The use of antimicrobial

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1 Antimicrobial mouthrinses and the management of periodontal diseases Introduction to the supplement Ira B. Lamster, DDS, MMSc The use of antimicrobial mouthrinses is an approach to limiting the accumulation of dental plaque, with a primary objective of controlling the development and progression of periodontal diseases. Antimicrobial mouthrinses allow patients to deliver active agents in a cost-effective manner, while controlling dosage and timing. Mouthrinses treat all accessible surfaces of the oral cavity and may reduce the number of bacteria in accumulations on mucosal surfaces. Depending on the chemistry of the rinse preparation, active agents can have sustained therapeutic benefits on the hard- and soft-tissue surfaces of the oral cavity, thereby extending their therapeutic benefits. This supplement to The Journal of the American Dental Association explores issues of importance to dental practitioners regarding the use of antimicrobial mouthrinses as part of a daily oral care regimen to control the accumulation of dental plaque. Numerous studies are cited that demonstrate the efficacy of antimicrobial mouthrinses in reducing plaque and gingivitis. Patients may ask their dental professionals about the use of antimicrobial mouthrinses, and this ABSTRACT Background. Periodontal diseases are complex disorders that have been associated with multiple risk factors. These disorders are triggered by the accumulation of dental plaque, and the clinical signs are caused by the resultant inflammatory and immune responses. Tissue destruction that defines periodontitis has been linked to excessive production of proinflammatory molecules including matrix metalloproteinases, interleukin-1 beta and prostaglandin E 2. Important risk factors for periodontitis can be grouped into four categories: microbial, systemic, behavioral and local. These risk factors can be considered modifiable or unmodifiable. Controlling risk factors is important in the management of chronic diseases and is a valid strategy for controlling periodontal diseases. Limiting the accumulation of dental plaque is an important part of controlling the development and progression of periodontal diseases. By adhering to a daily oral hygiene regimen that includes brushing, flossing and rinsing, patients play an essential role in disease management. Conclusion. Patients play an important role in controlling the oral microbial biofilm that is essential to the initiation, development and progression of periodontal diseases. A daily oral hygiene regimen that includes the use of an antimicrobial mouthrinse can modify patients microbial risk of developing periodontal disease. Clinical Implications. Patients can help reduce their risk of developing periodontal disease by controlling the accumulation of plaque. This can be accomplished, in part, by adhering to a daily oral hygiene regimen that includes brushing, flossing and using an antimicrobial mouthrinse. Key Words. Periodontal disease; pathogenesis; risk factors; microbial plaque. JADA 2006;137(11 supplement):5s-9s. Dr. Lamster is the dean, Columbia University College of Dental Medicine, 630 W. 168 St., New York, N.Y , ibl1@columbia.edu. Address reprint requests to Dr. Lamster. JADA, Vol November S

2 supplement is intended to provide the latest available information on the use of antimicrobial rinses in the daily oral care regimen. Thomas and Nakaishi 1 provide an overview of our understanding of periodontal microbiology and the concept of dental plaque as a biofilm. Barnett 2 reviews the rationale for, and benefits of, incorporating effective antimicrobial mouthrinses into a daily oral hygiene regimen. Silverman and Wilder 3 review safety issues associated with these products and outline factors that may influence patient compliance with or adherence to daily oral care. Douglass 4 examines how the inclusion of risk assessment and disease management in daily practice gives dentists the opportunity to affect patient outcomes favorably both in the general population and within groups at increased risk of developing periodontal diseases. As dental practitioners, it is our responsibility to disseminate this information and influence our patients adherence to a daily oral care regimen that includes brushing, flossing and rinsing. ETIOLOGY OF PERIODONTAL DISEASE A great deal of information concerning the etiology of periodontal diseases has been obtained in the past 15 years. 5 Periodontal disease is initiated by the accumulation of microbial plaque above the gingival margin, which extends into the subgingival environment (Figure). Dental plaque is a biofilm that induces an inflammatory response in the tissues, leading to increased leakage of fluid from the small vessels (capillaries) and movement of acute inflammatory cells (neutrophils) from the vasculature into the tissues and ultimately into the gingival sulcus. In this early stage, the sulcular epithelium begins to invaginate, and there is evidence of cellular and morphological changes in the connective tissue. Some of the collagen in the connective tissue is lost, and immune cells (lymphocytes) and neutrophils start to accumulate in the area below the sulcular epithelium. At this stage, the lesion still is defined as gingivitis and has classical signs of inflammation, including redness, swelling and pain when the tissue is probed. Since there are no changes in the position of the junctional epithelium or in the underlying bone, periodontitis is not present. The mechanisms that are responsible for the This supplement is intended to provide the latest available information on the use of antimicrobial rinses in the daily oral care regimen. shift from gingivitis to periodontitis have not been defined fully. What is clear, however, is that bacteria are needed to drive tissue destruction. The shift to a periodontitis lesion is characterized by a dramatic increase in the number of neutrophils and chronic inflammatory cells (macrophages). These cells are recruited into the tissues from the vasculature as a result of both bacteria and host-derived signals (chemotactic factors) that activate cell movement and increase the expression of adhesion molecules on the surface of cells that line the vasculature (endothelial cells). The T and B lymphocytes also are involved, which leads to increased antibody production and release of molecules that activate neutrophils and macrophages. Antibody production, which can be detected both locally and systemically, is a prominent part of the host response in periodontitis, 6 while increased production of proinflammatory molecules (cytokines) can be detected locally in the gingival crevicular fluid. 7 The transition from gingival inflammation to destructive periodontal disease appears to be triggered by dysregulation of the host response, which leads to an exaggerated inflammatory response. Macrophages and other constituent cells of the periodontium (for example, fibroblasts) release enzymes that degrade connective tissue (matrix metalloproteinases). Bone destruction in periodontal disease is mediated primarily by the cytokine interleukin-1 beta and the arachidonic acid metabolite prostaglandin E 2, both of which are released from macrophages and other cells. It is important to emphasize that the activation of neutrophils, macrophages and constituent cells is due to the effects of the complex microflora that comprise the subgingival biofilm. In addition to inducing an immune response and the recruitment of inflammatory cells into the tissues, microbial constituents such as lipopolysaccaride (from gram-negative microorganisms) and teichoic acid and lipoteichoic acid (both from grampositive microorganisms) can stimulate tissue breakdown that results in the loss of soft and hard tissues supporting the dentition. RISK FACTORS Individual patients differ greatly in their susceptibility to periodontal disease. A robust body of 6S JADA, Vol November 2006

3 Figure. The critical pathway for periodontitis. The pathological process is initiated with the accumulation of dental plaque and maturation of the biofilm. This biofilm induces a complex host response characterized by activation of both the immune and inflammatory responses. Persistence of the inflammatory response, with excess production of proinflammatory cytokines, arachodonic acid metabolites and degradative enzymes (matrix metalloproteinases [MMP]), leads to destruction of the soft and hard tissues supporting the dentition. Active phases of periodontitis are intermittent. Eventually the lesion becomes quiescent and may become active again at some later point. LPS: Lipopolysaccharide. PMN: Polymorphonuclear leukocyte. Adapted from Kornman 5 with permission of Quintessence Publishing. literature has examined factors that place a patient at risk of developing periodontal disease. 8 By all measures, periodontitis can be considered a complex disease with a range of risk factors. 9,10 While some overlap is recognized, risk factors for periodontitis can be categorized as microbial, systemic, behavioral or local (Box). Furthermore, these risk factors can be considered modifiable or unmodifiable. Microbial risk factors. Specific periodontal pathogens, including Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia, have been identified consistently with advanced periodontitis. 11 The importance of Actinobacillus actinomycetemcomitans in aggressive periodontitis also has been documented. 12 These bacteria reside in the subgingival and supragingival plaque, and dental plaque meets the criteria of a biofilm, and, thus, are difficult to eliminate. The total microbial mass, or challenge, as well as specific microbial species contributing to the endotoxin challenge, also are important variables. Microbial risk factors are modifiable and are the target of most of the antimicrobial mouthrinses discussed in this supplement. Systemic risk factors. A number of specific systemic conditions and the intrinsic nature of the patient contribute to the patient s overall risk of developing periodontitis. 13 The most important of the systemic conditions is diabetes mellitus, though other diseases such as leukocyte adhesion deficiency, cyclic neutropenia and HIV infection also can increase the risk of developing periodontitis. A person s genetic makeup greatly influences his or her risk of developing periodontitis. 14 In terms of genetics, the major focus has been on specific polymorphisms for the genes that control the production of inflammatory mediators. 15 These polymorphisms appear to account for differences in the production of proinflammatory cytokines that will translate into the intensity of the inflam- JADA, Vol November S

4 BOX Risk factors for periodontitis. MICROBIAL RISK FACTORS dspecific periodontal pathogens* dpathogenic potential of the biofilm dtotal microbial burden SYSTEMIC RISK FACTORS ddiabetes mellitus* dgenetic risk factors (genes controlling proinflammatory cytokines) dsex (male), race/ethnicity (African-American) dosteoporosis dhiv infection dpsychological factors BEHAVIORAL RISK FACTORS dtobacco use and cigarette smoking* dpatient compliance (oral hygiene practice and regular dental visits) LOCAL RISK FACTORS dfaulty dental restorations duntreated dental disease ddental anatomy and malocclusion and furcations * Primary risk factor (strong relationship, supported by association, prospective cohort and intervention studies). Secondary risk factor (moderate relationship, supported by association studies). Tertiary risk factor (limited supporting data). matory response. In addition, sex (male) and race/ethnicity (African-American) can be considered systemic risk factors for periodontitis. 16,17 Systemic risk factors can be modifiable (for example, improved metabolic control of diabetes mellitus) or unmodifiable (for example, genetic determinants of proinflammatory cytokine production, sex and race/ethnicity). Behavioral risk factors. The most important behavioral risk factors, which also have been considered environmental risk factors, are tobacco use and cigarette smoking. Cigarette smoking may account for one-half of the cases of advanced periodontitis in the United States. 18 Another important behavioral risk factor is patient compliance, which includes many patient-centered behaviors such as attention to recommended oral hygiene practices and regular visits for dental care. Behavioral risk factors are modifiable. Local risk factors. Local risk factors include malocclusion and faulty dental restorations or fractured teeth, and are not recognized to be as important as the other types of risk factors. These factors likely act by promoting plaque accumulation. Local risk factors are modifiable. MANAGEMENT OF PERIODONTAL DISEASE Periodontal disease management presents a challenge for clinicians and patients. Periodontitis can be prevented, but once it is present it can be controlled but not eliminated. A relatively new paradigm for managing periodontal disease focuses on modifying risk factors. The World Health Organization has proposed an approach to the management of noncommunicable chronic diseases based on control of important risk factors. Certain risk factors can affect many chronic disorders, and this effort has focused on diabetes mellitus, the use of tobacco products, the use of alcohol and promotion of a healthy diet. 19,20 The concept of controlling risk factors is relevant for periodontal disease. The most important behavioral and environmental risk factor for periodontitis is tobacco use and cigarette smoking, and the most important systemic risk factor is diabetes mellitus. In that same context, controlling the oral microbial biofilm is an approach to periodontal disease management that is focused on the modification of an important risk factor. Dental professionals should be involved in helping their patients who have diabetes mellitus improve their metabolic control and in helping their patients efforts to stop using tobacco products. 21,22 In addition, dental professionals have a primary responsibility to help their patients control the oral microbial biofilm that is critical to the initiation, development and progression of periodontal disease. CONCLUSIONS Understanding the pathogenesis and risk factors associated with periodontal disease is essential in properly managing the treatment of these common disorders. Patients must play an active role in controlling the development and progression of gingivitis and periodontitis by controlling the accumulation of dental plaque. 1. Thomas JG, Nakaishi LA. Managing the complexity of a dynamic biofilm. JADA 2006;137(11 supplement):10s-15s. 2. Barnett ML. Rationale for the daily use of an antimicrobial mouthrinse. JADA 2006;137(11 supplement):16s-21s. 3. Silverman S Jr, Wilder R. Safety and compliance factors for comprehensive daily oral care that includes an antiseptic mouthrinse (or Antiseptic mouthrinse as part of a comprehensive oral care regimen). JADA 2006;137(11 supplement):22s-26s. 4. Douglass CW. The practice of risk assessment and disease management. JADA 2006;137(11 supplement):27s-32s. 5. Kornman KS. The pathogenesis of periodontitis. In: Wilson TG, Kornman KS. Fundamentals of periodontics. 2nd ed. Chicago: Quintessence; 2003: Schenkein HA. Host responses in maintaining periodontal health and determining periodontal disease. Periodontol ;40: Armitage GC. Analysis of gingival crevice fluid and risk of progression of periodontitis. Periodontol :34; Borrell LN, Papapanou PN. Analytical epidemiology of periodontitis. J Clin Periodontol 2005;32(supplement 6): Glazier AM, Nadeau JH, Aitman TJ. Finding genes that underlie complex traits. Science 2002;298(5602): S JADA, Vol November 2006

5 10. Rees J. Complex disease and the new clinical sciences. Science 2002;296(5568): Holt SC, Ebersole JL. Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia: the red complex, a prototype polybacterial pathogenic consortium in periodontics. Periodontol ;38: Haffajee AD, Socransky SS. Microbial etiological agents of destructive periodontal diseases. Periodontol ;5: Ronderos M, Ryder MI. Risk assessment in clinical practice. Periodontol ;34: Michalowicz BS, Diehl SR, Gunsolley JC, et al. Evidence of a substantial genetic basis for risk of adult periodontitis. J Periodontol 2000;71(11): Brett PM, Zygogianni P, Griffiths GS, et al. Functional gene polymorphisms in aggressive and chronic periodontitis. J Dent Res 2005;84(12): Albandar JM, Brunelle JA, Kingman A. Destructive periodontal disease in adults 30 years of age and older in the United States, (published correction appears in J Periodontol 1999;70[3]:351). J Periodontol 1999;70(1): Borrell LN, Burt BA, Gillespie BW, Lynch J, Neighbors H. Periodontitis in the United States: beyond black and white (published correction appears in J Public Health Dent 2002;62[3]:139). J Public Health Dent 2002;62(2): Tomer JL, Asma S. Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health and Nutrition Examination Survey. J Periodontol 2000;71(5): World Health Organization. The World Health report 2002: Reducing risks, promoting healthy life. Geneva: World Health Organization; Petersen PE, Ogawa H. Strengthening the prevention of periodontal disease: the WHO approach. J Periodontol 2005;76(12): Kunzel C, Lalla E, Albert DA, Yin H, Lamster IB. On the primary care frontlines: the role of the general practitioner in smoking cessation activities and diabetes management. JADA 2005;136(8): Kunzel C, Lalla E, Lamster IB. Management of the patient who smokes and the diabetic patient in the dental office. J Periodontol 2006;77(3): JADA, Vol November S