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The chemosensory functions of taste and smell play avital role in human physiology. They determine the fla-vor and palatability of foods and beverages, the selec-tion of nutrients essential for life, and the warning offire, toxic vapors, and spoiled foodstuffs. The hedonicrole of chemosensation is experienced daily by every-one. Alterations in these pleasurable sensations haveserious implications for the preservation of oral and sys-temic health, with dramatic effects on quality of life.

Chemosensory disorders can be caused by a varietyof oral conditions, upper respiratory tract problems,peripheral or central nervous system (CNS) pathologies,systemic complications, and other factors (aging, circa-dian variations, menses, and pregnancy). Many patientsinitially complain to their dentist of altered taste orsmell. Unfortunately, it is difficult to diagnose manychemosensory disorders, and occasionally no effectivetreatment can be found. However, oral health practi-tioners can assess smell and taste function, identify andtreat disorders with orofacial causes, and refer patientsto other medical providers when appropriate.

When eating, smell is first perceived through thenasal passages before food is placed into the mouth.Taste is then perceived when food comes in contact withtaste receptors located throughout the mouth. A secondsmell perception occurs retronasally via the nasopharynxas the food bolus is chewed and swallowed. Trigeminalstimulation (pain, tactile, temperature) contributes toflavor perception throughout the eating process.

Smell and taste disorders are common in the generalpopulation, although accurate epidemiologic informa-tion is lacking. In the 1970s, the consensus was that

more than 2 million adults in the United States had adisorder of taste or smell. A large nonrandom surveyconducted by the National Geographic Society in 1987found that 1% of their 1.2 million respondents couldnot smell three or more of six odorants using a “scratchand sniff” test. A 1994 National Health Interview Sur-vey given to 42,000 randomly selected householdsreported adjusted national estimates of a prevalence of2.7 million (1.4%) adults with an olfactory problemand 1.1 million (0.6%) adults with a gustatory problem.When smell or taste problems were combined, 3.2 mil-lion (1.65%) adults indicated a chronic chemosensoryproblem. The prevalence rates increased exponentiallywith age, with nearly 40% of all problems (1.5 million)existing in adults aged 65 years or older.

Before considering disorders of these special senses indetail, it would be advisable to define the terminology inthis field of oral medicine. Smell is the perception ofodor by the nose, whereas taste is the perception of salty,sweet, sour, or bitter by the tongue. Flavor is the combi-nation of taste, smell, and trigeminal sensation. Halito-sis is defined as bad breath, and can contribute to tasteand smell changes. Alterations in taste and smell aredefined with relative and absolute terms (Table 27–1).

Oral sources of altered taste function are commonand can be evaluated by a dentist. Trauma (burns, lac-erations, local anesthesia, surgery, reflux), localantiplaque medicaments and drugs excreted into saliva,infections (periodontal, dentoalveolar, soft tissue),vesiculobullous conditions, removable prostheses,metallic dental restorations, and salivary dysfunctioncan directly or indirectly affect taste function. Oral

Molecular and pathophysiologic

correlates of disease, 278

Taste, 279

Smell, 281

Halitosis, 282

Clinical findings of common taste

and smell problems, 284

Diagnosis and treatment of common

taste problems, 285

Diagnosis and treatment of common

smell problems, 286

Diagnosis and treatment of halitosis, 287

Suggested reading, 288

27 Special Senses: Disorders of Taste and SmellJonathan A. Ship, DMD, and Elisa M. Chávez, DDS

278 C H A P T E R 2 7

sources of olfactory problems are also common. Halito-sis, gingivitis, poor oral hygiene, and periodontal dis-eases can cause abnormal smell sensations.

Molecular and pathophysiologic correlates of disease

Taste buds mediate taste sensation (Figure 27–1). Threetypes of lingual papillae contain taste buds: fungiform

(anterior two-thirds of the tongue), folate (lateral bor-ders of the tongue in vertical folds), and circumvallate(crateriform nodules on the posterior border of thetongue). Taste buds are also present in the soft palate,pharynx, larynx, epiglottis, uvula, upper third of theesophagus, lips, and cheeks. Taste buds are constantlyreplaced, approximately every 10 days; if damaged,they can be repaired rapidly.

Taste receptors detect four basic tastes (sweet, salty,bitter, sour) and also perceive a wide range of othertastes that are poorly described by these categories (eg,astringent, metallic, savory, electric). Each taste bud hasreceptors at the apical portion exposed to the oral cavityand a basolateral area separated by a tight junction. Theapical portion of the taste bud begins the chain of eventsleading to taste sensation (Figure 27–2). Saliva plays amajor role in this process since it dissolves and carriestastants to, and rinses them away from the taste buds.Saliva also serves as a protective agent for the taste andepithelial cells by diluting stimulant concentration.

Smell receptors reside in the olfactory epithelium ofthe nasal septum, superior turbinate, and the roofbetween the two (Figure 27–3). The bipolar ciliatedneurons of olfactory receptors are replaced approxi-mately every 30 to 60 days. They are connected by theolfactory nerve to the olfactory bulb via the cribriformplate. Signal transduction begins at the peripheral neu-rons when the stimulus is inhaled and transported ordissolved in the mucosal secretions, and processing iscompleted in the olfactory bulb.

Input received by the taste buds is transmitted bythree cranial nerves (CN): VII (chorda tympani andgreater petrosal components), IX (glossopharyngeal),and X (vagus) via the nucleus of the solitary tract andthe thalamus to the cortex and the hypothalamus. Thegustatory innervation system is designed so that contra-lateral nerves or those with overlapping functions fre-quently compensate for nerve damage.

Fungiform

Foliate

Circumvallate

Figure 27–1 Distribution of taste buds on the tongue dorsum. Adaptedfrom Annals of the New York Academy of Sciences.

villiTaste pore microv

Tight junctions

Nerve profile

Taste bud cellSynapse

Afferent fibers

Figure 27–2 Anatomy of a taste bud. Adapted from Annals of theNew York Academy of Sciences.

Table 27–1 Commonly Used Terms for Gustation and Olfaction

Term Definition Example

GustationNormal taste Normal taste Healthy adult (any age)Hypogeusia Diminished taste Alzheimer or Parkinson

diseaseDysgeusia Distortion of taste with Poor oral hygiene,

or without a stimulus medicationspresent

Ageusia Loss or absence of Exposure to toxic taste chemicals, stroke

OlfactionNormosmia Normal smell Healthy young adultHyposmia Diminished smell Older adultDysosmia Distortion of smell Oral candidiasis, brain

tumor, migranePhantosmia Perception of smell

without a stimulus present

Parosmia Distortion of smell with a stimulus present

Anosmia Loss or absence of smell Upper respiratory infection, stroke

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Several cranial nerves contribute to taste sensation,whereas only one cranial nerve (CN I, olfactory) isresponsible for smell. Olfactory neurons aggregate toform glomeruli in the olfactory bulb. Information is sentto and processed in the pyriform lobe, the hippocampalformation, and the hypothalamus. Since the olfactoryreceptors are themselves nerves with long turnoverrates, dysfunction caused by damage to either theperipheral or central components of this system is morecommon than gustatory dysfunction.

The trigeminal nerve (CN V) also plays a role inolfactory and gustatory sensation by identifying nox-ious chemicals or irritants. This has been referred to asa “common chemical sense” or as “chemesthesis.” Pun-gent spices and chemicals that cause tearing or sneezingstimulate the trigeminal nerve and its related branches.The ethmoid (branching from the ophthalmic divisionof CN V) and the nasopalatine (branching from themaxillary division of CN V) both arrive in the nasalcavity and become “free” nerve endings in the nasalmucosa. Some are so close to the surface that chemicalstimuli may act directly on the nerve endings.

The maxillary and mandibular branches of the fifthcranial nerve give rise to the lingual, nasopalatine, pos-terior palatine, and buccal nerves in the oral cavity. Thetrigeminal nerve (CN V) functions as a nociceptor pri-marily in the anterior region of the oral cavity, and theglossopharyngeal nerve (CN IX) serves as the mainreceptor in the posterior regions. Several free nerve end-ings also reside in the oral mucosa. They occur primar-ily in the anterior region in the filiform papillae andaround the circumvallate papillae, although they can befound in any of the taste papillae.

Disease and the process of aging are often difficult tosegregate. Aging, even independent of major medicalproblems and medications, has significant deleteriousinfluences on olfaction. Detection and recognitionthresholds for smell are raised in elderly individuals. Theglomeruli of the olfactory bulb deteriorate with age, and

alterations in the olfactory epithelium and the reductionin protein synthesis that occurs with normal aging maycontribute to diminished smell perception and identifica-tion. Olfaction can be further compromised by medica-tions, chemotherapy, radiotherapy, and systemic dis-eases. There is little information about possibledegenerative changes in the neural pathways attributableto normal aging; however, there is some evidence oflosses in trigeminal (CN V) sensitivity with aging.

Losses in gustatory function are not a commonsequela of aging, and most changes occur later in lifethan olfactory dysfunction. Taste-specific (ie, sweet,salty, sour, bitter) changes have been reported, yet itappears that global changes in gustation do not occur asa result of the aging process. Further, there is no evi-dence that numbers of papillae and taste buds decreaseover time. However, numerous older adults are treatedfor systemic conditions that may affect the gustatorysystem either directly or indirectly. For example, manymedications taken by the elderly directly affect tasteperception and inhibit salivary output, impairing gusta-tion. Head and neck cancer treatment (surgery,chemotherapy, radiotherapy) causes short- and long-term damage to the anatomic and nerve pathwaysresponsible for transmitting taste sensation.

Many older adults complain of taste losses, but theyare typically attributable to problems with olfaction.Age- and disease-related losses in olfaction play a largerole in diminished gustatory function. Any conditionthat results in a compromised environment for themediators of chemosensation (eg, tongue, saliva, oraland nasal mucosa, neural pathways, neurotransmitters)results in altered taste and smell perception at any age.

There are three major processes that result in loss oftaste and smell function: transport, sensory, and neu-ronal disorders that involve the oral cavity, head andneck region, and major organs (Table 27–2).

Taste

Many oral and systemic diseases affect the gustatorysystem (Table 27–3). Antiplaque mouthrinses, tooth-pastes, and gels are associated with taste alterations.Iatrogenic injury during or subsequent to dental treat-ments and the use of local anesthetics can cause a tastedisorder. Other trauma, such as exposure to excessivelyhot food or liquids or chemical burns, is common.Metal restorations have been reported to cause a tran-sient metallic taste in some patients. Complete and par-tial dentures can block access to taste receptor cells.Intraoral infections and inflammatory conditions, suchas candidiasis, gingivitis, periodontal disease, dentalcaries, dental-alveolar infections, herpetic lesions, pul-pal necrosis, traumatic lesions, vesiculobullous diseases

Olfactory bulb Olfactory nerve

Bone

Epithelium

Sensory cells

Volatile molecules

Figure 27–3 Distribution of olfactory receptors and nerves in thenasal cavity.

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(eg, pemphigus, pemphigoid, lichen planus), and burn-ing mouth syndrome, can all contribute to unpleasanttastes or altered taste function (Figure 27–4).

Defective salivary function can result in altered tasteperception or elevation of detection thresholds (Figure27–5). Numerous medical problems (eg, Sjögren syn-drome, diabetes, Alzheimer disease), prescription andnonprescription medications (eg, anticholinergics, anti-hypertensives, antipsychotics, antihistamines), head and

neck radiotherapy, and chemotherapy cause salivarydysfunction. The extent to which salivary hypofunctionaffects gustation is still under debate. Nevertheless, it ishypothesized that in the absence of saliva there is adiminished ability to transport stimuli to taste buds andan increased risk of developing oral-pharyngeal micro-bial infections that alter taste perception. Saliva mayalso act as a reservoir for medications or their metabo-lites, resulting in an unpleasant taste.

Numerous medical problems and their treatmentwith medications and chemotherapy have been associ-ated with altered taste sensation. Infections (eg,influenza, sinusitis, herpes zoster, human immunodefi-ciency virus syndrome [HIV]), trauma (eg, motor vehi-cle accident), and head and neck surgery can result intemporary or permanent damage. Endocrine and meta-bolic disorders, including diabetes and hypothyroidism,have been associated with altered taste sensation. Forexample, diabetic neuropathies have been shown toincrease taste thresholds. Finally, there is some evidencethat genetics may determine the number of taste buds inan individual, which could cause variable gustatoryability and perhaps even predisposition to or increasedrisk of developing taste disorders.

The effect of medications on the gustatory systemmay be transient, modifiable, or chronic (Table 27–4).For example, 0.12% chlorhexidine rinse has beenreported to produce a reversible impairment of periph-eral taste receptors. Whereas some medications causealterations of specific tastes (sweet, bitter, salty, sour),others increase taste or recognition thresholds. Severaldrugs have been associated with total loss of taste: localanesthetics (lidocaine), antineoplastics (bleomycin),and antirheumatics (penicillamine). The mechanismsbehind these effects are complex and not yet clearlydefined, but medication-induced taste dysfunction canoccur at any of the transport, sensory, or neuronal lev-els of the gustatory system.

Finally, little is known regarding pollutants and theireffect on the gustatory system. Environmental pollu-tants range from airborne chemicals, to metallic parti-cles, to dust. Some pollutants, such as insecticides, canactually bind to the tongue, altering taste-bud morphol-ogy and, consequently, function.

Table 27–2 Overview of Mechanistic Causes of Gustatory and Olfactory Disorders

Disorder Description Gustatory Examples Olfactory Examples

Transport problem Stimulus cannot reach receptor Salivary dysfunction, oral candidiasis Blockage of nasal airway, nasal polyp

Sensory problem Damage to peripheral sensory Radiotherapy, chemotherapy, burn, Radiotherapy, chemotherapy, upper

organs trauma respiratory tract infection

Neuronal problem Damage to peripheral nerves Tongue surgery, neoplasm, brain Brain tumor, head trauma, Alzheimer

or CNS tumor disease

Table 27–3 Common Causes of Gustatory and Olfactory Disorders

Oral causesTrauma (burns, lacerations, chemical damage, anesthetic,

surgical)Oral mouthrinses, dentifrices, gelsGingival and periodontal diseasesDentoalveolar infectionsViral infectionsSoft-tissue lesionsCandidiasis, denture stomatitisRemovable prosthodontic appliancesBurning mouth syndromeSalivary dysfunction, drugs in salivaGalvanism

Upper respiratory tract problemsLesions or tumors of the nose or airwayViral and bacterial infectionsExposure to toxic airborne contaminants, pollutantsTobacco use

Peripheral or CNS problemsHead traumaTumors, lesionsNeurologic diseases (Alzheimer, Parkinson, Huntington disease;

stroke) Systemic complications

Systemic diseases (diabetes, thyroid diseases, renal failure)Nutritional deficiencies, alcoholismPrescription and nonprescription medicationsChemotherapy and radiotherapyPsychiatric disorders

OtherAgingCircadian variationMenses and pregnancyIdiopathic

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Smell

Olfaction, entirely dependent upon neural function atperipheral receptor sites and centrally at the first cranialnerve, is especially at risk from any disease or eventwith neurologic sequelae. The most common cause ofsmell changes is upper respiratory infection, which alsoalters gustation. These frequent viral and bacterialinfections alter or block peripheral receptor sites. Non-respiratory bacterial or viral infections, such as acutedentoalveolar infections, HIV, and candidiasis, canadversely affect olfaction.

Head trauma also results in a diminished sense ofsmell, owing to the location and fragility of the olfac-tory neurons and the susceptibility to fracture of thecribriform plate. Tumors and surgical procedures thataffect olfaction-related structures in the brain or nasalcavity are associated with smell loss. Similarly, neuro-logic diseases, such as epilepsy, Parkinson disease,Huntington chorea, and Alzheimer disease, impairolfaction. For example, patients with Alzheimer diseasedevelop problems with smell perception because manyof the same anatomic and neural structures destroyedby their disease also affect normal olfaction. Further-

more, the limbic system is adversely affected inAlzheimer disease, resulting in poor recognition, identi-fication, and recall of odorants.

Other diseases may have indirect effects on thesense of smell because of treatments or medicationsused to treat the disease. Numerous medications causeolfactory changes, including cardiovascular (nifedip-ine), antithyroid (methylthiouracil), antibacterial(streptomycin), and analgesic (codeine) drugs (Table27–5). Radiation, chemotherapy, and hemodialysisregimens can also interfere with olfactory pathways.Environmental pollutants (eg, acrylates, petrochemi-cals) have been reported to alter neurotransmitters,damage the structures involved in olfaction, or accu-mulate in the olfactory bulbs. These losses may betransient or chronic.

Halitosis

Halitosis, oral malodor, or bad breath can originatefrom physiologic or pathologic sources (Table 27–6),and has been estimated to occur chronically in approx-imately half the population. Odor-producing com-

Figure 27–4 Common etiologies of taste, smell, and halitosis problems: A, pseudomembraneous candidiasis of the tongue dorsum; B, atrophic can-didiasis beneath a maxillary denture; C, gingivitis, material alba, and impacted food; and D, pemphigus vulgaris and desquamative gingivitis.

A B

C D

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pounds are inspired into the lungs and then expired.This occurs when odors (from foods or tobacco) areingested and inhaled or when pathologically producedodiferous compounds (intraoral or systemic) are intro-duced into the lungs. Halitosis has been estimated to befrom oral sources in 40 to 90% of cases, however, it canalso arise from systemic diseases.

Bad breath originating from the mouth is caused byvolatile sulfur compounds (VSCs), such as hydrogen

sulfide, methylmercaptan, and dimethyl sulfide. Precur-sors to these molecules (cysteine, methionine) are foundin saliva. The dorsum of the tongue and the gingival sul-cus are reservoirs for microbes that can produce VSCs,specifically gram-negative anaerobic bacteria (eg, Por-phyromonas gingivalis, Prevotella intermedia, Fusobac-terium nucleatum, and Treponema denticola). Severalfactors can result in a shift from gram-positive to gram-negative bacteria in the oral cavity: alkaline salivary pH,diminished salivary flow, and inflammatory diseases (ie,gingivitis, periodontitis, major aphthous stomatitis, her-petic gingivostomatitis).

Salivary hypofunction diminishes the self-cleansingaction of the oral cavity, and lower levels overnight fre-quently result in “morning breath.” When saliva evapo-rates, nonsulfur-containing gases (eg, cadaverine,putrescine, butyric, indole) can be released in additionto the VSCs, contributing to halitosis in the patient withsalivary hypofunction. Sources of necrosis or hemor-rhage in the oral cavity (dentoalveolar infections, perio-dontal diseases, oral cancers) produce foul odors.Although dental caries does not produce bad breath, itcreates food traps as do overhanging, subgingival, andopen restorations. Debris remaining in these areasdecomposes and produces fetid odors. Similarly, poormaintenance and overnight use of dental prostheses can

Figure 27–5 Salivary hypofunction and the sequelae of dessicatedoral mucosal and dental tissues are common etiologies of taste, smell,and halitosis problems.

Table 27–4 Drugs that Cause Gustatory Disorders

Drug Category Drug

Amebicide and anthelmintic Metronidazole, niridazoleAnesthetic (local) Benzocaine, procaine HCl, lidocaineAnticholinergic and antispasmodic Dicyclomine, glycopyrrolate, hyoscyamineAnticoagulant PhenindioneAntihistamine Chlorpheniramine maleateAntilipidemic Cholestyramine, clofibrateAntimicrobial Amphotericin B, ampicillin, bleomycin, cefamandole, ethambutol HCl, ethionamide, griseofulvin,

lincomycin, metronidazole, sulfasalazine, tetracyclinesAntiproliferative and Azathioprine, bleomycin, carboplatin, carmustine, cisplatin, doxorubicin, 5-fluorouracil, interferon

immunosuppressive gamma (INF-γ), methotrexate, vincristineAntirheumatic, analgesic, Allopurinol, auranofin, colchicine, dexamethasone, flunisolide, gold, hydrocortisone, levamisole,

antipyretic, anti-inflammatory d-penicillamine, phenylbutazone, salicylatesAntithyroid Carbimazole, iodide, methimazole, methylthiouracil, propylthiouracil, thiouracilDental hygiene agent Sodium lauryl sulfate, chlorhexidine gluconate mouthrinsesDermatologic agent IsotretinoinDiuretic and antihypertensive Acetazolamide, amiloride and its analogues, captopril, diazoxide, diltiazem, enalapril, ethacrynic

acid, hydrochlorothiazide, nifedipineHypoglycemic Glipizide, phenformin and derivativesMuscle relaxant and drugs for Baclofen, chlormezanone, levodopa

treatment of Parkinson diseasePsychopharmacologic and antiepileptics Carbamazepine, flurazepam HCl, lithium carbonate, phenytoin, trifluoperazineSympathomimetic Amphetamines, amrinoneVasodilator Dipyridamole, nitroglycerin patch, oxyfedrineOther EDTA, etidronate, germine monoacetate, idoxuridine, iron dextran complex, vitamin D

EDTA = ethylenediaminetetraacetic acid.

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produce malodors as a result of poor hygiene ordecreased nighttime salivary flow. Candida may arise insimilar circumstances, and whereas Candida albicansitself does not produce malodors, it can change the oralenvironment, creating a shift in bacterial flora. A fis-sured tongue and tonsillar crypts provide reservoirs forfood, bacteria, cellular debris, and stagnating saliva,conditions conducive to oral malodor.

Medications, radiotherapy, and chemotherapy candirectly affect the oral cavity, resulting in halitosis. Themost common medications associated with halitosis arethose that inhibit salivary output. Chronic use ofinhaled corticosteroids alters the respiratory tract floraand leads to malodors. Cancer treatments (chemo-therapy, head and neck radiation) have transient orpersistent effects on the salivary system, oropharyngealtissues, and oral flora, resulting in oral malodors.

Several systemic diseases also produce halitosis. Respi-ratory diseases are a common source of these odors. Infec-tions involving gram-negative anaerobic bacteria (tuber-culosis, pneumonia), obstructions (foreign bodies),tumors (lung cancer), and the production of pus(empyema, bronchiectasis) can all contribute to the emis-sion of foul odors from the nasal cavity, sinuses,nasopharynx, pharynx, and lungs. The postnasal dripassociated with upper respiratory viral infections and alle-gric or infectious sinusitis is a common source of halitosis.

Odiferous by-products may result from drug metab-olism, systemic diseases (diabetic ketoacidosis), and diet(alcohol, high fat, garlic). The circulatory system carriesthese metabolites through the lungs, and they areexpired, resulting in halitosis. Individuals with gastro-intestinal diseases suffer from halitosis. Hiatal hernias,gastroesophageal reflux, and pyloric stenosis permit therelease of gastric odors into the oral cavity. Achalasia isa swallowing disorder in which there is a failure of thecontents of the esophagus to empty into the stomach;these patients experience halitosis when food debris andsaliva are trapped and decay in the esophagus. Gastriculceration, infection, carcinoma, and malabsorptioncan also contribute to oral malodors.

Diabetes is another common systemic cause of hali-tosis. Diabetic ketoacidosis produces oral malodors, anddiabetics are at increased risk of infections and poorwound healing, predisposing them to odor-producingperiodontal diseases and other intraoral infections.Dehydration, a major component of diabetes, can resultin decreased salivary flow, and a subsequently increasedrisk of developing halitosis. Hepatic and renal failure,leukemias and other blood dyscrasias, and trimethyl-aminuria produce malodors as well.

Finally, some persons suffer from a psychogenic hal-itosis. They do not have detectable malodors, yet theybelieve it is present (halitophobia). This phenomenon is

Table 27–5 Drugs that Cause Olfactory Disorders

Drug Category Drug

Anesthetic (local) Benzocaine, procaine HCl (Novocain), lidocaineAntiarrhythmic Propafenone HCl, tocainide HClAnticoagulant PhenindioneAntihistamine Chlorpheniramine maleateAntilipidemic and cholesterol-reducing agents Cholestyramine, clofibrate, lovastatinAntimicrobials Amphotericin B, ampicillin, bleomycin, cefamandole, ciprofloxacin HCl, doxycycline,

ethambutol HCl, griseofulvin, lincomycin, lomefloxacin HCl, metronidazole, niridazole, ofloxacin, pentamidine, rifabutin, silver nitrate, sulfasalazine, tetracyclines, terbinafine HCl

Antiproliferative and Azathioprine, bleomycin, carmustine, doxorubicin, 5-fluorouracil, methotrexate, immunosuppressive vincristine sulfate

Antirheumatic, analgesic, antipyretic, Allopurinol, auranofin, colchicine, dexamethasone, flunisolide, gold, hydrocortisone, anti-inflammatory levamisole, D-penicillamine, phenylbutazone, salicylates, 5-thiopyridoxine

Antithyroids Carbimazole, methimazole, methylthiouracil, propylthiouracil, thiouracilDental hygiene agents Sodium lauryl sulfate, chlorhexidine digluconate mouthrinsesDiuretic and antihypertensive Acetazolamide, amiloride and its analogues, amilodipine besylate, captopril, diazoxide,

diltiazem, enalapril, ethacrynic acid, felodipine, lisinopril, losartan potassium, nifedipine, propranolol, spironolactone

Hypoglycemic Glipizide, phenformin and derivativesMuscle relaxant and drugs for treatment Baclofen, chlormezanone, levodopa, pergolide mesylate, selegiline HCl

of Parkinson diseasePsychopharmacologic and antiepileptic Carbamazepine, lithium carbonate, phenytoin, psilocybin, triazolam, trifluoperazineSympathomimetic Amphetamines, amrinoneVasodilator Bamifyline HCl, dipyridamole, nitroglycerin patch, oxyfedrineOther Etidronate, germine monoacetate, idoxuridine, iron sorbitex, vitamin D

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associated with depression, hypochondriasis, schizo-phrenia, suicidal ideation, and temporal lobe epilepsy.Importantly, some individuals who have altered tasteand smell may perceive their changes as halitosis.

Clinical findings of common taste and smell problems

Most patients who present with a chemosensory prob-lem complain of a taste loss or diminished taste sensi-tivity. However, the majority of chemosensory deficitsare attributable to olfactory losses. True taste loss is rel-atively rare, and a careful interview can help distinguishbetween the two problems (Table 27–7). Dysgeusia is a

distortion of taste, or a persistent unexplained orunelicited taste sensation. It is particularly difficult toassess, especially when a taste is perceived without astimulus present (eg, phantom taste).

Objective findings may occur anywhere in the headand neck region. Oral disorders associated with tastechanges should be evaluated by the dentist. Examplesinclude pseudomembraneous candidiasis, dentoalveolarabscesses, and salivary dysfunction. Suspected neuralinjuries to cranial nerves, brain trauma, systemic dis-

Table 27–7 Steps for the Examination and Diagnosis of Chemosensory and Oral Malodor Disorders

I. History of chief complaintWhen did the patient first notice the altered taste, smell,

or halitosis?Was there a specific stimulus or coinciding event?What relieves and exacerbates the problem?Questions specific to taste, smell, and halitosis problems

(Table 27–8)II. Medical, surgical, and family history

Review of systemsDates of medical diagnoses and surgeriesCurrent management of medical problems

Medications (prescription, nonprescription)Chemotherapy, radiotherapy, surgeryDiet, homeopathyNo treatment

Unresolved medical issuesFamily history

III. Social historyTobacco and alcohol use (past and present)Exposure to environmental toxinsHas anyone else noticed a problem (for smell and halitosis

problems)?Dietary habits (before and after onset of chief complaint)Living arrangements (recent changes, reliance on caregivers)

IV. Dental historyOral chief complaintHistory of dental and oral surgical treatmentsUse of mouthrinses, gums, candies, mints, sprays, etc.Regular and irregular oral hygiene routinePresence of head, neck, nasal, and oral discomfort

V. Oral examinationExtra- and intraoral lesions, masses, or swellingsSalivary output from major glandsOral hygiene, presence of gingivitis or periodontitisStatus of tongue, palate, posterior oropharynxStatus of removable prosthesesStatus of teeth (erupted, erupting, and exfoliating), caries,

restorationsEvaluate breath and nasal odor separately (putrid, sweet,

ketonic, etc.)Imaging (intraoral and extraoral radiographs, CT, MRI)Laboratory tests (biopsy, culture, serologic tests)Specific taste, smell, and halitosis tests (see text and Tables 27–9

and 27–10)VI. Interdisciplinary consultation or referral

Table 27–6 Common Causes of Halitosis

Oral causesGram-negative anaerobic bacteriaImpacted foodGingivitis, periodontitisDentoalveolar infectionsVesiculobullous and erosive mucosal diseases (eg, aphthous

stomatitis, herpetic gingivostomatitis)Salivary dysfunctionCandida albicansTongue coating, fissured tongueMouth breathingOral cancersChronic use of alcohol-containing mouthwashes

Pharyngeal and esophageal problemsTonsillar cryptsCancersAchalasia

Respiratory problemsBacterial infectionsNasal congestion, postnasal dripDeviated septumAllergiesTumors

Gastrointestinal disordersRefluxHernia, gastric stenosisGastric ulceration, infectionCarcinomas

Systemic complicationsMedications, chemotherapy, radiotherapyBlood dyscrasiasDiabetesHepatic failureRenal failureAlcoholismTrimethylaminuria (fish odor syndrome)

OtherDiet (use of herbs, spices, garlic)Tobacco useHalitophobia

eases, and medications should be evaluated by medicalspecialists, with appropriate testing.

As with taste problems, a careful history can helpelucidate the problem and distinguish between a smellor taste disorder. For example, smell changes followingthe use of nitrous oxide analgesia can assist in estab-lishing a diagnosis. Halitosis may be the primary com-plaint, and is usually attributable to oral-pharyngealproblems that should be evaluated by the dentist. Con-duction injuries in the nasal cavity (eg, rhinosinusitis,nasal polyposis) and obstructions in the ear (eg, serousotitis media) should be evaluated by medical specialistsand may require computed tomography (CT) and mag-netic resonance imaging (MRI) studies to assist with adiagnosis. Patients suspected of having neural injuries toolfactory-related structures (eg, head trauma, neo-plasms) or certain medical problems (see Table 27–3),or taking medications (see Table 27–5) should be evalu-ated by medical specialists with appropriate tests.

Subjective complaints of halitosis and objective find-ings are often incongruent. Many people think they havebad breath but do not actually have halitosis, and othersare unaware that they have a problem. Typically, femalesare more likely than males to complain of malodor andtheir self-estimates of bad breath are significantly higherthan those made by males. If a patient complains ofchronic halitosis that is unrelenting, it is usually a resultof chronic oral or systemic disease (eg, periodontitis, dia-betes). Alternatively, complaints of intermittent halitosismay be more likely attributable to a gastrointestinal dis-turbance (eg, gastroesophageal reflux disease).

Volatile sulfur compounds contribute to oral mal-odor and are produced by gram-negative anaerobic bac-teria. Subgingival plaque has the highest levels of thesebacteria, and therefore, gingivitis, impacted food mate-rial, and periodontal disease are objective markers oforal malodor. Salivary hypofunction, tongue coatings,and tonsillar crypts are additional findings in patientswith oral malodor.

Diagnosis and treatment of common taste problems

Diagnosis begins with a careful history of the com-plaint. The history must include critical questions on thehistory of the taste problem, a comprehensive dentaland medical history, review of medications (prescrip-tion, nonprescription, oral-hygiene aids), and social his-tory. Some questions can assist in defining whether thechemosensory loss is related to smell or taste (Table27–8). For example, the complaint of taste loss follow-ing an oral procedure involving injection of a local anes-thetic in the vicinity of the chorda tympani helps estab-lish a diagnosis. A frequent complaint is the loss of

taste; however, if upon further questioning, it is revealedthat the patient can taste the bitterness of coffee, sweet-ness of ice cream, saltiness of potato chips, and sournessof lemons, then they probably have a smell disorder.

Document the severity by asking the patient to ratetheir smell/taste/halitosis problem on a scale of 0 to 10.The best score is 0, which should be described to thepatient as having “no problem,” and 10 is the worstscore, or a “severe problem.” Recording this subjectiveranking helps determine whether the patient perceiveshis or her problem to be improving, worsening, or notchanging over time.

After the most common etiologic agents for a tastedisorder have been eliminated from the differentialdiagnosis (see Table 27–3), specific taste tests are indi-cated (Table 27–9). The use of topical anesthetics ishelpful, particularly when the patient complains of dys-geusia or a phantom taste without any obvious stimu-lus. If the dysgeusia persists or even gets worse aftertopical anesthesia has been sequentially applied to thedorsum of the tongue, then a local etiology is unlikelyand a central mechanism should be pursued. If the taste

Table 27–8 Questions Useful in the Diagnosis of Chemosensory Disorders

I. General questions1. Have you experienced a loss in taste, smell, or both?2. Have you experienced changes in hot, cold, texture, or

feeling sensations in your mouth or nose?3. How long have you had smell or taste loss? Was the loss

sudden or gradual, intermittent or continuous, bilateral or unilateral, seasonal (describe the history)?

4. What was the precipitating event for your smell or taste problem?

5. Does eating food mask the smell or taste problem or does the smell or taste distortion mask your enjoyment of eating food?

II. Specific taste questions1. Can you taste anything? What is it?2. Can you taste the bitterness of coffee?3. Can you taste the sweetness of ice cream?4. Can you taste the sourness of lemons?5. Can you taste the saltiness of potato chips?6. Do you have altered tastes without a stimulus, with a

stimulus?7. Describe the altered taste.

III. Specific smell questions1. Can you smell anything? What is it?2. Have you lost your taste for steak?3. Do you have altered smells without a stimulus, with a

stimulus?4. Describe the altered smell.

IV. Specific halitosis questions1. Do you have a bad taste in your mouth? 2. Have you had any changes in your sense of smell?3. Has anyone told you that you have bad breath?

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problem is eliminated or diminished by topical anesthe-sia, then an oral etiology must be pursued.

The success of treatment for gustatory problemsdepends upon the etiology. An orofacial source of ataste problem can usually be treated and followed bydental professionals. Once oral problems have beeneliminated from the differential diagnosis, referral to theappropriate medical provider is warranted (eg, neurolo-gist for suspected central or peripheral neurologic prob-lem; internists for underlying metabolic disorder). Uni-lateral surgical ablation of a damaged chorda tympaninerve has been described for severe dysgeusia. Anothercause for a taste problem may be psychologic or behav-ioral. For example, if dysgeusia is associated withpatient-described episodes of stress, advise the patientto see a specialist in stress management. Ultimately, if acause cannot be established, patients should be referredto a multidisciplinary taste and smell center.

Taste as well as smell impairments are stressful forpatients, particularly if a diagnosis is not establishedand treatments are not effective. Practitioners shouldcounsel patients with coping strategies and behavioralmodification techniques. Moreover, patients need to beadvised on nutrition and appetite issues to preventnutritional deficiencies. The efficacy of zinc supplemen-tation for chemosensory deficiencies is controversial butprobably not harmful. High dosages are necessary (ie,100 mg zinc sulfate daily). Finally, supplementation offoods and beverages with taste (eg, herbs, spices), smell,temperature, and textural stimulants (eg, crunchy,smooth, fizzy) improves palatability and flavor as wellas the desirability of eating.

Diagnosis and treatment of common smell problems

The approach to diagnosis and treatment of smell prob-lems is similar to that for taste disorders. A comprehen-sive subjective assessment of the chief complaint, objec-tive head, neck, oral evaluation, and review of thepatient’s medical, dental, medication, and social historyis necessary. Complaints should be recorded (see Table27–7), and responses to certain questions can be usefulin the establishment of a diagnosis (see Table 27–8). Itis important, as with taste complaints, to differentiatebetween a gustatory and an olfactory disorder. Sincethere are intimate interactions of taste and smell in theperception of flavor, most chemosensory complaints arerelated to taste losses, whereas most problems areattributable to smell losses.

A thorough oral, head, neck, and medical examina-tion is required to evaluate the patient for stomatologic,neurologic, endocrinologic, and other systemic diseasesthat may cause smell losses. Any oral source of malodorshould be identified and treated. The nasal cavity andsinuses require examination for any masses, inflamma-tion, or obstructions; this is best accomplished by a spe-cialist in otolaryngology. A complete neurologic exami-nation of cranial nerves, cerebellar function, andsensorimotor function may be required. Head and neckimaging with CT and MRI may be warranted if anintracranial or nasal-sinus abnormality is suspected. If apsychiatric etiology is suspected, referral to qualifiedspecialists is recommended.

Several olfactory tests are available for use in thedental office (Table 27–10). The University of Pennsyl-vania Smell Identification Test (UPSIT, Sensonics, Inc.,Haddonfield, New Jersey) is a commercially availablestandardized scratch and sniff test consisting of 40microencapsulated odorants. Scores may be particularlyuseful in longitudinal serial examinations to determine ifa patient’s performance is constant or deteriorating over

Table 27–9 Clinical Evaluation of Gustatory Function

I. Methylene blue staining of the tongue1. Used to test gross innervation of taste buds.2. Taste pores remain stained (blue) if they are innervated.3. Taste pores do not remain stained if there is an interruption

of innervation.II. Topical anesthesia applied to the tongue

1. Used to distinguish between oral and nonoral sources of dysgeusia.

2. Apply 2% unflavored viscous lidocaine or 1% dyclonine hydrochloride to four quadrants of the tongue in a sequential fashion (left anterior 2/3, left posterior 1/3, right anterior 2/3, right posterior 1/3) with a cotton-tipped applicator.

3. Total-mouth rinse with topical anesthetic to anesthetize taste buds located in the anterior portion of the oropharynx and hard and soft palate.

4. Caution patients about a reduced gag reflex after application of anesthetics.

5. Advise patients to avoid eating and drinking until anestheticshave worn off.

6. If dysgeusia is reduced, cause may be local.7. If dysgeusia is greater, cause may be central (eg, phantom

taste).8. If no changes in dysgeusia, cause is probably not oral.

III. Taste test1. Used to test for local and test-specific taste loss.2. Four standardized tastants applied to four quadrants of the

tongue in a sequential fashion (left anterior 2/3, left posterior 1/3, right anterior 2/3, right posterior 1/3) with cotton-tipped applicators.

3. Number of correct identifications noted.4. Four commonly used tastants easily prepared by a pharmacy:

a. 1.0 M sodium chlorideb. 1.0 M sucrosec. 0.03 M citric acidd. 0.001 M quinine hydrochloride

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There are three types of evaluation for halitosis:organoleptic examination, molecular evaluation ofexpired air, and bacterial identification tests. Organolep-tic measures (odor judge) are qualitative and based upondirectly sniffing sources, such as expired air from thenose or mouth, dried saliva, or plaque scrapings fromthe anterior or posterior of the tongue, teeth, or gingiva.Gas chromatography units, such as sulfide monitors (eg,Halimeter; Interscan Corp., Chatsworth, California),detect volatile sulfur gases in expired air. Gas chro-matography combined with mass spectrometry can pro-vide more elaborate analyses of expired air but are costlyand impractical. Plaque or saliva samples can be mea-sured for the presence of bacteria capable of producingodor-causing gases (eg, BANA or Perioscan; Oral-B Lab-oratories, Redwood City, California). Of these tech-niques, the most subjective (organoleptic) is still the mostreliable method of assessment and diagnosis and can beperformed by any health care provider. The other meth-ods are useful in monitoring treatment progress. Thesemeasures should be used in conjunction with a thoroughexamination and, if necessary, further diagnostic testing,or referral, to identify the source of the malodor.

Treatment for halitosis begins with improved oralhygiene. Reducing the oral microbes, specifically anaer-obes, improves halitosis. Patients should be instructedin proper and daily toothbrushing and flossing tech-niques, and regular prosthesis hygiene (when appli-cable). Tongue cleaning, particularly the posterior por-tion, is essential for the treatment of bad breath, andcan be accomplished with tongue cleaners, scrapers, andbrushes. Nonprescription mouthwashes may providesome improvement, but only for brief periods, and theycan actually exacerbate halitosis, because of the drying

time compared to age- and gender-matched adults. IfUPSIT scores diminish more rapidly that those of age-and gender-matched controls, then appropriate referraland treatment is justified, since the evidence suggeststhat smell losses are greater than attributed to agingalone. When a diagnosis cannot be established or treat-ment is unsuccessful, patients should be referred to amultidisciplinary research and clinical care taste andsmell center, where additional olfactory testing can beadministered.

Treatment for olfactory problems is based upon thedetermination of a diagnosis. Any organ-based etiology(eg, oral candidiasis, nasal polyp, hypothyroidism, useof nifedipine) should be treated by the appropriate spe-cialist. Dentists can treat any orofacial cause. If halito-sis is suspected as the etiology, then diagnosis and treat-ment should be performed. As with gustatory disorders,patients should be referred to appropriate health careproviders or smell and taste centers for evaluation andtreatment of systemic diseases, medications, environ-mental toxins, psychobehavioral problems, central orperipheral neurologic disorders that could be respon-sible for the olfactory dysfunction. Medical and surgicalcorrection of nasal disorders and upper respiratoryinfections, and the use of topical (nasal) and systemicsteroids has some success.

Another aspect of treatment is counseling on fourmajor issues: (1) use of additional smoke detectors inthe living environment, (2) avoidance of dwellings withnatural gas, (3) use of additional food spoilage precau-tions, and (4) maximum use of flavor enhancers toimprove the flavor of foods. Refrigerated food itemsmust be dated to keep track of potential spoilage.Spices, herbs, and other food additives can be used tostimulate taste, temperature, and textural sensation andto enhance the flavor of foods and the hedonic experi-ence of mealtime. Finally, patients should be remindedthat a diminished ability to smell is a sequelae of grow-ing older. Importantly, these losses do not present assudden disruptions of smell function or dysosmias, butoccur gradually and do not become clinically observableuntil the sixth or seventh decade of life.

Diagnosis and treatment of halitosis

Diagnosis requires a careful review of the chief com-plaint, dental, medical, medication, and social history(see Table 27–7). A thorough head, neck, and oral exam-ination must be completed to identify a cause of oral mal-odor (see Table 27–6). On the day of the appointment thepatient should be instructed not to wear any perfumes,colognes, or other scented products (eg, cosmetics, hair-sprays, powders), and not to eat, drink, smoke, or per-form oral hygiene 2 hours before the appointment.

Table 27–10 Clinical Evaluation of Olfactory Function

I. Odor stix1. Used to evaluate gross perception of olfaction.2. Commercially available odor-producing magic marker-like

pen.3. Wave approximately 3 to 6 inches in front of patient’s nose.

II. Twelve-inch alcohol test1. Used to evaluation gross perception of olfaction.2. Open an isopropyl alcohol packet and wave it approximately

12 inches in front of patient’s nose.III. Scratch and sniff cards

1. Used to evaluate gross sensation of olfaction.2. Commercially available three-odorant card.

IV. UPSIT (University of Pennsylvania Smell Identification Test)1. Used to quantitate olfactory loss (anosmia, hyposmia) and

adjusts for age and gender of the patient.2. Commercially available test of 40 scratch and sniff odors.3. Delivered by forced choice testing.4. High test-retest reliability.

effect caused by high alcohol content. Oxidizing agents(dioxide, peroxide), zinc chloride, and triclosan rinses,and prescription antimicrobial rinses (chlorhexidine)are slightly more effective, but all have side effects andlack prospective long-term research confirmation.

If the source of the malodor is suspected to arisefrom oral disorders, such as defective dental restora-tions and prostheses, periodontal diseases, or candidia-sis, definitive treatment diminishes the number of oralmicrobes. Salivary hypofunction contributes to halito-sis; sugarless candies, mints, or gums, artificial salivas,and pilocarpine (5 mg tid and qhs) can increase salivaryoutput and may improve malodor.

It has been estimated that only 10% of all cases oforal malodor are of systemic origin. However, if an oralsource of halitosis has been ruled out and the problempersists, referral to the appropriate health care practi-tioner is indicated. Ultimately, if an oral and systemiccause cannot be discerned and the patient does notrespond to conventional therapy, a psychobehavioraletiology should be considered and a referral made to atrained specialist.

Suggested reading

Ackerman BH, Kasbekar N. Disturbances of taste and smellinduced by drugs. Pharmacotherapy 1997;17:482–96.

Ayers KM, Colquhoun AN. Halitosis: causes, diagnosis, andtreatment. N Z Dent J 1998;94:156–60.

Cullen MM, Leopold DA. Disorders of smell and taste. MedClin North Am 1999;83:57–74.

Deems DA, Doty RL, Settle RG, et al. Smell and taste disor-ders: a study of 750 patients from the University of Penn-sylvania smell and taste center. Arch Otolaryngol HeadNeck Surg 1991;117:519–28.

Fox PC. Management of dry mouth. Dent Clin North Am1997;41:863–76.

Getchell TC, Doty RL, Bartoshuk LM, Snow JB Jr. Smell andtaste in health and disease. New York: Raven Press, 1991.

Jones N, Rog D. Olfaction: a review. J Laryngol Otol 1998;112:11–24.

McDowell JD, Kassebaum DK. Treatment of oral and nonoralsources of halitosis in elderly patients. Drugs Aging 1995;6:397–408.

Rosenberg M. Clinical assessment of bad breath: current con-cepts. J Am Dent Assoc 1996;127:475–82.

Schiffman SS. Perception of taste and smell in elderly persons.Crit Rev Food Sci Nutr 1993;33:17–26.

Schiffman SS. Taste and smell losses in normal aging and dis-ease. J Am Med Assoc 1997;278:1357–62.

Ship JA. Gustatory and olfactory considerations in generaldental practice. J Am Dent Assoc 1993;124:55–61.

Ship JA. The influence of aging on oral health and consequencesfor taste and smell. Physiol Behav 1999;66:209–15.

Spielman AI. Interaction of saliva and taste. J Dent Res 1990;69:838–43.

Spielman AI. Chemosensory function and dysfunction. CritRev Oral Biol Med 1998;9:267–91.

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