Halitosis

BY:

Amir A. Kargoshaie Assistant professor of otorhinolaryngology Isfahan university of medical sciences

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Oral Malodor 4 Classes…. 3 Sub-types

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Above Carina (URTI’s) Below Carina (LRTI’s)-

STOMATODYSODIA OZOSTOMIA

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HALITOSIS:

i) Physiological ii) Pathological iii) Psychological

FETOR EX ORE/ FETOR ORIS:

Oral Hygiene, Perio, and Decay

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Breath odor the subjective perception after smelling someone’s breath

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pleasant, unpleasant, or even disturbing, if not repulsive

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. If unpleasant, the terms breath malodor, halitosis, bad breath, or fetor ex ore can be applied. not synonymous with oral malodor. This term is restricted to halitosis with an origin in the oral cavity.

three main categories of halitosis:

genuine halitosis pseudo-halitosis halitophobia

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Genuine halitosis

when the breath malodor really exists and can be diagnosed organoleptically or by measurement of the responsible compounds.

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physiologic halitosis

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The transient disturbing odor caused by food intake (e.g., garlic, onions, and certain spices), smoking, or medication (e.g., metronidazole) do not reveal a health problem and are common examples of physiologic halitosis.

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The same is true for “morning” bad breath, as habitually experienced on awakening. This malodor is caused by a decreased salivary flow and increased putrefaction during the night and spontaneously disappears after breakfast or after oral hygiene measures.

pathologic halitosis . A persistent breath malodor, reflect s some pathology

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The causes of this will be discussed later

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pseudo-halitosis

. When an obvious breath malodor cannot be perceived, but the patient is convinced that he or she suffers from it,

halitophobia,

If the patient still believes that there is bad breath after treatment of genuine halitosis or diagnosis of pseudo-halitosis, is a recognized psychiatric condition.

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OZOSTOMIA

… above carina

[G. ozo, to smell, + stoma, mouth]

• Obstruction, Nasal discharge, Tonsillitis, Tonsoliths, Laryngitis, • Dysphagia, Voice problems • Previous ENT pathology • Sinusitis, Rhinitis, Pharyngitis, Foreign Bodies • Stagnation and Infection • Malignancies

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STOMATODYSODIA

…below carina • Tobacco Smokers • Bronchitis • Bronchiectasis • Lung Abscess • Pleuritis • Pneumonia • Blood • Foreign Body • Neoplasia, Mucous Stagnation/Infection

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HALITOSIS

physiological • Poor hydration • Menstruation • Diet • Constipation • Starvation, Morning breath • Habits (Mouth breathing, thumb sucking)

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HALITOSIS

pathological

• Lungs release blood-borne catabolic products • Stomach--Gastritis, Liver hepatitis, Kidney nephritis • Pancreas--Diabetes mellitus (Ketosis) • Anorexia/Bulimia nervosa • IgA deficiency • Xerostomia (Sjogrens, Radiation therapy, Stress) 10

HALITOSIS

psychological • “Halitophobia” not very accurate term • Delusional cacosmia • Psychogenic dysosmia • Symptomatic schizophrenia • Temporal lobe epilepsy (Aura) • Cerebral tumors

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Fetor ex Ore/ Fetor Oris

• From Mouth: Gums &Teeth • Gingivitis/Periodontitis • Percoronitis/Peri-implantitis • Dorsum of tongue • Interdental areas • ANUG/NUG • Post-extraction, Dry socket • Plaque & Calculus Oral Hygiene, Stagnation areas • Caries: Tooth decay • Brushing and Flossing • Reduced salivary flow • Faulty fillings, Overhangs • Dental materials • Cements: Eugenol, Cajeput, Creosote, Kri3 • Fixed bridgework, Pontics • Appliances– Orthodontic, Prosthodontic • Denture hygiene • Oral medicine conditions • Ulcerations, Abrasions, Wounds • Neoplasias • Hemorrhagic diatheses 12

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Epidemiology Breath malodor is a common complaint among the general population .(as high as 50% in some articles) It has a significant socioeconomic impact but unfortunately has been neglected until recently by scientists and clinicians hardly covered in the medical curricula Halitosis can lead to personal discomfort and social embarrassment, and is still one of the biggest taboos of society. Almost $1 billion a year is spent in the United States on deodorant-type mouth (oral) rinses, mints, and related over-the-counter products to manage bad breath.

It would be preferable to spend this money on a proper diagnosis and etiologic care instead of short-term and even inefficient masking attempts.

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Etiology In the vast majority, breath malodor originates from the oral cavity. Gingivitis, periodontitis, and especially tongue coating are the predominant causative factors.

In general, one can identify two pathways for bad breath. The first one involves an increase of certain metabolites in the blood circulation (e.g., due to a systemic disease), which will escape via the alveoli of the lungs during breathing (blood breath exchange) and it is commonly referred as “ extraoral halitosis .” The second pathway (intraoral halitosis ) involves an increase of either the bacterial load or the amount of substrate for these bacteria at one of the lining surfaces of the oropharyngeal cavity, the respiratory tract, or the esophagus. All types of infections, ulcerations, or tumors at one of the previously mentioned areas can thus lead to bad breath. Studies also suggest that oral malodor is associated with the total bacterial load of anaerobic bacteria in both saliva and tongue coating.

The most commonly involved bacteria are Porphyromonas gingivalis, Prevotella

intermedia/nigrescens, Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Campylobacter rectus, Fusobacterium nucleatum, Peptostreptococcus micros, Tannerella forsythia, Eubacterium spp, and spirochetes.

A study conducted by Niles and Gaffar made clear that these gram-negative species in particular cause an unpleasant smell by the production of sulfur compounds .

However, because of the large species diversity found in patients with halitosis, it can be suggested that breath malodor is the result of complex interactions between several bacterial species. A recent study indicates that some gram-positive microorganisms, such as Streptococcus salivarius, also contribute to oral malodor

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production by deglycosylating salivary glycoproteins, thus exposing their protein core to further degradation by gram-negative microorganisms.

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There are few studies that document the prevalence of oral malodor. Moreover, the studies that exist used different methodologies ranging from self-reported breath malodor to more objective assessments such as the measurement of the volatile sulfur compounds (VSCs). Because self reported halitosis correlates weakly with objective measurements and tends to overestimate the problem, data should be interpreted carefully.

The incidence of halitosis remains poorly documented in most countries. Large-scale studies have been performed for the Japanese,Swedish,and Chinese populations.

Smaller investigations in Brazilian,Polish,and Israeli habitants have also been reported.

Despite the different approach of each study, if a VSC level of 75 ppb (limit for social acceptance) is used as a threshold for halitosis, the prevalence reported in the different populations can be calculated as 23% (late-morning group) and 20% for the Japanese and Chinese studies, respectively. In line with this, prevalences of 27.5% and 29.8% for the Chinese and the Israeli groups, respectively, can be calculated when an organoleptic score of at least 2 is considered as being representative for halitosis. With the same criterion, the calculated prevalence varied between 11.0% and 29.7% for the different age groups in the Polish population. In conclusion, independent of the method used to assess oral malodor and independent of the study population, the results point out that about one in four subjects suffer from persistent bad breath.

From large-scale inventories in multidisciplinary outpatient clinics for breath odor, no gender predominance seems to exist for bad breath, although other studies indicate a higher prevalence in women .

It has also been observed that women seek treatment more often than men.

Age can range from 5 years to more than 80 years. No association was found between increased age and oral malodor.

Most of the patients had been complaining about breath malodor for several years before seeking proper advice (recent report of the department involving 2000 patients).

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A recent large-scale study including 2000 patients with halitosis complaints showed that for those where bad breath could be objectively detected, the cause of it was mostly found within the oral cavity (90%) . Tongue coating (51%), gingivitis/periodontitis (13%), or a combination (22%) accounted for the majority of the cases.

Because a large part of the population has a tongue coating or gingivitis/periodontitis, there is a risk that an intraoral condition is too easily considered as the cause while more important pathologies are overlooked. Indeed, for a minority of patients (4% in the same recent study), extraoral causes could be identified, including ear-nose-throat (ENT) pathologies, systemic diseases (e.g., diabetes), metabolic or hormonal changes, hepatic or renal insufficiency, bronchial and pulmonary diseases, or gastroenterologic pathologies.

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Recently, the presence of Solobacterium moorei, a gram positive

bacterium, has also been linked to oral malodor.

For oral malodor, the unpleasant smell of the breath mainly originates from volatile sulphur compounds (VSCs), especially hydrogen sulfide (H2S), methylmercaptan (CH3SH), and (less significantly) dimethyl sulfide [(CH3)2S], as first discovered by Tonzetich.

However, in certain conditions (e.g., when the saliva dries out on the mucosal surfaces), other compounds in mouth air may also play a role such as diamines (e.g., putrescine, cadaverine), indole, skatole, and volatile organic acids like butyric or propionic acid.

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Most of these compounds result from the proteolytic degradation by oral microorganisms of peptides present in saliva (sulfurcontaining or non –sulfur-containing amino acids) ,shed epithelium, food debris, gingival crevicular fluid (GCF), interdental plaque, postnasal drip, and blood. In particular, gram negative, anaerobic bacteria possess such proteolytic activity.

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Proteolytic degradation by oral microorganisms of four amino acids (two containing sulfur and two not containing sulfur) to malodorous compounds.

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For the extraoral causes of halitosis, other compounds besides the VSCs may be involved.

Bad-smelling metabolites can be formed/absorbed at any place in the body (e.g., the liver, the gut) and transported by the bloodstream to the lungs. Exhalation of these volatiles in the alveolar air then causes halitosis, at least when the concentrations of the bad-smelling metabolites are sufficiently high. The crevicular fluid reflects the circulating molecules in the blood and can thus also play a relevant role but due to the small amount probably not a very dominant one. The extraoral causes are much more difficult to detect, although they can sometimes be recognized by a typical odor. Uncontrolled diabetes mellitus can be associated with a sweet odor of ketones, liver disease can be revealed by a sulfur odor, and kidney failure can be characterized by a fishy odor because of the presence of dimethylamine and trimethylamine.

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In a special patient category, subjects imagine they have breath malodor; this is called imaginary breath odor or

halitophobia.

The latter has been associated with obsessive-compulsive disorders and hypochondria. Well-established personality disorder questionnaires (e.g., Symptom Checklist 90) allow the clinician to assess the patient’s tendency for illusional breath malodor.

The presence of a psychologist or psychiatrist at the malodor consultation can be especially helpful for such patients. Because of the complexity of this pathology, a malodor consultation is thus preferably multidisciplinary, combining the knowledge of a periodontologist or dentist, an ENT specialist, an internist (if necessary), and a psychologist or psychiatrist. In a recent study of 2000 patients, 16% were diagnosed with pseudo-halitosis or halitophobia.

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Biological Sources of Oral Malodor

• BLOOD • NECROSIS • PUS • MUCOUS • BACTERIA

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Oral Malodor

Volatile Sulfur Compounds

• VSC mainly responsible for stench • Measure with the Halimeter

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• VSC’s include hydrogen sulfide, methyl mercaptan, and dimethyl sulfide

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Oral Malodor CLINICAL

Management I

• Full comprehensive Oral Examination • Detect, record all gingival problems • Gingivitis and Periodontitis • Scale and Polish: Root Planing; Pocket elimination • Restore faulty restorations • Oral Hygiene PIx<10% • Recall: re-measure VSC’s • Outcome analysis: Results/Proof 23

Oral Malodor CLINICAL

Management II

• OHI: Brushing, Flossing, Gargle, Rinse • Teeth, Gums, Tongue, Tonsils, pharynx • Prosthesis: Hygiene, Repair, or Replace • Remove all plaque 24

Oral Malodor CLINICAL

Management III

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Floss Anti-bacterial Paste Peroxide paste Bicarbonate of Soda Paste Tongue scraper - Commercial vs Spoon Pre-sleep Oral Hygiene

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Intraoral Causes

Tongue and Tongue Coating. The dorsal tongue mucosa, with an area of 25 cm , shows a very irregular surface topography.

The posterior part exhibits a number of oval cryptolymphatic units, which roughen the surface of this area. The anterior part is even rougher because of the high number of papillae: the filiform papillae with a core of 0.5 mm in length, a central crater and uplifted borders; the fungiform papillae, 0.5 to 0.8 mm in length; the foliate papillae, located at the edge of the tongue, separated by deep folds; and the vallate papillae, 1 mm in height and 2 to 3 mm in diameter. These innumerable depressions in the tongue surface are ideal niches for bacterial adhesion and growth, sheltered from cleaning actions.

Moreover, desquamated cells and food remnants also remain trapped in these retention sites and consequently can be putrefied by the bacteria.

A fissurated tongue (deep fissures on dorsum, also called scrotal

tongue or lingua plicata) and a hairy tongue (lingua villosa) have an even rougher surface

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The accumulation of food remnants intermingled with exfoliated cells and bacteria forms a coating on the tongue dorsum. The latter cannot be easily removed because of the retention offered by the irregular surface of the tongue dorsum . As such, the two factors essential for putrefaction are united. Several investigators have identified the dorsal posterior surface of the tongue as the primary source of breath malodor.

Indeed, high correlations have been reported between tongue coating and odor formation.

Both in healthy individuals and periodontitis patients with or without complaints of oral halitosis, a significant positive correlation was found between the presence or amount of tongue coating and levels of VSCs and/or organoleptic scores of the mouth odor.

In a group of 2000 patients visiting a multidisciplinary halitosis clinic, significant correlations were found between the organoleptic scores and tongue coating (R = 0.52; p < 0.001). In another study,it was also observed that the amount of tongue coating was significantly greater in the halitosis-positive group compared to the halitosis-negative group.

Morita and Wang found that the volume of tongue coating and the percentile of sites with bleeding on probing, were significantly associated with oral malodor.

In 1992, Yaegaki and Sanada demonstrated that, even in patients with periodontal disease, 60% of the VSCs were produced from the tongue surface.

Recent research showed that the strongest determinant for the presence of tongue coating is suboptimal oral hygiene. Other influencing factors were: periodontal status, presence of a denture, smoking, and dietary habits.

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Different clinical pictures of heavily coated tongues

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Periodontal Infections. A relationship between periodontitis and oral malodor has been shown. However, not all patients with gingivitis and/or periodontitis complain about bad breath, and there is some disagreement in the literature as to what extent oral malodor and periodontal disease are related.

Bacteria associated with gingivitis and periodontitis are indeed able to produce VSCs.

Several studies have shown that the VSC levels in the mouth correlate positively with the depth of periodontal pockets (the deeper the pocket, the more bacteria, particularly anaerobic species) and that the amount of VSCs in breath increases with the number, depth, and bleeding tendency of the periodontal pockets.

It is important to realize that VSCs aggravate the periodontitis process by, for example, increasing the permeability of the pocket and mucosal epithelium and therefore exposing the underlying connective tissues of the periodontium to bacterial metabolites. Moreover, methylmercaptan enhances interstitial collagenase production, interleukin-1 (IL-1) production by mononuclear cells, and cathepsin B production, thus further mediating connective tissue breakdown.

It was also shown that human gingival fibroblasts developed an affected cytoskeleton when exposed to methylmercaptan.

The same gas alters cell proliferation and migration. VSCs are also known to impede wound healing. Thus, when periodontal surgery is planned, especially the

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Some studies, however, have shown that when the presence of tongue coating is taken into account, the correlation between periodontitis and oral malodor is much lower, indicating that tongue coating remains a key factor for halitosis. The prevalence of tongue coating is six times higher in patients with periodontitis, and the same bacterial species associated with periodontal disease can also be found in large numbers on the dorsum of the tongue, particularly when tongue coating is present.

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The reported association between periodontitis and oral malodor may thus primarily be due to the effects of periodontal disease on tongue coating. And may explain why other articles did not find a correlation.

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Other relevant malodorous pathologic manifestations of the periodontium are pericoronitis (the soft tissue “cap” being retentive for microorganisms and debris), major recurrent oral ulcerations, herpetic gingivitis, and necrotizing gingivitis/periodontitis. Microbiologic observations indicate that ulcers infected with gramnegative anaerobes (i.e., Prevotella and

Porphyromonas species) are significantly more malodorous than noninfected ulcers.

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Dental Pathologies

. Possible causes within the dentition are deep carious lesions with food impaction and putrefaction, extraction wounds filled with a blood clot, and purulent discharge leading to important putrefaction. The same applies to interdental food impaction in large interdental areas and crowding of teeth favor food entrapment and accumulation of debris. Acrylic dentures, especially when kept continuously in the mouth at night or not regularly cleaned, can also produce a typical smell. The denture surface facing the gingiva is porous and retentive for bacteria, yeasts, and debris, which are compounds needed for putrefaction.

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Dry Mouth.

Saliva has an important cleaning function in the oral cavity. Patients with xerostomia often present with large amounts of plaque on teeth and an extensive tongue coating. The increased microbial load and the escape of VSCs when saliva is drying up explain the strong breath malodor.

• Several studies link stress with VSC levels, but it is not clear whether this can simply be explained by a reduction of salivary flow.

• Other causes of xerostomia are medication, • alcohol abuse, • Sjögren syndrome (a common autoimmune rheumatic disease), • and diabetes.

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Extraoral Causes

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Ear-Nose-Throat. During chronic or purulent tonsillitis, the

• deep crypts of the tonsils accumulate debris and bacteria, especially periopathogens, resulting in putrefaction. In the crypts, even calculus (e.g., subgingivally) can be formed (tonsilloliths or tonsil stones). Other examples include acute pharyngitis (viral or bacterial) and postnasal drip. The latter is a rather common condition, which is perceived by patients as a liquid flow in the throat, originating from the nasal cavity.

• It is often associated with chronic sinusitis or regurgitation esophagitis, in which the acidic content of the stomach reaches the nasopharynx and causes mucositis. Ozena (caused by

Klebsiella ozaenae) is a rare atrophic condition of the nasal mucosa, with the

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Bronchi and Lungs. Pulmonary causes include chronic bronchitis, bronchiectasis (infection of standing mucus secretion in cystic dilations through walls of bronchioles), pneumonia, pulmonary abscesses, bronchial carcinoma, and carcinoma of the lung.

• The relevance of an early diagnosis is evident.

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Gastrointestinal Tract. In contrast to the common public opinion, even among medical physicians, gastrointestinal pathologies are rarely responsible for bad breath.

• The following pathologies might be responsible for less than 1% of malodor cases: • • • • • •

• A Zenker diverticulum (a hernia in the esophageal wall, allowing accumulation of food and debris and thus putrefaction) can cause a significant breath odor because it is not separated from the oral cavity by any sphincter.

• A gastric diaphragmatic hernia (the fundus of the stomach protrudes through the diaphragm with relative sphincter insufficiency, allowing gases to escape or contents to flow back in the esophagus) can cause reflux of the gastric contents up to the oropharynx. This is sometimes combined with ructus, in which air from the stomach suddenly regurgitates.

• Regurgitation esophagitis (ulceration of the mucosal lining of the esophagus by acidic stomach contents flowing back because of an improper function of the sphincter).

• Intestinal gas production: Some gases (e.g., dimethyl sulfide) are absorbed but not metabolized by the intestinal endothelium and thus transported by the blood. These gases can then be exhaled through the lungs.

There is some disagreement in the literature whether Helicobacter pylori infection is

associated with halitosis.

In a recent paper, H. pylori was shown to produce hydrogen sulfide and

methylmercaptan, which suggests that this microorganism can contribute to the development of halitosis.

Tangerman et alfound no association between halitosis and H. pylori infection.

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Liver. Patients with various degrees of hepatocellular failure and/ or portosystemic shunting of blood may acquire a sweet, musty, or even slightly fecal aroma of the breath, termed fetor hepaticus, which has been

mainly attributed to the accumulation of dimethyl sulfide.

• Moreover, if the metabolizing function of the liver fails, the concentration of certain metabolites, normally processed in the liver, will increase and they will enter the systemic circulation again and will be exhaled.

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Kidney. Kidney insufficiency, primarily caused by chronic glomerulonephritis, will lead to an increase of the amines dimethylamine and trimethylamine, which causes a typical fishy odor of the breath.

Systemic Metabolic Disorders. Uncontrolled diabetes mellitus results in the accumulation of ketones, which have a sweet smell, like the odor of rotten apples. Insulin resistance leads to an increase of triglycerides and free fatty acids and ketones (such as acetone, acetoacetate, and hydroxybutyrate) are formed during lipolysis.

Trimethylaminuria. Trimethylaminuria is a hereditary metabolic disorder that leads to a typical fishy odor of the breath, urine, sweat, and other bodily secretions. Trimethylaminuria is an enzymatic defect that prevents the transformation of trimethylamine to trimethylaminoxide, resulting in abnormal amounts of this molecule. The prevalence is unknown but approaches 1% in the United

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Kingdom.

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Hormonal Causes. At certain moments during the menstrual cycle, a typical breath odor can develop; partners are often well aware of this odor. Evidence also indicates that VSC levels in the expired air are increased twofold to fourfold around the day of ovulation and in the perimenstrual period. Increases in VSCs are smaller in midfollicular phases.

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In a study by Kleinberg and Codipilly, aqueous solutions of oral odoriferous volatiles were placed on the skin of the back of the hand.

Afterwards, odor scores were given (organoleptic score, cfr. supra). The results are shown in Table 52-2. All metabolites caused an explicit odor, which decreased in intensity over time. Some molecules disappeared very fast (e.g., hydrogen sulfide and methylmercaptan), whereas others produced a bad smell for a longer period of time (e.g., indole and skatole, for 10 minutes and longer).

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The olfactory response, rated by an organoleptic scale, follows an exponential curve when correlated with the concentration of different gases. In other words, when the concentrations of the molecules were compared to their organoleptic outcome, an optimal fit was only obtained when the concentrations of the gases were transformed to log values. The latter implies that all types of breath “measurements” (gas chromatography [GC], portable breath analyzers [e.g., Halimeter]) require log transformation to be comparable with organoleptic scores.

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Oral Malodor CLINICAL

Management VI

• Rectify URT and LRT • Treat systemic disease Diabetes, Hypertension, CCF • Oral Health: Teeth and Gum problems cause >90% cases of oral malodor • Keep records • Record on VAS scales • Note measures of VSC • Educate the patient 42

OM CLINICAL

Management VII

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Medicinal

Oral Irrigation A

Mouthwash

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Physiological

• Short-term for specific effect • Associated risks • Daily use • Long tem • Examples: Peridex (Chlorhexidine gluconate); Phenol Based with oils (Listerine); Cetyl-pyridinium Cl (Cepacol) Chlorine dioxide, herbal remedies, etc.

• Minimal side effects if any • Physiological substances: Examples: Salt, Bicarbonate of soda, Urea crystals • Fluoride rinse: correct • Side effects: staining, taste changes, toxicity, overgrowth of bacteria, fungi etc.

physiological concentration 1ppm 43

OM CLINICAL

Management VIII Saline Mouthwash &

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PREPARATION:

• NaCl common Table Salt • Hypertonic solutions: stir one teaspoonful of salt in about 300ml water.

• Salt should remain at base of glass=Saturated solution  hypertonic • Freshly prepared for each use.

• Not costly; available

Gargle

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MODE OF ACTION

• Hypertonicity dehydrates bacteria  bacteriostatic initial  then bacteriocidal • Edema: Swollen Cells are reduced • Saline debridement of tonsillar crypts • Washes and irrigates mucous membranes; mucolytic • Slows inflammation 44

Oral Malodor Clinics

• Part of Practice: NOT isolated • Must have accurate clinical measuring devices- Halimeter ® (VSC’s ppb) • Must have ALL oral therapeutic back-up • Refer and COMMUNICATE • Clinical Protocol: Quote fees • Examinations, Radiographs, Bacteriology, Histopathology, Periodontics, Endodontics, Restorative, Prosthodontics, Otolaryngology, Psychological referrals • Written Report Mandatory 45