Compend Contin Educ Dent. 2011;32(suppl 3):13-17.
5. Elworthy AJ, Edgar R, Moran J, et al. A 6-month home-usage trial of 0.1% and 0.2% delmopinol mouthwashes (II). Effects on the plaque microflora. J Clin Periodontol. 1995;22(7):527-532.
About the Author
Samuel B. Low, DDS, MS, MEd
College of Dentistry, University of Florida