Halitosis

Offensive breath odour. It is a common complaint with a well defined and largely treatable set of causes, and the clinical failure in this area is the tendency to dismiss it as trivial when it produces genuine social withdrawal, occupational difficulty and psychological distress.

Biochemistry

Odour arises predominantly from volatile sulphur compounds produced by anaerobic Gram negative bacteria degrading sulphur containing amino acids:

• Hydrogen sulphide, from cysteine, with the smell of rotten eggs.
• Methyl mercaptan, from methionine, with the smell of decaying cabbage, which is the compound most strongly associated with periodontal disease.
• Dimethyl sulphide, which is the predominant compound in extraoral and blood borne halitosis, and which is therefore a diagnostic pointer when it dominates.

Other contributors include cadaverine, putrescine, indole, skatole and short chain fatty acids including butyric and propionic acid.

The organisms responsible are anaerobes including Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, Treponema denticola, Tannerella forsythia and Solobacterium moorei.

Classification

• Genuine halitosis, subdivided into:
• Physiological halitosis: morning breath and hunger breath, resulting from reduced salivary flow and increased bacterial metabolism overnight, which resolves with eating and oral hygiene and is not pathological.
• Pathological halitosis, oral in origin, which accounts for 85 to 90 percent of genuine halitosis.
• Pathological halitosis, extraoral in origin, accounting for 10 to 15 percent.
• Pseudohalitosis: the patient believes they have halitosis but it cannot be demonstrated objectively, and they accept reassurance and objective evidence.
• Halitophobia: persistent belief in halitosis despite objective evidence to the contrary and despite treatment and reassurance. This is a psychiatric condition on the spectrum of olfactory reference syndrome and body dysmorphic disorder, and it requires psychiatric rather than dental or otolaryngological management. Repeatedly investigating and treating these patients reinforces the belief and causes harm.

Causes

Oral, 85 to 90 percent:

• Tongue coating, which is the single largest contributor. The posterior dorsum of the tongue has a large surface area with papillary crypts harbouring anaerobes, desquamated epithelium and food debris.
• Periodontal disease and gingivitis, with periodontal pockets providing an anaerobic environment.
• Dental caries and food impaction.
• Pericoronitis around partially erupted third molars.
• Necrotising ulcerative gingivitis, which produces a characteristic and intense foetor.
• Dry socket after extraction.
• Ill fitting or unclean dentures and orthodontic appliances.
• Xerostomia from drugs, radiotherapy, Sjögren syndrome, mouth breathing and dehydration.
• Oral candidiasis.
• Oral malignancy with necrotic tissue.

Otolaryngological:

• Tonsilloliths and chronic cryptic tonsillitis, which are a specific and frequently overlooked cause.
• Chronic rhinosinusitis with postnasal purulent discharge.
• Nasal foreign body, particularly in a child with unilateral foul discharge.
• Atrophic rhinitis with crusting.
• Nasopharyngeal and oropharyngeal malignancy with necrosis.
• Adenoiditis.
• Zenker diverticulum, in which retained decomposing food produces halitosis together with dysphagia and regurgitation.

Gastrointestinal:

• Gastro oesophageal reflux disease and laryngopharyngeal reflux.
• Helicobacter pylori infection, whose contribution is debated but which is worth treating where present with other indications.
• Achalasia and oesophageal stricture with food retention.
• The general belief that halitosis commonly originates in the stomach is largely wrong. The oesophagus is normally collapsed, and gastric gas reaches the mouth only on belching. Attributing halitosis to the stomach without evidence delays the correct diagnosis.

Systemic and blood borne, in which the odorant is carried in the blood and excreted through the lungs. These characteristically produce dimethyl sulphide and are unaffected by oral hygiene measures:

• Diabetic ketoacidosis, with a sweet acetone odour.
• Uraemia in chronic kidney disease, with an ammoniacal fishy odour.
• Hepatic failure, with foetor hepaticus described as sweet and musty.
• Trimethylaminuria, that is fish odour syndrome, a metabolic disorder with a defect in flavin containing monooxygenase 3, producing a fishy odour in breath, sweat and urine.
• Bronchiectasis, lung abscess and empyema.
• Certain foods and drugs: garlic, onion, alcohol, dimethyl sulphoxide, disulfiram, and drugs causing xerostomia.

• Bad breath reported by the patient, or more often by a family member, partner or colleague. The source of the complaint matters diagnostically: halitosis reported only by the patient, with no confirmation from others, raises the possibility of pseudohalitosis or halitophobia.
• Bad taste, which frequently accompanies genuine halitosis.
• Social avoidance, covering the mouth when speaking, excessive use of mints and mouthwash, and reluctance to be close to others.
• Anxiety and depression, which may be secondary to the halitosis or, in halitophobia, primary.

History that directs investigation

• Who noticed it, and has anyone else confirmed it.
• Duration, timing through the day, and relation to meals, hunger and sleep.
• Oral hygiene practices including frequency of brushing, interdental cleaning and tongue cleaning.
• Dental history, dentures, and time since the last dental visit.
• Nasal and sinus symptoms, tonsilloliths, and recurrent sore throats.
• Reflux symptoms, dysphagia and regurgitation.
• Systemic symptoms and known renal, hepatic, respiratory and metabolic disease.
• Medication list, with attention to xerostomia inducing agents: anticholinergics, antidepressants, antihistamines, antipsychotics, diuretics and antihypertensives.
• Smoking, alcohol and dietary habits.
• Psychiatric history and the degree of preoccupation with the symptom.

Examination

• Full oral examination including the tongue dorsum with attention to coating, the periodontium, all teeth, the dentures and the fitting surfaces.
• Tonsils examined for cryptic debris and tonsilloliths, with gentle pressure on the anterior pillar to express material.
• Nasal examination and flexible nasoendoscopy in adults, assessing the nasopharynx, postnasal space, hypopharynx and larynx. This step is essential and is frequently skipped, and it is what identifies sinus disease, tonsilloliths, malignancy and a foreign body.
• Assessment of salivary flow and the salivary duct orifices.
• General examination directed by the history.

• Organoleptic assessment, which remains the reference standard. The examiner smells the patient's exhaled breath at a distance of around 10 cm through a tube, scoring intensity on a 0 to 5 scale. Compare mouth breath with nose breath: odour predominantly from the mouth indicates an oral or oropharyngeal source; odour predominantly from the nose indicates a nasal or sinus source; equal odour from both indicates a systemic or blood borne source. This simple comparison is the single most useful discriminating test and requires no equipment.
• Patients should avoid eating, drinking, smoking, oral hygiene products and scented cosmetics for at least 2 to 3 hours before assessment, and should avoid antibiotics for 3 weeks and garlic, onion and spicy food for 48 hours.
• Portable sulphide monitors, which quantify total volatile sulphur compounds, giving an objective and reproducible measure that is particularly useful for demonstrating absence of odour to a patient with suspected pseudohalitosis.
• Gas chromatography, which separates and quantifies individual compounds, and which is the definitive method. A dimethyl sulphide predominant pattern points strongly to an extraoral or blood borne source.
• Tongue coating index, scoring coating across the tongue dorsum.
• Periodontal assessment with probing depths, bleeding on probing and radiographs, by a dentist.
• Full blood count, glucose and HbA1c, renal function, liver function.
• Helicobacter pylori testing where there are dyspeptic symptoms.
• Sinus computed tomography where sinusitis is suspected.
• Upper gastrointestinal endoscopy or a barium swallow where dysphagia, regurgitation or a pharyngeal pouch is suspected.
• Chest imaging where bronchiectasis or lung abscess is possible.
• Urinary trimethylamine to creatinine ratio after a choline load where trimethylaminuria is suspected.
• Psychiatric assessment where halitophobia is suspected.

The great majority is oral in origin and responds to mechanical measures. Antimicrobial mouthwashes alone, without mechanical debridement, fail.

Tongue cleaning, which is the highest yield single intervention

• Clean the posterior dorsum of the tongue daily using a tongue scraper, which is more effective than a toothbrush and provokes less gagging.
• Scrape from posterior to anterior with light pressure, repeated 5 to 10 times, rinsing between strokes.
• Reach as far posteriorly as tolerated, since the posterior third harbours most of the coating and is the part usually missed.
• Explain and demonstrate the technique, since patients who are simply told to clean their tongue generally clean only the anterior visible part, which achieves little.

Oral hygiene and dental treatment

• Twice daily brushing with a fluoride toothpaste, and daily interdental cleaning with floss or interdental brushes.
• Professional scaling, root planing and periodontal treatment for periodontal disease, which produces substantial improvement.
• Treat caries, extract unrestorable teeth, and address food traps and overhanging restorations.
• Denture hygiene: remove overnight, clean daily, soak in chlorhexidine 0.2 percent or dilute hypochlorite for acrylic dentures, and assess fit.
• Treat pericoronitis, with extraction of the impacted tooth where recurrent.
• Treat oral candidiasis.

Antimicrobial adjuncts

• Chlorhexidine gluconate 0.12 to 0.2 percent mouthwash, 10 mL twice daily, which is the most effective antimicrobial mouthwash. Warn about tooth staining, taste disturbance and, with prolonged use, calculus formation. Use for defined periods rather than indefinitely.
• Cetylpyridinium chloride mouthwash.
• Zinc containing mouthwashes and toothpastes, which chemically neutralise volatile sulphur compounds by forming insoluble sulphides. Combined zinc and chlorhexidine preparations are more effective than either alone.
• Chlorine dioxide and sodium chlorite rinses, which oxidise sulphur compounds.
• Essential oil mouthwashes.
• Avoid alcohol containing mouthwashes in patients with xerostomia, since they worsen dryness and therefore worsen halitosis.
• Mints and chewing gum give brief masking only; sugar free gum has some benefit by stimulating salivary flow.

Management of xerostomia

• Frequent sips of water, sugar free gum, saliva substitutes and gels.
• Review and substitute xerostomia inducing medications where feasible.
• Pilocarpine 5 mg three times daily where there is residual gland function, with attention to contraindications including asthma, chronic obstructive pulmonary disease, bradycardia and narrow angle glaucoma.
• Treat Sjögren syndrome with rheumatology involvement.

Otolaryngological causes

• Tonsilloliths: oral irrigation with a water flosser directed at the crypts, salt water gargles, and manual expression. Laser or coblation cryptolysis under local anaesthesia for persistent cases. Tonsillectomy where conservative measures fail and the tonsils are demonstrably the source, with the important caveat that dental and tongue causes must be excluded and treated first, since tonsillectomy performed for halitosis of dental origin fails and leaves a dissatisfied patient who has undergone a painful operation for nothing.
• Chronic rhinosinusitis: intranasal corticosteroid, saline irrigation, antibiotics for exacerbations, and endoscopic sinus surgery for medically refractory disease.
• Nasal foreign body: removal.
• Atrophic rhinitis: alkaline nasal irrigation, emollients and glucose in glycerine drops.
• Zenker diverticulum: endoscopic stapling or laser cricopharyngeal myotomy with diverticulotomy, or open diverticulectomy with myotomy.
• Malignancy: oncological management.

Systemic causes

• Optimise diabetes control.
• Manage renal and hepatic disease.
• Treat bronchiectasis and lung abscess.
• Trimethylaminuria: dietary restriction of choline, carnitine, trimethylamine N oxide and lecithin, avoiding eggs, offal, seafood and legumes; low dose metronidazole or neomycin to reduce gut bacterial trimethylamine production; riboflavin supplementation to maximise residual enzyme activity; and acidic soaps and lotions to trap trimethylamine on the skin. Genetic counselling and psychological support are important, since the condition is lifelong and socially disabling.
• Reflux: proton pump inhibitor such as omeprazole 20 mg twice daily for 8 to 12 weeks with lifestyle modification, and alginates after meals.

Pseudohalitosis and halitophobia

• For pseudohalitosis, provide objective evidence with organoleptic scoring and sulphide monitoring, explain the results, reinforce normal oral hygiene, and most patients accept the reassurance.
• For halitophobia, recognise it and stop investigating. Repeated tests, mouthwashes, antibiotics and surgery reinforce the belief and cause harm. Refer for psychiatric assessment, since the condition responds to cognitive behavioural therapy and to selective serotonin reuptake inhibitors, and it sits within the olfactory reference syndrome and body dysmorphic disorder spectrum.
• Handle the referral carefully and without dismissiveness, since these patients are genuinely distressed and often have long histories of feeling disbelieved. Frame it as treatment for the distress rather than as a statement that the problem is imaginary.

Follow up

Review at 4 to 6 weeks with repeat organoleptic and sulphide assessment to demonstrate objective improvement, which is both a clinical measure and a therapeutic reassurance. Persistent halitosis after adequate oral treatment requires reassessment for an extraoral source, with particular attention to the nose, sinuses, tonsils, pharyngeal pouch and systemic disease.