Abstract: Diagnostic and treatment services for patient complaints of “bad breath” are currently being offered in many dental offices. There are no accepted standards of care for these services, and clinical protocols for the diagnosis and treatment of breath malodor vary widely. This article attempts to review the biological and psychological bases of patients’ complaints of bad breath and to describe a clinical protocol for the evaluation and treatment of such complaints. This protocol resulted in a 99% success rate in eliminating objectively measured breath malodor. However, 24% of patients continued to believe that at least some of their bad breath persisted after treatment. The merits of various diagnostic procedures are discussed in light of the psychogenic component of the symptomatology of halitosis sufferers.
Learning Objectives: After reading this article the reader should be able to
- Identify if a patient is experiencing breath malodor without the use of any specialized equipment.
- Explain how to determine whether a patient’s breath malodor is originating from the mouth or another part of the airway
- Describe the location, origin, and cause of most breath malodor
- Discuss how to distinguish between real and “imagined” halitosis
- Describe the difference between VSC generation in the mouth and VSC emission in the breath
- Describe the relationship between periodontal disease and bad breath
Most adults and many children suffer from halitosis (bad breath). This affliction may occur occasionally, regularly, or chronically at specific times of the day or month.1,2 For the purposes of this article, the terms bad breath, halitosis, and breath malodor all mean an unpleasant breath odor that is objectionable to others. Public awareness and concern for this phenomenon is evidenced by the support of an estimated $850 million mouthwash industry in the United States despite wide agreement that commercially available products have no significant effect on breath malodor.3,4 Recent public opinion polls5,6 (taken between 1994 and 1995) have revealed that 55- to75-million Americans consider bad breath a principal concern in social encounters.
In general, physicians and dentists are generally poorly informed about the causes and treatments for halitosis. This article briefly reviews the current understanding of the etiologies of halitosis and introduces a clinical protocol for diagnosis and treatment. The clinical strategies and techniques for diagnosis and treatment were drawn from the research methods and results of Tonzetich1, 7-9 Preti,10,11 Rosenberg,4, 12-13 Yaegaki,15,16 Bosy17 et al, and our own experience treating more than 3,000 patients presenting with chief complaints of “bad breath.”
Studies on the etiologies of breath malodor agree that hydrogen sulfide (H2S), methylmercaptan (CH3SH), and dimethyl sulfide (CH3SCH3), collectively referred to as volatile sulfur compounds (VSC), are the principal odorants in bad breath.1 Volatile sulfur compounds originate with the anaerobic bacterial degradation of sulfur containing amino acids within the oral cavity. Therefore, it is reasonable for dentists to assume the responsibility for diagnosing and managing breath malodor. When systemic or other non-oral etiologies are suspected, dentists must be prepared to make appropriate medical referrals. There are many common non-oral diseases cited in the literature for which halitosis can be a symptom.18-19 However, halitosis typically occurs late in the pathogeneses of these diseases when other more obvious or more urgent symptoms are present.18,20,21 Rapid onset and progressively intensifying breath malodor are suggestive of an infective process, possibly secondary to carcinomas or other localized pathologies in the airway.18,20 However, in our experience for patients with a chief complaint of long-standing, chronic halitosis, there is, almost without exception, either an oral origin or no halitosis at all.
Oral Origins of Breath Malodor: Tonzetich1 showed that incubated whole saliva produces a putrid odor and that hydrogen sulfide, methyl mercaptan and, to a lesser extent, dimethyl sulfide are the principal, responsible malodorants. When fresh saliva was filtered, the incubated supernate alone produced very little VSC. Saliva filtrate was shown to contain dead epithelial cells, live and dead bacteria, white blood cells, other blood elements and food debris, all of which are rich in proteins, peptides and free amino acids. Through a series of systematic studies, Tonzetich and coworkers established that the malodorous volatiles produced by incubated whole saliva evolve from anaerobic bacterial activity on sulfur-containing amino acids derived from degraded proteins present in salivary filtrate. They also observed that the incubated saliva of patients with periodontal disease produced a more rapidly developing, and intense malodor and evolution of VSC. Volatile sulfur compounds that evolved from substrates high in the amino acid cystine were high in hydrogen sulfide, while VSC that evolved from high methionine substrates were high in methylmercaptan.
Direct measurements of breath volatiles using gas chromatography-flame photometric detection confirmed that the distribution of VSC generated from incubated saliva is similar to that which can be identified in malodorous, human mouth air. Kostelc et al22 and others15-23 have shown that patients suffering from periodontal disease produced more breath malodor and mouth-air VSC than patients with healthy periodontium. However, it has been reported that periodontal disease is not a prerequisite for the production of high levels of orally generated VSC or oral malodor as measured organoleptically.17,24 In our practice with periodontal disease is not a routine finding. We routinely see dentally healthy children, young adults with no clinical evidence of periodontal diseases, adults with inactive and/or well-controlled periodontitis, and totally edentulous patients who have high levels of oral malodor. Some of these patients have extremely intense breath malodor and extremely high VSC in their mouth air (Fig. 1.). Yaegaki15 et al1,25-26 have identified the dorsoposterior surface of the tongue as the principal location for intraoral generation of VSC and breath malodor. That anaerobic bacteria capable of producing VSC are routinely recoverable from this location is well established.21,31 The benefits of tongue cleaning for controlling dental plaque and breath malodor have been extolled in the literature for decades.25-26,32-33
The incidence, intensity and duration of episodes of breath malodor vary considerably within one individual depending on a number of conditions.1,8,25 Using a modified industrial sulfide monitor, called the Halimeter™ (Interscan Corp., Chatsworth, CA) (Fig 2.), Rosenberg14 demonstrated a diurnal cycle for oral emission of VSC. Tonzetich et al34 showed that oral VSC production varies in accordance with the menstrual cycle. The concentrations of VSC in the saliva35,36 and perhaps the surface soft tissue of the mouth37considerably exceed that of the breath. Because VSC are permeable in soft tissue and toxic to gingival connective tissue,37 a major role for VSC has been postulated for the pathogenesis of periodontitis (Fig. 3)23,38 Within this context, the VSC associated with oral malodor may constitute only a relatively small proportion of intraoral VSC that volatilizes when the VSC in saliva and soft tissues exceed saturation. If, in fact, the saliva and oral soft tissues store significant quantities of VSC by absorbing them into solution, then it is likely that the concentration of VSC in mouth air at any moment may not always correlate well with the instantaneous rate of VSC generation within the mouth.
To measure the rate of VSC generation within the mouth, we developed a modified anaerobic bacterial growth medium enriched with cystine and methionine and a trace of lead acetate which undergoes a color change when exposed to VSC (HaliTest™, ProFresh, Inc., Philadelphia, PA). We observe the time it takes for a standardized sample of tongue coating, collected on a cotton swab and submerged in the medium, to produce a barely observable color change. We interpret this time to be a measure of the rate of VSC generation by the tongue coating (VSGT). The less time it takes for the color change to occur, the faster the rate of VSC generation. We then compared rates of VSC generation from tongue coating samples, measured by this simple technique, with mouth air VSC (VSCm) and organoleptic malodor assessments (ORQ,.) in patients preconditioned with at least six hours of abstention from oral activities (eating, oral hygiene, etc.). We also recorded results of our attempts to verbally confirm episodes of bad breath perceived by friends or relatives identified by the patients. Table 1 is a sample of these data. There appears to be associations between the four measures of breath malodor, but the associations are, by no means, perfect. Nevertheless, with only one exception (MS), all patients with organoleptic scores which we judged as significant (ORGm>2) or elevated mouth air VSC (VSCm>180) had high rates of VSC generation from tongue coating (VSGT < 30 min). It is interesting that several patients had high rates of VSC generation (low VSGT’s) but normal VSCm and low ORGm at the time of testing. However, each of these patients had verified episodes of bad breath as reported by friends or relatives. This means that even fasted patients who, at a particular evaluation, exhibit no evidence of breath malodor except high rates of VSC generation from tongue coating (low VSGT) may have, at least, occasional episodes of perceptible bad breath. We could not confirm episodes of bad breath with friends or relatives for any patient with a VSGT of 50 or above (low rates of VSC generation). Assuming that most VSC are produced by the tongue coating,1,8,16,25 we have interpreted the data in Table 1 to suggest that a high rate of intraoral VSC generation need not result in an episode of breath malodor unless and until the quantity of VSC in the mouth exceeds the capacity of the saliva and soft tissue to absorb them into solution.
Of additional interest in Table 1 is that several patients who had high VSCm, had low ORGm and vice versa. This observation has been previously attributed to the general unreliability of organoleptic scoring.13 In our experience, it is not uncommon to see patients whose breath odor is significantly offensive according to multiple judges but whose peak VSC, as measured by the Halimeter, is normal. It is well established that the proportion of CH3SH to H2S in VSC varies considerably.15 Tonzetich25 demonstrated that the air concentration threshold for organoleptic objectionability of CH3SH (0.5 ng/10cc) was one-third that of H2S (1.5ng/10cc). Since the Halimeter is approximately twice as sensitive to H2S as to CH3SH,39 it is possible that patients with high CH3SH relative to H2S in their mouth air may produce normal Halimeter measurements despite significant organoleptically detectable breath malodor. Conversely, patients with low CH3SH relative to H2S may have elevated Halimeter measurements and no organoleptically discernible breath malodor.
Imaginary Halitosis: In dealing with patients seeking professional care for halitosis, one must be prepared to differentiate between those patients who emit above average malodor, those who emit average or near average malodor, but are more sensitive to it, and those who emit below average or no malodor, but believe that their breath is offensive (imaginary halitosis). In the former two cases, treatment for organic causes of malodor is warranted; in the latter, it is not. That is not to say that sufferers of imaginary halitosis cannot be helped.
There are many patients who complain of chronic bad breath for whom no objective evidence of breath malodor can be identified.12,18,40,41 Olfactory reference syndrome42,43 is a recognized psychiatric condition. It has been described as a somatization of some psychological distress resulting in a belief that an offensive odor emanates from some body part, usually the mouth. This condition interferes with normal social interactions for fear of offending others with breath malodor and has been described in the psychiatric literature for over100 years.40,43 Affective disorders and schizophrenia were reported to develop in patients whose initial complaints were limited to malodor, and some success has been reported in treating olfactory reference syndrome with tricyclic antidepressants and the neuroleptic primozide.40,41,44 We have had some preliminary success in treating this condition with the serotonin reuptake inhibitor, Zoloft®,c (verbal communication, March 1995, E Schweitzer, MD, Hospital of the University of Pennsylvania).
Breath malodor can be episodic14 and may be provoked or diminished by a variety of transient conditions1,9 which cannot always be controlled. Consequently, an incorrect diagnosis of imaginary halitosis can result if a patient’s evaluation is limited to a single occasion of VSC and organoleptic assessment. We have found that many patients who suffer mild or occasional episodes of breath malodor may test negative for elevated VSC and/or organoleptically determined malodor at a particular office visit even if pre-visit conditions are imposed which enhance breath malodor (Figures 6A and 6B). Therefore, we have established guidelines to avoid mistaking mild or occasional breath malodor problems for imaginary halitosis. A diagnosis of imaginary halitosis is considered only if all the following conditions are met after repeated testing under various properly selected conditions conducive to the production of breath malodor:
- Breath malodor cannot be organoleptically identified, and above normal levels of VSC cannot be demonstrated instrumentally in any breath samples taken from various airway locations,
- A sample of tongue coating is demonstrated to have a poor ability to convert bioavailable sulfur to VSC (VSGT>60).
- The patient cannot provide reliable third-party verification of his/her bad breath.
Unlike the discomfort we associate with traditional dental diseases, the discomfort caused by halitosis is totally psychological. The social and sexual taboos associated with halitosis originate in antiquity. Commercial mouthwash and “breath freshener” advertising reinforces and exaggerates the stigma of bad breath to the public. Such repeated exposure to the social anathema of halitosis may account for the high level of disproportionate concern about bad breath that we have observed in patients who present for halitosis treatment. This phenomenon can occur with real or imagined halitosis, and it appears in two forms which often coexist in the same patient: (1) an exaggerated perception by the patient of the intensity of the halitosis; and (2) an excessive preoccupation with the personal consequences of the halitosis. Patients manifesting these symptoms often exhibit inappropriate behavior that interferes significantly with their everyday lives. Halitosis sufferers commonly identify their halitosis as the cause for limited career choices, poor job performance, loss of jobs, failed marriages, impotency, social isolation, inability to concentrate, and thoughts of suicide. Therefore, any protocol for evaluating patients for complaints of halitosis, whether real or imagined, must include criteria that reveal the degree to which a patient may be inappropriately preoccupied with or psychologically impaired by his/her condition.
Documentation and Diagnosis: The following is a protocol that we have developed for the diagnosis and management of complaints of bad breath:
- Visit Preparation
In preparation for their first visit to the office, patients are instructed to abstain from food, breath fresheners, and oral hygiene for 6 to 12 hours; smoking for 12 hours; scented cosmetics for 24 hours; onions, garlic, and spicy foods for 48 hours; and antibiotics for 3 weeks.
- Halitosis History
After reviewing the medical history, a thorough history of the patient’s halitosis is taken. This history is divided into six sections; each designed to reveal specific objective and subjective information about the patient and his/her complaint. Some of the issues raised in the interview may be emotionally charged, and patients may resist open and frank discussion about them. Therefore, it is important that the interviewer establishes a relaxed and communicative atmosphere at the outset. The six sections of the halitosis history are described briefly below:
Age and circumstances of onset of halitosis – When and how did the patient first become aware that he/she had halitosis? If the onset was recent and/or accompanied by other physical signs or symptoms, one might suspect the origin to be a systemic or localized respiratory disease. If first recognition can be traced to a particular comment from another person, the degree to which this initial awareness is supported by subsequent events becomes important. Among our patients, it is not uncommon for a comment received in childhood to trigger a life-long, debilitating preoccupation with halitosis.
Current methods used by the patient for judging his/her halitosis – Patients rely on three methods for assessing or knowing about their halitosis: (1) Self-perceived taste or odor; (2) body language, including verbal and non-verbal “hints” from other people; and (3) direct verbal corroboration from other people. In our experience, only direct verbal corroboration is objectively reliable evidence of a breath malodor problem. Patients who rely heavily on the first two methods sometimes have difficulty perceiving improvement when their breath malodor is eliminated.
Blood borne malodorant volatiles – Ethnic diets that regularly include large amounts garlic and other mercaptan- or thiol containing foods can result in conspicuous and prolonged episodes of breath malodor. These and other dietary volatiles, such as ethanol, are rapidly absorbed into the bloodstream through the gastrointestinal tract and are carried to the lungs where they volatilize and enter the breath18. Other potential sources of blood-borne malodorant volatiles are metabolic disorders such as trirnethylaminuria11 amino acid absorption deficits42 and medications.18 Patients with these conditions may also present with complaints of bad taste and/or body odors.47
Conditions which may result in elevated salivary proteins – Breath malodor production is favored by elevations in the saliva concentrations of the VSC precursors, cystine and methionine, whether they appear as free amino acids or in peptide configuration.1 Periodontal disease, xerostomia, oral ulcers, rampant caries, poor oral hygiene or oral inflammations associated with excessive use of irritants such as tobacco and some commercial breath fresheners may be expected to result in elevations in salivary proteins. The cyclic variations in oral VSC production associated with the menstrual cycle3,4 (see Figure 6A) may also correspond to variations in salivary protein concentrations.
Inaccurate perception of the intensity of halitosis – In our experience, many patients seeking treatment for bad breath have, to varying degrees, exaggerated perceptions of the frequency and intensity of their episodes of breath malodor. The amount of exaggeration can be estimated by asking the patient to assess the intensity of his/her own malodor at the moment and then comparing this self-assessment to organoleptic assessment(s) by examiners(s). A patient’s estimate of the distance from which his/her halitosis can offend people is also helpful in this regard. Estimates of up to 3 feet are probably realistic, whereas estimates over 5 feet suggest exaggeration.
Disproportionate concern about halitosis – The degree to which a patient’s concern about his/her halitosis interferes with normal, daily activities reveals the appropriateness of the patient’s adaptation to his/her condition. Patients may disclose that their halitosis is interfering substantively with their ability to work, participate in social activities, express affection or concentrate. Some admit to thoughts of suicide. Some patients betray an excessive preoccupation with their halitosis by having undergone unreasonable numbers of invasive dental and/or medical tests and procedures in search of a cure.
Volatile sulfur-compound concentrations in mouth, nose, and lung air are recorded with a Halimeter™, a modified sulfide monitor first described by Rosenberg et al13 and a pen-writer Linear model 1101d (Figure 3). According to the manufactuerer, the sensitivity of the monitor is 0-1900-ppb to H2S with a 60% response to equal concentrations of methylmercaptan.3 The Halimeter™ output signal is adjusted with a variable potentiometer so that a 500-ppb response by the Halimeter™ produces a 5-cm deflection of the pen-writer set at a sensitivity of 500 mV/cm. Before each recording, the monitor is adjusted to zero for ambient room air. Samples of the mouth, nose, and lung air are collected in plastic bags. (6 5/8” x 5 7/8”) through flexible straws (7 5/8” x 15/64” diameter) and fed into the Halimeter™ immediately on collection. Because we have found no differences in the recordings obtained from the mouth air fed directly from the mouth to the Halimeter™ through a vented straw and those obtained through bag collection method, we generally feed air directly to the Halimeter™ from the mouth through a vented straw for convenience. Detailed instructions for preparation, sample collection, and recording with the Halimeter™ and pen-writer are available through Interscan Corp.a or ProFresh, Inc.b Figure 4 is an example of a recording obtained in this manner. Peak VSC values for each sample are recorded in the patient’s chart.
Separate organoleptic assessments of oral, nasal, and pulmonary air are performed and recorded independently by two operators. A 0 to 5 scoring system is used. “1,” barely detectable malodor; “2,” slightly offensive malodor; “3,” moderately offensive malodor; “4,” strongly offensive malodor; “5,” overwhelmingly offensive malodor. Oral air is assessed immediately after a 3-minute incubation period during which the patient keeps the lips sealed and breathes through the nose. Then the patient opens the mouth wide and breathes out slowly through the mouth. The operator, having positioned his/her nose 4 to 6 inches from the patient’s open mouth, assesses the odor of the patients mouth air (ORGm) with a series of two to four strong, but brief, staccato like sniffs. The patient then pinches the nose closed for 3 minutes while breathing through the mouth. The operator repeats the assessment procedure on the initial air sample expelled through the nose (ORGn). The patient continues to expel air slowly while the operator turns his/her head away from the patient and sniffs room air to avoid olfactory adaptation to any perceived odor by reacclimating his/her sense of smell to the ambient room air. As the patient approaches the end of exhalation, the operator turns back to the patient and assesses the last sample of air that the patient can force out of the lungs through the nose (ORGn). The two operators’ scores for each air sample are averaged and recorded in the patient’s chart.
An assessment of the relative capacity of the patient’s tongue coating to convert bioavailable sulfur to VSC is obtained by gently drying the dorsoposterior surface of the tongue with a gauze square of air syringe, collecting a sample of dorsoposterior tongue coating on a cotton swab 1 to 3 cm anterior to the lingual cecum, and then plunging the cotton swab into HaliTestTM,b. The operator then records in the chart the time required for a yellow-brown coloration, which indicates evolution of VSC, to first appear on the cotton swab. At room temperature, a time of 30 minutes or less is considered a strong positive; 31 to 90 minutes, a weak positive; and more than 90 minutes, a negative test result.
Separate organoleptic assessments (0 to 5) of intraoral appliances, tongue coating, and interdental samples are performed by a single operator and then recorded in the chart. Dental appliances are removed, dried to remove saliva, and assessed organoleptically for malodor. Next, a 2 x 2 gauze square is applied with finger pressure to the midline of the dorsoposterior border of the tongue and drawn anteriorly for about 1 inch. The gauze is removed and immediately assessed organoleptically for malodor. Finally, Superfloss 7TM,e, an absorbent dental floss, is drawn interproximally between all of the posterior teeth. A separate piece of floss is used for each sextant and is immediately assessed organoleptically and discarded.
Ears, nose, and oropharynx are examined with an otoscope and tongue depressor for evidence of acute or chronic upper respiratory diseases or conditions commonly associated with complaints of bad breath (tonsillitis, postnasal drip, nasal polyps, etc).18 Dental radiographs (panoramic x-ray and bite-wings) are taken, and a complete dental examination is performed. During these examinations, particular attention is given to conditions that may cause patients to perceive bad tastes or odors, such as endodontically infected teeth, cryptic tonsils, or defective dental restorations. It is not usual for such conditions to be a source of bad breath (as perceived by others), but they may promote or intensify a patient’s concern about bad breath. (eOral-B, Redwood City, CA 94065)
With the information obtained from the malodor history, testing and examination, a diagnosis is proposed. In virtually all apparently health patients who have breath malodor, the cause of malodor is the degradation of host tissue proteins by anaerobic bacteria on the dorsoposterior surface of the tongue. We have called this condition “anaerobic bacterial glossitis.” We feel this term, which implies infection, is warranted because of the clinical signs of inflammation and the frequency of frank ulceration of the tongue surface that accompanies this condition (Figures 7A through 7C). The apparent similarities between anaerobic bacterial glossitis and periodontitis are striking. Consequently, we have proposed a model for the pathogenesis of anaerobic bacterial glossitis (Figure 8) that parallels the model for the pathogenesis of periodontal disease depicted in Figure 5.
The most important and challenging aspects of diagnosis are estimating: (1) the degree to which the patient produces breath malodor (this includes estimating the frequency and intensity of episodes of breath malodor); (2) the degree to which the patient’s perception of his/her breath malodor is exaggerated; and (3) the degree to which the patient’s concern about bad breath provokes inappropriate behavior or preoccupation with the condition. The relative contributions of these three factors to the patient’s overall level of discomfort with his/her condition must be considered when formulating a treatment plan.
Treatment: The objectives of treatment are elimination of the patient’s breath malodor and the discomfort the patient experiences in situations in which breath malodor was a problem in the past. While these two objectives are somewhat interdependent, success in achieving the former is not always followed by success in achieving the latter. Treatment for breath malodor consists of three phases: (1) elimination of all breath malodor; (2) instruction of the patient in objective methods for the evaluation of his/her breath malodor; and (3) monitoring the patient’s progress in divesting him/herself of the social apprehension and psychological discomfort associated with having bad breath.
Orally generated breath malodor is caused by VSC that volatilize from the saliva and oral soft tissues. Elimination of breath malodor is directed toward reducing the oral generation of VSC and removing volatilized and non-volatilized VSC from the mouth. For these purposes, an intraoral liquid-air spray device, Prophy-Jet® 30f, and an ultrasonic intraoral dental cleaner, BOBcat® Ultrasonic Scalerf, have been modified to deliver a 20-ppm molecular chlorine dioxide irrigant, ProFresh™ Irrigantb, for debridement and deodorization of the hard and soft tissues of the mouth. Sodium bicarbonate is not used with the Prophy-Jet® 30. A spray deflector is attached to the Prophy-Jet® 30 handpiece to localize the impact of the spray to a small area and to prevent the spray from causing gagging when debriding (f Dentsply International Inc, York, PA 17405) posterior oral soft-tissue surfaces. The tip of the Prophy-Jet® 30 nozzle is positioned about 1 cm from the intraoral tissues at approximately a 45-degree angle and moved in a slow, circular motion over all accessible soft-tissue surfaces (Figures 7A through 7C). Particular attention is given to the circumvallate region of the tongue. Bleeding can be expected from this area as a result of the spray. Supragingival calculus is removed, and interdental areas are flushed with molecular chlorine dioxide (ClO2) irrigant using the Cavitron TFI®- 1000 insert.f
The deodorizing and antibacterial characteristics of molecular ClO2 in aqueous solutions are well known.44-46 It is safe and nontoxic in solutions in the range of concentrations described here.44,45 The physical and chemical properties of molecular ClO2 are different from those of so-called “stabilized chlorine dioxide.” Stabilized ClO2 mouth rinses contain no chlorine dioxide when measured spectrophotometrically in the laboratory. Chlorine dioxide deodorizes by oxidizing malodorous sulfides and thiols (VSC) to nonodoriferous salts.46 It also oxidizes other malodorous volatiles, such as aliphatic amines, phenols, and alcohols.44,45 Chlorine dioxide’s high solubility in nonpolar solvents,46 suggest it may concentrate itself in plaque and on soft-tissue surfaces. These properties may enhance the deodorizing effect of ClO2 because a large proportion of oral VSC is dissolved in soft tissue, saliva, and plaque. The antibacterial effect of ClO2 is not well understood but presumably derives from interference with protein synthesis and alterations of membrane permeability to electrolytes within bacterial cells.44,45 Chlorine dioxide also may reduce VSC generation by oxidizing sulfur-containing, free amino acids and peptides,46 which are the precursors of VSC.
After professional debridement and irrigation of the soft tissues with aqueous chlorine dioxide, the patient is introduced to a regimen that is designed to prevent recurrences of breath malodor. The purpose of the regimen is to mechanically remove surface plaque and pellicle so that all potentially accessible anaerobic sites in the mouth become exposed directly to the oxidizing effects of ClO2. Patients are instructed to brush their teeth, check, lips, and palate for 1 minute with 1/3 oz of an 8-ppm molecular ClO2 mouthrinse, such as ProFresh™ Mouthrinseb. This is followed by flossing, tongue cleaning of the posterior third of the dorsoposterior surface of the tongue with a tongue blade, and a final 30-second rinse, taking care to saturate the dorsoposterior surface of the tongue with the ClO2 mouthrinse. This regimen, performed once in the morning and again in the evening, is sufficient for nearly all individuals to maintain complete control of breath malodor 24 hours per day after undergoing the in-office antiseptic debridement and irrigation.
After treatment and maintenance instruction, patients are instructed to keep a log of organoleptic breath odor assessments performed by family members or friends at 2 or more randomly selected times each day for 2 to 4 weeks. This exercise is important for patients to “unlearn” previous, unreliable methods of breath odor self-assessment. Without such direct, cognitive feedback from other people, many patients cannot achieve confidence that their breath odor is controlled.
Two to 4 weeks after treatment, the patient returns for retesting under the same pretesting conditions that produced the greater level of breath malodor of the 2 visits. Attention is given to the time of day, time without food, drink, oral hygiene, and, for women, day of the menstrual cycle. The patient is instructed to bring the assessment log to this visit for review. If episodes of breath malodor persist after treatment, the log is helpful in determining the periodicity of such episodes so that appropriate alterations in the timing and/or frequency of the patient’s maintenance regimen can be recommended.
Results: Of the 2,837 patients who visited our clinic between February 1993 and February 1995, verifiable breath malodor was evident for 2,243. Because many of these patients traveled considerable distances to our clinic, we were unable to perform posttreatment assessments on all of them. Of the 923 patients who presented with verifiable breath malodor for whom posttreatment organoleptic and VSC assessments were performed, breath malodor was eliminated in 918 (99%) (Table 3). A patient was identified as having no breath malodor if all organoleptic assessment scores were below 1.0, all VSC measurements were below 180 ppb, tongue coating VSC generation time exceeded 60 minutes, and no reliable confirmation from a third party could be obtained.
When a posttreatment follow-up questionnaire was mailed to 1,343 patients between 4 and 20 weeks after in-office treatment, 1,047 (78%) indicated that they had experienced “significant improvement” in their breath odor as a result of treatment and maintenance. Another 243 (18%) indicated “somewhat improved” while 53 (4%) indicated “no improvement” (Table 4). Of the 53 who indicated no improvement, only 1 could provide reliable third-party confirmation of a persistence of breath malodor. Many of these patients received no in-office, posttreatment evaluation.
Conclusion: Bad breath is a major concern for many people. Because it nearly always originates in the mouth, it can and should be diagnosed and treated professionally by dentists. There is no known “stand-alone” product or solution for halitosis, nor do traditional standards of dental or periodontal care eliminate the problem. Recent developments in the understanding of the etiologies of breath malodor have spawned new techniques for its assessment and management. This article outlined a clinical protocol for diagnosing and treating chronic halitosis that is highly effective and reliable and consistently produces patient satisfaction.
- Tonzetich J: Production and origin of oral malodor. J Periodontal 28: 13-20, 1977.
- Prinz H: Offensive Breath. Its causes and prevention. Dent Cosmos 72: 700-707, 1930.
- Consumer Reports Sept. 1 992: 607- 10..
- Rosenberg M: Bad breath – Diagnosis and Treatment. University of Toronto Dental Journal 3-2: 7- 1 1 , 1990.
- Krieger E: Excell Survey No. J808. Media, PA, ICR Survey Research Group. pp 1 -4, Feb. 23, 1994.
- Lescher J: OCR Study No. 70403. Princeton, NJ , Opinion Research Corp. Jan. 1 9, 1995.
- Tonzetich J, Richter VJ: Evaluation of odiferous components of saliva. Arch Oral Biol 9: 39-45, 1964.
- Tonzetich J: Oral malodour: an indicator of health status and oral cleanliness.Int Dent J 28: 309-319, 1978.
- Tonzetich J, Preti G, Huggins,GR: Changes in concentration of Volatile Sulphur Compounds of mouth air during the menstrual cycle. J Int Med Res 6: 245-254, 1978.
- PretiG,Labows JN,Kostelc JG, Aldinger S, Daniele R: Analysis of lung air from patients with bronchogenic carcinoma and controls using gas chromatography-mass spectrometry. J Chromatogr 432: 1-1 1, 1988.
- Preti G, ClarkL, Cowart B J, Feldman R S,LowreyL D, Weber E, Young I M: Non-oral etiologies of oral malodor and altered chemosensation. J Periodontal 63: 790-796, 1992.
- Rosenberg M,Barki M, Portnoy S: A simple method for estimating oral microbial levels. J Microbiol Meth 9: 253 -256, 1989.
- Rosenberg M, Septon I, Eli F, Bar-Ness R,Gelemter I, Brenner S, Gabbay J: Halitosis measurement by an industrial sulphide monitor. Am J Periodontal 62: 487-489, 1991.
- Rosenberg M, McCullouch CAG: Measurements of oral malodor: current methods and future prospects. J Periodontal 63: 776-782, 1992
- YaegakiK, Sanada K: Volatile sulfur compounds in mouth air from clinically healthy subjects and patients with periodontal disease. J Periodont Res 27: 233-238, 1992.
- YaegakiK, SanadaK: Biochemical and clinical factors influencing oral malodor in periodontal patients. J Periodontol 63: 783-789, 1 992.
- Bosy A, Kulkarni GV, Rosenberg, M, McCullouch CAG: Relationship of oral malodor to periodontitis: evidence of independence in discrete subpopulations. J Periodontol 65: 37-46, 1994.
- Attia EL, MarshallKG. Halitosis: Can MedAssoc J 1 26: 128- 1 3 5, 1 982.
- McDowell J D, Kassenbaum. DK: Diagnosing and treating halitosis. JADA 1 24: 55-64, 1993.
- Lorber B, Bad breath: presenting manifestation of anaerobic pulmonary infection. Amer Rev Resp Dis1 1 2: 875-877, 1 975 .
- Chen S, Zieve L, Mahadeven V: Mercaptans and dimethyl sulfide in the breath of patients with cirrhosis ofthe liver. J Lab C/in Med 75: 628-63 5, 1976.
- Kostelc JG, PretiG, Zelson P R, BraunerL, Baehni P: Oral odors in early experimental gingivitis. J Perio Res 19 : 303-3 1 2, 1984.
- Coil, J M, Tonzetich J: Characterization of volatile sulfur compounds production at individual gingival cervicular sites in humans. J Clin Dent 3: 97-103, 1993.
- YaegakiK: Oral Malodor and Periodontal Disease. In Rosenberg M (ed): Bad Breath: Research Perspectives. Ramat Aviv, Israel, Ramot , pp 87- 108, 1995.
- Tonzetich J, Ng SK: Reduction of malodor by oral cleansing procedures. Oral Surg 42: 172-181, 1976.
- Jacobson S E, Crawford J J, McFall W R: Oral physiotherapy ofthe tongue and palate: Relationship to plaque control. JADA 87: 13 4-13 9, 1973.
- Gibbons RJ, Kapsimalis B, Socransky SS: The source of salivary bacteria. Arch Oral Bio 9: 101-103, 1964.
- Zambon JJ, Reynolds HS, Slots J: Black-pigmented Bacteroides spp . in the human oral cavity. Infect and lmmun 32: 1 98- 103, 1981.
- Van Winkelhoff AJ, Van der Velden U, Clement M, DeGraf J: Intra-oral distribution of black-pigmented Bacteroides species in periodontitis patients. Oral Microbiol lmmunol 3: 83-85, 1988.