Safety and efficacy of antimicrobial mouthrinses in clinical practice

Safety and efficacy of antimicrobial mouthrinses in clinical practice

Louis G. DePaola


Efficacy Overview. The use of an antimicrobial mouthrinse is an important adjunct to toothbrushing and interdental cleaning. To varying degrees, chlorhexidine gluconate (CHG), cetylpyridinium chloride (CPC), and essential oils (EO) interrupt the integrity of the bacterial cell membrane, leading to lysis and death. CHG binds to salivary mucins, tooth structure, dental plaque, and oral soft tissues and is released slowly into the mouth, where it inhibits adsorption of bacteria onto teeth. CHG is active against a wide range of gram-positive and gram-negative microorganisms. CPC binds to teeth and plaque to a lesser degree than CHG and is generally less efficacious than CHG. CHG and EO penetrate plaque biofilm and produce changes in microbial cell surface morphology that alter coaggregation, recolonization, and, thus, survival. CHG, CPC, and EO are active against a wide variety of aerobic and anaerobic bacteria. An overview of the Food and Drug Administration and American Dental Association rigorous approval processes for efficacy and safety is provided.

Safety Overview. Long-term use of CHG or EO does not adversely affect the ecology of oral microbial flora, including microbial overgrowth, opportunistic infection, or development of microbial resistance. Long-term use of CHG, CPC, or EO does not contribute to soft tissue lesions or mucosal aberrations and has no serious adverse effect on salivary flow, taste, tooth deposits, or dental restoration. There is no evidence of a causal link between alcohol-containing mouthrinses and the risk of oral and pharyngeal cancer.

Key words: Antimicrobial mouthrinse, efficacy, gingivitis, mechanism of action, safety


Mechanical plaque removal through toothbrushing and flossing has been the universally accepted “gold standard” for maintaining oral health since the early 1960s. However, numerous studies have shown that most patients do not effectively clean interdentally to remove dental plaque daily. (1-3) By the early 1980s, chemotherapeutic agents were marketed as adjuncts to brushing and flossing; however, no definitive guidelines for the evaluation of their safety and efficacy were available. Both the American Dental Association (ADA) and the Food and Drug Administration (FDA) have established standards for assessing the safety and efficacy of over-the-counter (OTC) and prescription mouthrinses.

ADA Safety and Efficacy Guidelines for Mouthrinses

Since 1931, the ADA, through its voluntary Seal of Acceptance Program, has promoted the use of oral and dental products that are both safe and effective. Published guidelines developed by the ADA list the acceptance criteria for each type of agent, product, or device. In order to obtain the Seal of Acceptance, a company must provide evidence establishing that a submitted agent, product, or device meets or exceeds the guidelines for that particular usage and is safe and effective. Additionally, the product must have been approved for marketing in the United States by the FDA. In 1985, the ADA recognized the potential benefits of some chemotherapeutic formulations, giving impetus to the development of guide lines for the evaluation of antiplaque and antigingivitis chemotherapeutic agents for inclusion in the Seal Program, which are still in use today. (4) In order to be awarded the Seal, an antiplaque and antigingivitis chemotherapeutic must (5)

* Be tested in populations of typical product users in a randomized, parallel-group, or crossover clinical trial in which the test product is compared with a negative control and, if appropriate, an active control

* Be supported by data from at least two 6-month studies conducted at independent sites, with assessment of gingivitis and qualitative and quantitative assessment of plaque performed at baseline, an intermediate point (usually 3 months), and 6 months

* Document a statistically significant reduction of supragingival plaque and gingivitis as compared with a negative control in each of the 2 studies and demonstrate a statistically significant reduction of gingivitis for the mouthrinse group of at least 15% for any one study and an average reduction of 20% in the 2 studies compared with the control group

* Establish product safety with respect to soft tissues, teeth, toxicology, and effects on the oral flora (eg, adverse shifts in microbial populations, the development of microbial resistance, and the emergence of opportunistic organisms)

Data from the studies are then presented to and reviewed by the ADA Council on Scientific Affairs. If the product meets the established standards, it is awarded the ADA Seal of Acceptance. (4,5)

For the professional and consumer, the ADA Seal for antimicrobial mouthrinses indicates that

* Product data have successfully undergone an intensive, nonbiased safety and efficacy review

* Evidence supports the manufacturer’s claim for effectiveness against supragingival dental plaque and gingivitis

* The product is safe when used as directed

FDA Regulation

The FDA regulates prescription drugs as well as any OTC products that make therapeutic claims, such as the reduction of gingivitis. The FDA has accepted key elements for gingivitis assessment used by the ADA Seal Program as appropriate for its review. However, in contrast to the ADA, which evaluates products, the FDA evaluates active ingredients while recognizing that the way in which an ingredient is formulated may affect its clinical activity. In 2003, the recommendations of the FDA’s Dental Plaque Subcommittee of the Non-prescription Drugs Advisory Committee were published, and they included the conditions under which OTC products for the reduction or prevention of dental plaque and gingivitis would be recognized as safe, effective, and not misbranded. (6,7) In addition to data supporting effectiveness, the following criteria are examined by the FDA (6):

* Incidence and risk of adverse reactions and significant side effects when used according to adequate directions

* Margin of safety with normal use

* Potential for harm from abuse or misuse

* Potential for inducing adverse side effects (such as irritation, ulceration, inflammation, erosion, damage to teeth/restorations)

* Benefit-risk ratio

After assessing an OTC ingredient, the FDA assigns the ingredient to a category of I, II, or III (6,7).

* Category I: The ingredient is both safe and effective and is not misbranded.

* Category II: The ingredient is not generally recognized as safe and effective or is misbranded.

* Category III: There are insufficient data to evaluate safety and/or effectiveness.

The FDA may also approve products, both prescription and OTC, through the New Drug Application (NDA) process. The NDA process is a more lengthy one that also requires documentation of both the safety and efficacy of the product.

Mouthrinses That Meet ADA and/or FDA Guidelines

Two antiseptic mouthrinses (and their generic equivalents) have been awarded the ADA Seal for chemotherapeutic control of supragingival plaque and gingivitis: 0.12% chlorhexidine gluconate (CHG) mouthrinse (Peridex[R]) and essential oils (EO) mouthrinse (Listerine[R]). Because of a recent change in the ADA Seal Program, Peridex[R] and its generic equivalents as prescription products no longer carry the ADA Seal. However, no CPC formulation has yet to obtain the ADA Seal. (See also page 32 for more information on the ADA Seal Program.)

The FDA’s Dental Plaque Subcommittee of the Nonprescription Drugs Advisory Committee has classified 20TC mouthrinse ingredients as both safe and effective and not misbranded (Category I): cetylpyridinium chloride (CPC; examples of products include Colgate Viadent[R] and Crest[R]Pro-Health[TM] Rinse) and EO. (6,7) CHG was reviewed and found to be safe and effective by the FDA by means of an NDA and is available in the United States only by prescription.

Although many commercial mouthrinse manufacturers claim antiplaque and antigingivitis properties, most lack the efficacy data required to earn the ADA Seal. Stannous fluoride has received Category I recommendation by the FDA’s advisory committee, and triclosan has received NDA approval by the FDA. However, these agents are not found in mouthrinse formulations in the United States. This article discusses the safety and efficacy data of mouthrinses that have been approved by the FDA, recommended as Category I by the advisory committee, or awarded the ADA Seal.

Antimicrobial Mouthrinse Safety

Two essential criteria for any product are safety and efficacy (see also pages 19 to 22, Efficacy of Mouthrinses). The most effective product would be use less if it were not safe; conversely, the safest product would be inconsequential if it did not work. Issues related to safety in mouthrinses include the following:

* Are there any adverse effects on the oral microbial flora?

* Are there any oral soft tissue aberrations?

* Does routine use adversely affect dental restorative materials?

* Are there any contraindications for the use of these products?

Each of these concerns merits careful consideration.

Do Mouthrinses Have Adverse Effects on Oral Microbiota?

Some dental professionals may fear that antiseptic mouthrinses pose a risk in killing or inhibiting normal flora with subsequent repopulation with opportunistic and/or more pathogenic or resistant organisms. The microbial shift would manifest as an overgrowth of opportunistic organisms, such as Candida. Fortunately, studies document no adverse effects on supragingival dental plaque microflora after 6 months of continued use with either CHG or EO. (8-12) Table I describes the findings of several studies of the impact of EO and CHG on normal oral flora. Evidence confirms that daily, long-term use (6 months or longer) of CHG or EO does not adversely affect oral microbial flora, including no microbial overgrowth, opportunistic infection, or development of microbial resistance.

Do Mouthrinses Cause Oral Mucosal or Other Soft Tissue Aberrations?

Concerns about potential adverse effects on oral mucosa and other soft tissue include the following:

* Does alcohol cause adverse effects such as an increased risk of oral and pharyngeal cancer (OPC)?

* Are the active ingredients found in CHG, CPC, and EO safe for long-term use on the oral mucosa?

* Do mouthrinses affect salivary flow?

* Are there adverse effects on taste or tooth deposits?

Several studies have addressed these issues and are discussed below.

Does alcohol cause adverse effects such as an increased risk of OPC? Many mouthrinses contain pharmaceutical-grade alcohol to solubilize active ingredients, make them biologically active, or dissolve flavoring agents. Typical alcohol levels in mouthrinses include the following:

* CHG: generally 12.6% alcohol

* CPC: 6% to 18% alcohol (traditional) and alcohol free, with high-bioavailability CPC, 0.07% (17)

* EO: 26.9% alcohol (original “gold” product) and 21.6% alcohol (flavored products)

Oral care professionals may be reluctant to recommend an alcohol-containing mouthrinse (ACM) because of perceived risk for developing OPC. It is well known that tobacco usage and excessive alcoholic beverage consumption cause a substantial portion of the OPC. (18-20) Since most mouthrinses contain alcohol, do ACMs increase cancer risk as well? A number of studies have examined a cause-effect relationship between ACMs and OPC with varying results. (19,21-27) A critical review of investigations that suggested a cause-effect relationship revealed a number of deficiencies and study design flaws that necessitate rethinking the ACM-cancer link (28,29):

* Lack of a dose-response based on frequency and/or duration of mouthwash use

* Inconsistent findings among studies

* Lack of a scientific or biological basis to explain inconsistent findings between males and females

* Absence of correction for alcoholic beverage ingestion and tobacco use

* Inclusion of pharyngeal cancer, an improper classification as mouthrinses only contact the oral cavity

* Inclusion of other head and neck carcinomas, lymphomas, and sarcomas as oral cancer, an improper classification as mouthrinses only contact the oral cavity

A widely referenced study by the National Cancer Institute erroneously concluded that OPC risks were elevated 60% among female and 40% among male users of mouthwash (with >25% alcohol). (27) This epidemiologic retrospective investigation consisted of interviews with 866 patients with OPC, diagnosed January 1984 through March 1985, and 1249 controls from the general population without OPC sampled from 4 areas of the United States. Reanalysis of this report by independent reviewers concluded that many patients in the OPC group (6.6% of men and 12.6% of women) had tumors of nonmucosal histology that could not have been contacted by an ACM. Reanalysis of the data showed no relationship between ACMs and OPC. (6,30,31) Additional investigators continue to report that there is no evidence that ACM use increases OPC risk. (28,32,33)

Data comparisons of topical alcohol exposure of the oral mucosa from ACMs and alcoholic beverage consumption may be invalid. Two or even 3 topical administrations of a 25% ACM, each lasting 30 seconds, seem unlikely to produce the same effect as long-term, habitual alcoholic beverage consumption. Pharmaceutical alcohol is not a carcinogen. (6,28) However, chemicals and additives found in alcoholic beverages can cause cancer; for example, urethane, a known carcinogen, is commonly found in alcoholic beverages. (6,19,28) Commercial mouthrinses contain pharmaceuticalgrade denatured alcohol (pure ethanol), which is free from contaminating carcinogens.

Taking the following precautions should limit any potential problems with ACMs:

* Advise patients to consult with their abuse sponsor (counselor) before using an ACM.

* EO is indicated for use in individuals over the age of 12 years. The effectiveness and safety of CHG have not been established in individuals under 18 years. (35,36)

* Use of an ACM in persons taking disulfiram (Antabuse[R]) and metronidazole (Flagyl[R]) is contraindicated, because in combination they may induce nausea, vomiting, and other unpleasant side effects. (37,38)

Do the active ingredients of CHG, CPC, and EO adversely affect the oral mucosa? Evidence supports that long-term use of CHG, CPC, or EO does not contribute to soft tissue lesions or mucosal aberrations. Long-term clinical trials (at least 6 months’ duration) produced substantial evidence documenting the safety of the active ingredients of CHG, CPC, and EO mouthrinses on the oral mucosa and periodontium. (39-52) Complete oral soft tissue examinations were performed at each data collection period (baseline, 3 months, and 6 months) in these studies. Findings revealed no differences in the incidence or severity of adverse events between the CHG, CPC, or EO groups and control/placebo groups. With EO, users report an initial tingling/burning sensation that lessens rapidly with time and is considerably reduced by the addition of flavoring such as citrus. (29,42) A burning sensation and occasional mild desquamation have also been reported with CPC use. (53)

Do mouthrinses affect salivary flow? Xerostomia is a common side effect of many systemic diseases, radiation/chemotherapy, and numerous OTC and prescription medications. A misconception is that the use of an ACM desiccates the oral mucosa, leading to xerostomia. However, studies have shown that rinsing with an EO mouthrinse does not induce mucosal drying or aberration. (54,55) Table II summarizes these study findings.

Are there adverse effects on taste and tooth deposits? Some patients may experience a bitter taste with EO use. (56) Taste alteration, as well as increased supragingival calculus formation and brown staining of the teeth and tongue, is associated with use of CHG and CPC. (42,46,56-60) CHG stains teeth, esthetic restorations, and implant abutments, and this staining can be problematic in a society that desires cosmetic dentistry and whiter and brighter teeth. (36,56)

Does Routine Use of Mouthrinses Adversely Affect Dental Restorative Materials?

A number of studies have addressed the concern raised about the effect of antimicrobial mouthrinses on dental materials. Other than the potential for staining with CHG and CPC, there are no documented adverse effects on dental materials. Table III summarizes the findings of these studies.

Efficacy of Mouthrinses

How Antimicrobial Mouthrinses Work

Antiseptics are chemical agents used to eliminate oral microorganisms in a variety of ways:

* By producing cell death

* By inhibiting microbial reproduction

* By inhibiting cellular metabolism

Most antiseptic agents are bactericidal, although some are bacteriostatic. The effectiveness of these agents varies widely and is dependent upon product formulation, concentration of the active agent, dose, substantivity, compliance, and interactions with other chemicals present in the oral cavity at the time of use. Different antimicrobial mouthrinses have demonstrated efficacy against bacteria, fungi, viruses, and spores. Some products produce a wide spectrum of activity, while others are effective against selected microorganisms only. (56) Notably, most studies, including longitudinal trials, testing the efficacy of CHG used the commercial product Peridex[R], and Listerine[R] was the EO commercial product used for all studies cited in this paper. CPC commercial preparations used in research studies vary by product concentration and brand.

Mechanism of action of CHG. CHG (0.12%) is a bactericidal bisbiguanide antiseptic, with demonstrated efficacy against the following organisms:

* A wide range of gram-positive and gram-negative organisms (64)

* Aerobes and anaerobes, many of which are associated with plaque and gingivitis, including Fuso-bacterium and Prevotella intermedia (65)

* Herpes simplex virus 1 and 2, human immunodeficiency virus 1, cytomegalovirus, influenza A, parainfluenza, and hepatitis B. (12,66,67) CHG is not approved for the prevention and treatment of viral infections

* Seven species of Candida and other yeasts (13,68,69) (often used alone or in combination with other anti-fungal medications to reduce opportunistic infections in at-risk populations, such as those undergoing treatment for leukemia or bone marrow transplantation (70,71))

Exposure to CHG causes rupturing of the bacterial cell membrane, which allows for leakage of the cytoplasmic contents, resulting in cell death. (72,73) CHG binds to salivary mucins, reducing pellicle formation and inhibiting colonization of plaque bacteria. (64,74) It also binds to bacteria, which inhibits their adsorption onto the teeth. (64) CHG has been shown to penetrate the dental plaque biofilm, which enables CHG to access and kill pathogens embedded within the biofilm. (72)

CHG binds tightly to tooth structure, dental plaque, and oral soft tissues. It is released slowly into the mouth, which allows antimicrobial effects to be sustained for up to 12 hours, thus its high degree of substantivity. (64,75) A 30-minute interval is optimal between toothbrushing and rinsing with CHG to avoid an interaction between the positively charged detergents found in dentifrices (eg, sodium lauryl sulfate) and the cationic CHG rinse. This interaction, and possible inactivation of CHG, can also occur with the anionic fluoride ion found in stannous fluoride and in some toothpastes and mouthrinses. (73,76)

Mechanism of action of CPC. CPC, a quaternary ammonium compound, demonstrates bactericidal activity. Its mechanism of action is similar to CHG in that it ruptures the bacterial cell wall membrane, resulting in leakage of the intracellular contents and eventual cell death. CPC is also thought to alter bacterial metabolism and inhibit cell growth. (73,77)

CPC binds to tooth structure and dental plaque biofilm; however, the degree of binding is not as strong as with CHG. Further, CPC is rapidly released from binding sites, which explains why it is generally less efficacious than CHG. (73) Like CHG, this cationic rinse may adversely interact with other charged ions found in dentifrices and mouthrinses, possibly limiting its biological activity.

Published data regarding the efficacy of CPC-containing mouthrinses are limited. In the United States, CPC is available in 2 concentrations: 0.05% found in cosmetic mouthrinses (Cepacol[R] and Scope[R]) and 0.07% found in therapeutic mouthrinses (BreathRx[R] and Crest[R] ProHealth[TM] Rinse). It has been suggested that the unique vehicle found in Crest[R] Pro-Health[TM] Rinse is purported to increase the product’s oral bioavailability when compared with other CPC-containing mouthrinses. (78)

In vitro studies have documented that CPC can be effective against the following organisms:

* Actinomyces viscosus, Porphyromonas gingivalis, Campylobacter rectus, Streptococcus sanguis, Eikenella corrodens, Salmonella typhimurium, Fusobacterium nucleatum, Haemophilus actinomycetemcomitans, Lactobacillus casei, and P intermedia (78)

* Several species of Candida (68,69,79,81)

CPC, like CHG, has been suggested as a possible agent for the prevention and treatment of fungal infections. However, CPC mouthrinses may adversely affect systemic azole drug treatment of oropharyngeal candidiasis in immunocompromised persons. This negative outcome may be attributed to either a cross-resistance to the azole drugs against CPC-resistant organisms or drug antagonism between CPC and azole antifungal medications when they are used in combination. (82) Two of 5 fluconazole-resistant C albicans strains have also exhibited reduced susceptibility to CPC. (82)

Mechanism of action of EO. EO antiseptic mouthrinse is a bactericidal combination of phenolic essential oils, including eucalyptol, menthol, methyl salicylate, and thymol. Phenolic compounds exert their antimicrobial effects by the following mechanisms (77,83-87):

* Cause protein denaturation

* Alter the cell membrane, resulting in leakage of the intracellular contents and eventual cell death

* Alter bacterial enzyme activity

* Exhibit anti-inflammatory properties by inhibiting prostaglandin synthetase, an enzyme involved in the formation of prostaglandins, which are primary inflammatory mediators. Note that the anti-inflammatory effect of phenolic compounds occurs at concentrations lower than those needed for antibacterial activity

* Cause perforation of the cell membrane and rapid efflux of intracellular contents (especially thymol)

* Alter neutrophil function by suppressing the formation of and scavenging existing free radicals generated in neutrophils and by altering neutrophil chemotaxis (especially thymol)

A 30-second exposure time to EO produces morphologic cell surface alterations in a variety of oral pathogens that suggest the loss of cell membrane integrity. (88) Cell surface changes may also alter bacterial coaggregation and recolonization that could potentially affect the growth and metabolism of these organisms. Microscopic evidence of cell surface roughening was obtained for the following microorganisms:

* C albicans

* F nucleatum

* A viscosus

* Actinobacillus actinomycetemcomitans

* S sanguis

Cell surface changes that result from a short exposure time to EO may adversely affect bacterial and fungal survival. (88) Exposure to levels of EO sublethal to microorganisms also reduces bacterial coaggregation with gram-positive pioneer species, an essential step in plaque maturation and the development of the complex pathogenic flora found in gingival disease. Decreased bacterial coaggregation reduces the rate of plaque maturation, which in turn may result in a decreased plaque mass, as is observed clinically with EO use. (89) EO also has been shown to extract endotoxins from gramnegative bacteria. (90) Endotoxins play an important role in pathogenesis; thus, reduction in endotoxin level should manifest as a decrease in gingival inflammation.

Unlike other OTC mouthrinses, EO has been shown to penetrate the dental plaque biofilm and is active against bacteria embedded within the biofilm. (72,91-93) EO kills a wide variety of aerobic and anaerobic bacteria associated with plaque biofilm and gingivitis, including the following (94)

* A actinomycetemcomitans

* A viscosus

* S mutans

* S sanguis

* Bacteroides species

Efficacy against gram-positive and gram-negative organisms occurs even at concentrations that are less than full strength. (94,95) A single 30-second rinse reaches and exerts an antibacterial effect interproximally, an important consideration given that gingival disease starts between the teeth and that individuals often cannot access interproximal areas with mechanical plaque removal techniques such as toothbrushing and flossing. Total recovered bacteria from proximal tooth surfaces was 43.8% lower following a single 30-second rinse of EO compared with a control (P =.001). (96) Rinsing twice daily with EO as an adjunct to brushing for 11 days reduced total recoverable streptococci in interproximal plaque by 69.9% (P<.001), with EO producing a 37.1% greater activity against S mutans than other streptococci. A significant reduction of 75.4% in total recoverable S mutans count was observed (P<.001). (14) Studies also have demonstrated significant suppression of the oral flora for several hours after rinsing, documenting that the antimicrobial activity of EO extends beyond the rinsing period. (97-99)

In vitro studies have shown that EO is also active against viruses, including herpes simplex virus 1 and 2, hepatitis B, human immunodeficiency virus 1, and influenza A virus, as well as against 7 species of Candida. (13,67,100) Like CHG, EO is not approved for the prevention and treatment of viral infections.

Unlike CHG and CPC, EO has a neutral electrical charge and does not interact negatively with other charged ions found in dentifrices and mouthrinses. (73) Moreover, its action is not inhibited by proteins in blood serum that inactivate many antimicrobial agents, including CHG. (94,95)

Efficacy of Mouthrinses on Plaque Biofilm and Gingivitis

The primary indication for antimicrobial mouthrinse use is the reduction of supragingival plaque biofilm and gingivitis in patients. A recent meta-analysis of 6-month clinical trials to evaluate the efficacy of a variety of antiplaque and antigingivitis products revealed that the largest body of studies supported the efficacy of EO. (101) A smaller body of studies supported the antiplaque and antigingivitis efficacy of 0.12% CHG. Results regarding the efficacy of CPC varied and were dependent upon product formulation. (101) Efficacy studies of CHG, CPC, and EO are summarized in Tables IV, V, and VI, respectively.

The following observations can be made from these study results:

* CHG generally reduces more plaque than either CPC or EO, a predictable outcome given its greater substantivity; the longer an antimicrobial agent stays in contact with plaque bacteria, the greater its effect.

* CHG and EO are comparable in reducing gingivitis. (39-41,43-45,48-50,102-104)

* In head-to-head comparison studies that evaluated both CHG and EO in the same participants, antiplaque effects were greater for CHG, but antigingivitis effects were similar for both agents. (42,46,47)

* Both CHG and EO demonstrate greater reductions in supragingival plaque and gingivitis as corn pared with CPC (see Tables IVVI).

Perhaps one EO study best summarizes the effectiveness of mouthrinses as an aid to reducing supragingival plaque and controlling gingivitis. In a large, randomized, controlled clinical trial involving 237 participants, those who added twice-daily rinsing with EO to their homecare routine of regular brushing and flossing demonstrated a 51.9% greater reduction in plaque and a 21.0% greater reduction in gingivitis, as compared with those who brushed and flossed only. (45) This study demonstrates the benefit of adding an EO mouthrinse to regular mechanical plaque removal and shows that mouthrinses are able to reach bacteria in areas that are difficult to access and where mechanical methods often leave residual plaque behind.

Approved Mouthrinses Are Efficacious Throughout the Entire Mouth

Using an antiseptic mouthrinse produces an antimicrobial effect throughout the entire mouth, including areas easily missed during toothbrushing and interdental cleaning. Studies have demonstrated that antiseptics kill bacteria in saliva and on the soft tissues of the mouth, including the tongue and oral mucosa, which are reservoirs of pathogenic bacteria that are able to transfer and colonize onto the teeth. (98,105-108) These collective research findings, with consideration given to the respective adverse events profiles of antiseptic agents, reinforce the value of using CHG, CPC, and EO in addition to mechanical plaque control for long-term maintenance of gingival health.


Antimicrobial mouthrinses that are approved by the FDA and carry the ADA Seal of Acceptance are safe and effective for the reduction of supragingival plaque and gingivitis. Products that have not been evaluated in long-term clinical trials have no scientific evidence documenting safety or efficacy and should be used with caution. Antimicrobial mouthrinses with established safety and efficacy are an important and effective addition to mechanical plaque control methods to establish a healthy mouth. Most patients will benefit by adding an ADA-Accepted antimicrobial mouthrinse to their self-care daily regimen of brushing and interdental cleaning.


The ADA and FDA have rigorous approval processes

The ADA grants its Seal of Acceptance to mouthrinses that have documented safety and efficacy through at least 2 longitudinal, controlled clinical trials. The FDA evaluates OTC ingredients making therapeutic claims. It has adopted key elements for gingivitis assessment from the ADA Seal of Acceptance criteria and assigns categories (I, II, or III) based on level of safety and efficacy. For certain prescription mouthrinses, the FDA evaluates safety and efficacy via the New Drug Application (NDA) process.

No link between ACMs and OPC

According to the FDA, National Cancer Institute, and ADA, there is no evidence of a causal relationship between ACMs and OPC. (6,28) Most mouthrinses accepted by the ADA as safe and effective contain alcohol. The ADA Seal documents a product’s safety and efficacy, and the ADA recommends that patients continue to use antiseptic mouthrinses as advised by their dental hygienist and dentist. (28,34)

CHG, CPC, and EO cause no serious adverse effects in a generally healthy population when used according to directions

This includes effects on salivary flow, taste, tooth deposits, and dental restorations. Some users may experience minor taste alteration, staining, and supragingival calculus formation with some CHG and CPC formulations.


(1.) Beals D, Ngo T, Feng Y, et el. Development and laboratory evaluation of a new toothbrush with a novel brush head design. Am J Dent. 2000;13:5A-14A.

(2.) Bader HI. Floss or die: implications for dental professionals. Dent Today. 1998;17:76-82.

(3.) Oliver RC, Brown LJ , Loe H. Periodontal diseases in the United States population. J Periodontol. 1998;69:269-278.

(4.) Council on Dental Therapeutics. Guidelines for acceptance of chemotherapeutic products for the control of supragingival dental plaque and gingivitis. J Am Dent Assoc. 1986;112:529-532.

(5.) American Dental Association Council on Scientific Affairs. Acceptance Program Guidelines: Chemotherapeutic Products for Control of Gingivitis. Available at: http://www. Published July 1997. Accessed May 1, 2007.

(6.) Food and Drug Administration. Oral health care drug products for over-the-counter human use; antigingivitis/ antiplaque drug products; establishment of a monograph; proposed rules. Fed Regist. May 29, 2003;68:32232-32287.

(7.) Wu CD, Savitt ED. Evaluation of the safety and efficacy of over-the-counter oral hygiene products for the control of plaque and gingivitis. Periodontol 2000. 2002;28:91-105.

(8.) Minah GE, DePaola LG, Overholser CD, et al. Effects of 6 months use of an antiseptic mouthrinse on supragingival dental plaque microflora. J Clin Periodontol. 1989; 16:347-352.

(9.) Walker C, Clark W, Tyler K, et al. Evaluation of microbial shifts following long-term use of an oral antiseptic mouthrinse [abstract]. J Dent Res. 1989;68:412. Abstract 1845.

(10.) Emilson CG, Fornell J. Effect of toothbrushing with chlorhexidine gel on salivary microflora, oral hygiene, and caries. Scand J Dent Res. 1976;84:308-319.

(11.) Schiott CR, Briner WW, Loe H. Two year oral use of chlorhexidine in man. II. The effect on the salivary bacterial flora. J Periodontal Res. 1976;11:145-152.

(12.) Briner WW, Grossman E, Buckner RY, et al. Effect of chlorhexidine gluconate mouthrinse on plaque bacteria. J Periodontal Res. 1986;21 (suppl):44-52.

(13.) Meiller TF, Kelley JI, Jabra-Rizk MA, et al. In vitro studies of the efficacy of antimicrobials against fungi. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001;91:663670.

(14.) Fine DH, Furgang D, Barnett ML, et al. Effect of an essential oil-containing antiseptic mouthrinse on plaque and salivary Streptococcus mutans levels. J Clin Periodontol. 2000;27:157-161.

(15.) DePaola LG, Minah GE, Elias SA, et al. Clinical and microbial evaluation of treatment regimens to reduce denture stomatitis. Int J Prosthodont. 1990;3:369-374.

(16.) DePaola LG, Minah GE, Leupold RL, et al. The effect of antiseptic mouthrinses on oral microbial flora and denture stomatitis. Clin Prev Dent. 1986;8:3-8.

(17.) White DJ. An alcohol-free therapeutic mouthrinse with cetylpyridinium chloride (CPC)–the latest advance in preventive care: Crest Pro-Health Rinse. Am J Dent. 2005;18:3A-8A.

(18.) Parkin DM, Pisani P, Lopez AD, Masuyer E. At least one in seven cases of cancer is caused by smoking: global estimates for 1985. Int J Cancer. 1994;59:494-504.

(19.) Blot WJ, McLaughlin JK, Winn DM, et al. Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res. 1988;48:3282-3287.

(20.) Negri E, La Vecchia C, Franceschi S, Tavani A. Attributable risk for oral cancer in northern Italy. Cancer Epidemiol Biomarkers Prev. 1993;2:189-193.

(21.) Garro AJ, Leiber CS. Alcohol and cancer. Annu Rev Pharmacol Toxicol. 1990;30:219-249.

(22.) Weaver A, Fleming SM, Smith DB. Mouthwash use and oral cancer: carcinogen or coincidence? J Oral Surg. 1979;37:250-253.

(23.) Mashberg A, Barsa P, Grossman ML. A study of the relationship between mouthwash use and oral and pharyngeal cancer. J Am Dent Assoc. 1985;110:731-734.

(24.) Kabat GC, Herbert JR, Wynder EL. Risk factors for oral cancer in women. Cancer Res. 1989;49:2803-2806.

(25.) Young TB, Ford CN, Brandenburg JH. An epidemiologic study of oral cancer in a statewide network. Am J Otolaryngol. 1986;7:200-208.

(26.) Wynder EL, Kabat G, Rosenberg S, Levenstein M. Oral cancer and mouthwash use. J Natl Cancer Inst. 1983;70:255-260.

(27.) Winn DM, Blot W J, McLaughlin JK, et al. Mouthwash and oral conditions in the risk of oral and pharyngeal cancer. Cancer Res. 1991 ;51:3044-3047.

(28.) Ciancio SG. Alcohol in mouthrinse: lack of association with cancer. Biol Ther Dent. 1993;9:1-2.

(29.) Silverman S, Wilder R. Antimicrobial mouthrinse as part of a comprehensive oral care regimen: safety and compliance factors. J Am Dent Assoc. 2006;137:22S-26S.

(30.) Cole P et al. Alcohol-containing mouthwash and oropharyngeal cancer: an epidemiologic prospective. Unpublished study in OTC 2001;Vol 210476.

(31.) FDC Reports. Alcohol-containing mouthwash concern “alleviated” by existing data. The Tan Sheet. June 10, 1996;4(24): 1-5.

(32.) Cole P, Rodu B, Mathisen A. Alcohol-containing mouthwash and oropharyngeal cancer: a review of the epidemiology. J Am Dent Assoc. 2003; 134:1079-1087.

(33.) Elmore JG, Horwitz RI. Oral cancer and mouthwash use: evaluation of the epidemiologic evidence. Otolaryngol Head Neck Surg. 1995;113:253-261.

(34.) American Dental Association Council on Dental Therapeutics. Mouthrinse use and the risk of oral and pharyngeal cancer (position statement) Sept. 29, 1991.

(35.) Listerine[R] Antiseptic [package insert]. Skillman, NJ: Johnson & Johnson Healthcare Products Division of McNEIL-PPC, Inc.; 2007.

(36.) Peridex[R] (chlorhexidine gluconate 0.12% ) Oral Rinse [package insert]. West Palm Beach FL: 3M ESPE; 2007.

(37.) Antabuse[R] (disulfiram) [package insert]. East Hanover, N J: Odyssey Pharmaceuticals, Inc.; 2001.

(38.) Gage TW, Pickett FA. Mosby’s Dental Drug Reference. 6th ed. St Louis, MO. Mosby/Elsevier; 2003.

(39.) Gordon JM, Lamster IB, Seiger MC. Efficacy of Listerine antiseptic in inhibiting the development of plaque and gingivitis. J Clin Periodontol. 1985;12:697-704.

(40.) Lamster IB, Alfano MC, Seiger MC, et al. The effect of Listerine antiseptic on the reduction of existing plaque and gingivitis. Clin Prev Dent. 1983;5:12-16.

(41.) DePaola LG, Overholser CD, Meiller TF, et al. Chemotherapeutic inhibition of supragingival dental plaque and gingivitis development. J Clin Periodontol. 1989; 16:311-315.

(42.) Overholser CD, Meiller TF, DePaola LG, et al. Comparative effects of 2 chemotherapeutic mouthrinses on the development of supragingival dental plaque and gingivitis. J Clin Periodontol. 1990;17:575-579.

(43.) Charles CH, Sharma NC, Galustians HJ, et al. Comparative efficacy of an antiseptic mouthrinse and an antiplaque/antigingivitis dentifrice: a six-month clinical trial. J Am Dent Assoc. 2001;132:670-675.

(44.) Bauroth K, Charles CH, Mankodi SM, et al. The efficacy of an essential oil antiseptic mouthrinse vs. dental floss in controlling interproximal gingivitis: a comparative study. J Am Dent Assoc. 2003;134:359-365.

(45.) Sharma N, Charles CH, Lynch MC, et al. Adjunctive benefit of an essential oil-containing mouthrinse in reducing plaque and gingivitis in patients who brush and floss regularly: a six-month study. J Am Dent Assoc. 2004; 135:496-504.

(46.) Charles CH, Mostler KM, Bartels LL, Mankodi SM. Comparative antiplaque and antigingivitis effectiveness of a chlorhexidine and an essential oil mouthrinse: 6-month clinical trial. J Clin Periodontol. 2004;31:878-884.

(47.) Grossman E, Meckel AH, Issacs RL, et al. A clinical comparison of antibacterial mouthrinses: effects of chlorhexidine, phenolics and sanguinarine on dental plaque and gingivitis. J Periodontol. 1989;60:435-440.

(48.) Grossman E, Reiter G, Sturzenberger OP, et al. Six-month study of the effects of a chlorhexidine mouthrinse on gingivitis in adults. J Periodontal Res. 1986;21 (supp116):33-43.

(49.) Loe H, Schiott CR, Glavind L, Karring G. Two years oral use of chlorhexidine in man. I. General design and clinical effects. J Periodontal Res. 1976;11:135-144.

(50.) Lang NP, Hotz P, Graf H, et al. Effects of supervised chlorhexidine mouthrinses in children. A longitudinal clinical trial. J Periodontal Res. 1982;17:101-111.

(51.) Mankodi S, Bauroth K, Witt JJ, et al. A 6-month clinical trial to study the effects of a cetylpyridinium chloride mouthrinse on gingivitis and plaque. Am J Dent. 2005;18:9A-14A.

(52.) Stookey GK, Beiswanger B, Mau M, et al. A 6-month clinical study assessing the safety and efficacy of two cetylpyridinium chloride mouthrinses. Am J Dent. 2005;18:24A28A.

(53.) Ashley FP, Skinner A, Jackson P, et al. The effect of a 0.1% cetylpyridinium chloride mouthrinse on plaque and gingivitis in adult subjects. Br Dent J. 1984;157:191-196.

(54.) Fischman SL, Aguirre A, Charles CH. Use of essential oil-containing mouthrinses by xerostomic individuals: determination of potential for oral mucosal irritation. Am J Dent. 2004; 17:23-26.

(55.) Kerr AR, Katz RW, Ship JA. A comparison of the effects of two commercially available non-prescription mouthrinses on salivary flow rates and xerostomia: a pilot study. Quintessence Int. In press.

(56.) Ciancio SG. Antiseptics and antibiotics as chemotherapeutic agents for periodontitis management. Compend Contin Educ Dent. 2000;21:59-78.

(57.) Mandel ID. Chemotherapeutic agents for controlling plaque and gingivitis. J Clin Periodontol. 1988;15:488-498.

(58.) Kerr AR, Ship JA. Tooth discoloration. Available at: Accessed April 8, 2007.

(59.) Sheen S, Addy M. An in vitro evaluation of the availability of cetylpyridinium chloride and chlorhexidine in some commercially available mouthrinse products. Br Dent J. 2003;194:207-210.

(60.) Bascones A, Morante S, Mateos L, et al. Influence of additional active ingredients on the effectiveness of non-alcoholic chlorhexidine mouthwashes: a randomized controlled trial. J Periodontol. 2005;76:1469-1475.

(61.) Norman R. Surface hardness effects of various mouthrinses on a composite resin [abstract]. J Dent Res. 1997;76:325. Abstract 2490.

(62.) Von Fraunhofer JA, Kelley JJ, DePaola LG, Meiller TF. The effect of a dental unit waterline treatment solution on composite-dentin shear bond strengths. J Clin Dent. 2004; 15:28-32.

(63.) Von Fraunhofer J, Kelley JI, DePaola LG, Meiller TF. The effect of a mouthrinse containing essential oils on dental restorative materials. Gen Dent. 2006;54:403-407.

(64.) Wolff LF. Chemotherapeutic agents in the prevention and treatment of periodontal disease. Northwest Dent. 1985;64:15-24.

(65.) De Boever EH, Loesche WJ. Assessing the contribution of anaerobic microflora of the tongue to oral malodor. J Am Dent Assoc. 1995; 126:1384-1393.

(66.) Bernstein D, Schiff G, Echler G, et al. In vitro virucidal effectiveness of a 0.12% chlorhexidine gluconate mouthrinse. J Dent Res. 1990;69:874-876.

(67.) Baqui AA, Kelley JI, Jabra-Rizk MA, et al. In vitro effect of oral antiseptics on human immunodeficiency virus-1 and herpes simplex virus type 1. J Clin Periodontol. 2001;28:610-616.

(68.) Giuliana G, Pizzo G, Milici ME, et al. In vitro antifungal properties of mouthrinses containing antimicrobial agents. J Periodontol. 1997;68:729-733.

(69.) Giuliana G, Pizzo G, Milici ME, Giangreco R. In vitro activities of antimicrobial agents against Candida species. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999;87:44-49.

(70.) Sharon A, Berdicevsky I, Ben-Aryeh H, Gutman D. The effect of chlorhexidine mouth rinses on oral Candida in a group of leukemic patients. Oral Surg Oral Med Oral Pathol. 1977;44:201-205.

(71.) Epstein JB, Vickars L, Spinelli J, Reece D. Efficacy of chlorhexidine and nystatin rinses in prevention of oral complications in leukemia and bone marrow transplantation. Oral Surg Oral Med Oral Pathol. 1992;73:682-689.

(72.) Foster JS, Pan PC, Kolenbrander PE. Effects of antimicrobial agents on oral biofilms in a saliva-conditioned flowcell. Biofilms. 2004;1:5-12.

(73.) Ciancio SG. Chemical agents: plaque control, calculus reduction and treatment of dentinal hypersensitivity. Periodontol 2000. 1995;8:75-86.

(74.) Fine DH. Mouthrinses as adjuncts for plaque and gingivitis management: a status report for the American Journal of Dentistry. Am J Dent. 1988;1:259-263.

(75.) Weeks C, Briner W, Rebitski G, et al. Immediate and prolonged effect of 0.12% chlorhexidine on salivary bacteria [abstract]. J Dent Res. 1988;67:326. Abstract 1711.

(76.) Barkvoll P, Rella G, Svendsen AK. Interaction between chlorhexidine digluconate and sodium lauryl sulfate in vivo. J Clin Periodontol. 1989;16:593-595.

(77.) Scheie AA. Modes of action of currently known chemical antiplaque agents other than chlorhexidine. J Dent Res. 1989;68:1609-1616.

(78.) Witt J, Ramji N, Gibb R, et al. Antibacterial and antiplaque effects of a novel, alcohol-free oral rinse with cetylpyridinium chloride. J Contemp Dent Pract. 2005;6:1-9.

(79.) Meier S, Collier C, Scaletta MG, et al. An in vitro investigation of the efficacy of CPC for use in toothbrush decontamination. J Dent Hyg. 1996;70:161-165.

(80.) Nakamoto K, Tamamoto M, Hamada T. In vitro effectiveness of mouthrinses against Candida albicans. Int J Prosthodont. 1995;8:486-489.

(81.) Phillips B J, Kaplan W. Effect of cetylpyridinium chloride on pathogenic fungi and Nocardia asteroides in sputum. J Clin Microbiol. 1976;3:272-276.

(82.) Edlind MP, Smith WL, Edlind TD. Effects of cetylpyridinium chloride resistance and treatment on fluconazole activity versus Candida albicans. Antimicrob Agents Chemother. 2005;49:843-845.

(83.) Goodson JM. Response. In: Loe H, Kleinman DV, eds. Dental Plaque Control Measures and Oral Hygiene Practices. Oxford, England: IRL Press; 1986:143-146.

(84.) Walker CB. Microbiological effects of mouthrinses containing antimicrobials. J Clin Periodontol. 1988;15:499-505.

(85.) Shapiro S, Meier A, Guggenheim B. The antimicrobial activity of essential oils and essential oil components towards oral bacteria. Oral Microbiol Immunol. 1994;9:202-208.

(86.) Kuehl FA Jr, Humes JL, Egar RW, et al. Role of prostaglandin endoperoxide PGG2 in inflammatory processes. Nature. 1977;265:170-172.

(87.) Azuma Y, Ozaza N, Ueda Y, Takagi N. Pharmacological studies on the anti-inflammatory action of phenolic compounds. J Dent Res. 1986;65:53-56.

(88.) Kubert D, Rubin M, Barnett ML, Vincent JW. Antiseptic mouthrinse-induced microbial cell surface alterations. Am J Dent. 1993;6:277-279.

(89.) Fine DH, Furgang D, Lieb R, et al. Effects of sublethal exposure to an antiseptic mouthrinse on representative plaque bacteria. J Clin Periodontol. 1996;23:444-451.

(90.) Fine DH, Letizia J, Mandel ID. The effect of rinsing with Listerine antiseptic on the properties of developing dental plaque. J Clin Periodontol. 1985; 12:660-666.

(91.) Pan P, Barnett ML, Coelho J, et al. Determination of the in situ bactericidal activity of an essential oil mouthrinse using a vital stain method. J Clin Periodontol. 2000;27: 256-261.

(92.) Fine DH, Furgang D, Barnett ML. Comparative antimicrobial activities of antiseptic mouthrinses against isogenic planktonic and biofilm forms of Actinobacillus actinomycetemcomitans. J Clin Periodontol. 2001;28:697-700.

(93.) Ouhayoun JP. Penetrating the plaque biofilm: impact of essential oil mouthrinse. J Clin Periodontol. 2003;30(suppl 5):10-12.

(94.) Ross NM, Charles CH, Dills SS. Long-term effects of Listerine antiseptic on dental plaque and gingivitis. J Clin Dent. 1989; 1:92-95.

(95.) Whitaker EJ, Pham K, Feik D, et al. Effect of an essential oil-containing antiseptic mouthrinse on induction of platelet aggregation by oral bacteria in vitro. J Clin Periodontol. 2000;27:370-373.

(96.) Charles CH, Pan PC, Sturdivant L, Vincent JW. In vivo antimicrobial activity of an essential oil-containing mouthrinse on interproximal plaque bacteria. J Clin Dent. 2000;11:94-97.

(97.) Pitts G, Brogdon C, Hu L, et al. Mechanism of action of an antiseptic, anti-odor mouthwash. J Dent Res. 1983;62:738-742.

(98.) DePaola LG, Minah GE, Overholser CD, et al. Effect of an antiseptic mouthrinse on salivary microbiotia. Am J Dent. 1996;9:93-95.

(99.) Furgang K, Sinatra K, Schreiner H, et al. In vitro antimicrobial activity of an essential oil mouthrinse. J Dent Res. 2002;81 (special issue A). Abstract 2854.

(100.) Dennison DK, Meredith GM, Shillitoe EJ, Caffesse RG. The antiviral spectrum of Listerine antiseptic. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995;79:442448.

(101.) Gunsolley JC. A meta-analysis of six-month studies of antiplaque and antigingivitis agents. J Am Dent Assoc. 2006; 137:1649-1657.

(102.) Segreto VA, Collins EM, Beiswanger BB, et al. A comparison of mouthrinses containing two concentrations of chlorhexidine. J Periodontal Res. 1986;21(suppl):23-32.

(103.) Brightman LJ, Terezhalmy GT, Greenwell H, et al. The effects of a 0.12% chlorhexidine gluconate mouthrinse on orthodontic patients aged 11 through 17 with established gingivitis. Am J Orthod Dentofacial Orthop. 1991 ;100:324329.

(104.) Eaton KA, Rimini FM, Zak E, et al. The effects of a 0.12% chlorhexidine-digluconate-containing mouthrinse versus a placebo on plaque and gingival inflammation over a 3month period. A multicentre study carried out in general dental practices. J Clin Periodontol. 1997;24:189-197.

(105.) Allen DR, Davies R, Bradshaw B, et al. Efficacy of a mouthrinse containing 0.05% cetylpyridinium chloride for the control of plaque and gingivitis: a 6-month clinical study in adults. Compend Contin Educ Dent. 1998;19(2 suppl):20-26.

(106.) Dahlen G. Effect of antimicrobial mouthrinses on salivary microflora in healthy subjects. Scand J Dent Res. 1984;92:38-42.

(107.) Jenkins S, Addy M, Wade W, Newcombe RG. The magnitude and duration of the effects of some mouthrinse products on salivary bacterial counts. J Clin Periodontol. 1994;21:397-401.

(108.) Pitts G, Pianotti R, Feary TW, et al. The in vivo effects of an antiseptic mouthwash on odor-producing microorganisms. J Dent Res. 1981;60:1891-1896.

(109.) Fine DH, Furgang D, Sinatra K, et al. In vivo antimicrobial effectiveness of an essential oil-containing mouth rinse 12 h after a single use and 14 days’ use. J Clin Periodontol. 2005;32:335-340.

Louis G. DePaola, DDS, MS, and Ann Eshenaur Spolarich, RDH, PhD

Table I. Effect of CHG and EO on Normal Oral Flora

Mouthrinse Study Description Outcome References

0.12% Several studies of Routine use of CHG 8, 9, 12

Chlorhexidine 6 months’ duration and EO did not

gluconate (CGH) or longer; dental cause adverse

and essential plaque harvested at shifts in plaque

oils (EO) baseline, midpoint, ecology, emergence

and end. Minimum of opportunistic

inhibitory pathogens, or

concentration development of

microbial resistant

samples taken microbial strains

0.12% CHG Candida species Both agents 13

and EO (C albicans, C effective against

dubliniensis, C test fungal

krusei, C glabrata, species at

C tropicalis) grown commercially

in vitro and available

treated with 0.12% concentrations

CHG or EO with comparable

inhibition between

CHG and EO

EO Randomized, Reduction in S 14

crossover study mutans:

with 29 adults to Recoverable S

determine whether mutans counts from

regular anti- the participants’

microbial rinse use interproximal

had the potential spaces reduced by

for a selective 75.4% with EO

increase of compared with

Streptococcus control. Total

mutans or an streptococci in

overgrowth of interproximal

fungal species. plaque declined by

Participants rinsed 69.9%. EO activity

with EO or placebo 37.1 % greater

for 14 days against S mutans

than against other

streptococci. No

increase in risk

of caries

EO In vivo Rinsing with EO 15, 16

investigations in twice daily was as

persons with effective as

denture stomatitis nystatin oral

caused by an suspension in

overgrowth of C reducing clinical

albicans and other palatal

fungal species in inflammation

maxillary and candidiasis


Table II. Effects of EO on Salivary Flow

Study Description Outcome References

Effect of EO versus placebo Under exaggerated conditions 54

on the salivary flow rate (3 rinses/day instead of the

and oral mucosa of 19 recommended 2), no lesions

volunteers with documented attributable to EO observed

xerostomia who used 3 rinses in the majority of patients.

daily for 14 days followed No statistically significant

by a cross-over after a differences detected between

7-day washout period. Pre- pre- and postrinse salivary

and postrinse salivary flow flow rates for either the EO

rates were measured and or control group

oral soft tissues examined

for evidence of irritation

and inflammation

Effect on salivary flow or No significant effect on 55

symptoms of dry mouth salivary flow or dry mouth

of an EO mouthrinse and between the 2 groups

a non-alcohol-containing


Table III. Effects of Antimicrobial Mouthrinses on Dental Materials

Mouthrinse Study Description Outcome References

Seven In vitro study of No statistical 61

mouthrinses resin specimens difference among

(5 alcohol- placed in 1 of 7 the tested

containing mouthrinses and solutions. ACMs

mouthrinses vibrated for 30 caused no increased

[ACMs], 1 seconds or 1 minute reduction in

alcohol free, twice daily (to composite resin

and 1 plain simulate actual use hardness

water) exposure times) for

180 days

Essential In vitro study No differences in 62

oils (EO) measured effect of SBS found between

EO on resin bond the EO and control

strength on human groups at all

teeth embedded in dilutions. EO had

dental stone. Tooth no effect on resin

surfaces etched and bond strength

rinsed for 30

seconds with

distilled water or

various EO

dilutions. Each

tooth was then

dried, a film of

adhesive resin

applied followed by

composite resin, and

shear bond strength

(SBS) recorded

EO Direct effect of EO No significant 63

use on dental differences between

materials. Specimens the EO and control

of amalgam, glass groups detected in

ionomer, and vitro or in vivo.

composite subjected EO use had no

to EO or distilled adverse effect on

water for a restorative

continuous 10-day materials tested

period. For each


compressive strength

and water fluid

absorption were

compared; surface

porosity was

evaluated with

scanning electron

micrographs (SEM).

Also, 10 subjects

wore appliances with

implanted study

materials and rinsed

twice daily for 30

seconds with EO or

placebo. After 10

days, dental

materials examined

by SEM

Table IV. Effects on CHG on Supragingival Plaque and Gingivitis

Trial Concentration

Length No. of of CHG

(months) Subjects (%)

Loe et al, 24 120 0.20

1976 (49)

Lang et al, 6 158 0.10

1982 (50) 0.20

Segreto et al, 3 600 0.12

1986 (102) 0.20

Grossman et al, 6 430 0.12

1986 (48)

Grossman et al, 6 481 0.12

1989 (47)

Brightman et al, 3 34 0.12

1991 (103)

Overholser et al, 6 124 0.12

1990 (42)

Eaton et al, 3 121 0.12

1997 (104)

Charles et al, 6 108 0.12

2004 (46)

Plaque Gingivitis

Decrease Decrease

(%) (%)

Loe et al, 45 27

1976 (49)

Lang et al, 16.2 66.6

1982 (50) 19.4 80.4

Segreto et al, 36 37

1986 (102) 28 28

Grossman et al, 61 39

1986 (48)

Grossman et al, 49 31

1989 (47)

Brightman et al, 64.9 60.0

1991 (103)

Overholser et al, 50.3 30.5

1990 (42)

Eaton et al, 28 25

1997 (104)

Charles et al, 21.6 18.2

2004 (46)

Table V. Effects of CPC on Supragingival Plaque and Gingivitis


Trial tration Plaque Gingivitis

Length No. of of CHG Decrease Decrease

Investigator (months) Subjects (%) (%) (%)

Allen et al, 6 111 0.05 28.2 24.0

1998 (105)

Mankodi et al, 6 139 0.07 15.8 15.4

2005 (51)

Stookey et al, 6 366 0.075 17 23

2005 (52) * 0.10 19 20

* The mouthrinse formulations in this study were experimental.

Table VI. Effects of EO (Listerine[R]) on Supragingival Plaque and



Length No. of Rinsing

Investigator (months) Subjects Supervision

Lamster et al, 1983 (40) 6 145 Supervised

Gordon et al, 1985 (39) 9 85 Supervised

DePaola et al, 1989 (41) 6 107 Supervised

Overholser et al, 1990 (42) 6 124 Supervised

Charles et al, 2001 (43) 6 316 Unsupervised

Bauroth et al, 2003 (44) 6 326 Unsupervised

Sharma et al, 2004 (45) 6 237 Unsupervised

Charles et al, 2004 (46) 6 108 Unsupervised

Plaque Gingivitis

Decrease Decrease

Investigator (%) (%)

Lamster et al, 1983 (40) 22 28

Gordon et al, 1985 (39) 19.5 23.9

DePaola et al, 1989 (41) 34 34

Overholser et al, 1990 (42) 36.1 35.9

Charles et al, 2001 (43) 56.1 22.9

Bauroth et al, 2003 (44) 21 12

Sharma et al, 2004 (45) 51.9 21.0

Charles et al, 2004 (46) 18.8 14.0

COPYRIGHT 2007 American Dental Hygienists’ Association

COPYRIGHT 2008 Gale, Cengage Learning