The Oropharynx

The Oropharynx

Look to thy mouth; diseases enter there.


Order of Examination


The patient should sit up straight, facing the examiner, at a height such that the physician can comfortably look into the mouth. A flashlight or the otoscope may be used as a light source at the bedside, although the head mirror of the ear, nose, and throat (ENT) specialist provides superior illumination.

A Method

  • Inspect the lips (discussed later in this chapter), everting them to examine the labial mucosa. Ask the patient to open his mouth and inspect the oral aperture and then all the structures inside the mouth (with the dentures removed), including the dorsal surface of the tongue. Check for fibrillations and fasciculations of the tongue (for significance, see Chapter 26). This must be done with the tongue at rest and the patient breathing through his mouth. Most normal persons have “contraction fasciculations” when the tongue is held in forced extension. The method that involves the least amount of effort for the patient is for you to pull out his cheek by hooking your finger in the angle of the mouth, and then have the patient open his mouth slightly to permit inspection of the tongue at repose.

  • Use the tongue blade to retract the cheek and lips for a complete inspection of the buccal mucosa, the opening of the Stensen1 and Wharton ducts (the former directly opposite the second molar and the latter just under the tongue about 5 mm lateral to the frenulum), the teeth, and the gums.

  • Ask the patient to place his tongue on the roof of his mouth to permit inspection of its under surface and the floor of the mouth (all common sites for carcinoma, especially in older smokers).

  • Next, inspect the palate (for findings, see later in this chapter). Use of an intraoral mirror is very helpful.

  • Ask the patient to relax his tongue. (Do not ask him to protrude it for this part of the examination—see Chapter 26.) If you cannot see well, depress the middle third of the tongue with the tongue blade in your nondominant hand, and if you still cannot see well, pull the tongue forward. Do not touch the posterior portion of the tongue; you do not want him to gag until you are ready to test the gag reflex (see Chapter 26). The tonsils, tonsillar fossa, the anterior and posterior pillars, the posterior and lateral pharyngeal walls, a portion of the base of the tongue, and occasionally the tip of the epiglottis (discussed later in this chapter) can now be seen.

An Alternate Method

Stand behind the seated patient and have him extend his neck, open his mouth fully, and hold his breath in deep inspiration. The tongue and floor of the mouth will drop with gravity; a tongue blade is seldom needed (Greally, 1988; Sprackling, 1988).

imageAny single black mucosal lesion in any part of the oropharynx could possibly be a malignant melanoma, and a biopsy should be performed.


Palpate all symptomatic or unusual-appearing areas in the mouth and pharynx. (The examiner should wear disposable gloves.) In persons at high risk for carcinoma, the tongue and floor of the mouth should also be palpated because moderate-sized tumors and cysts lying deep within the oral tissues may be found only in this way. Calculi in the submaxillary ducts can be felt. (The salivary glands are discussed in Chapter 14.) A perfectly round, pale, subcutaneous mass in the floor of the mouth is due to the obstruction of a minor
salivary gland; this is called a ranula. The temporomandibular joints can be palpated by placing your fingertips in the external ear canals and having the patient open and close his mouth.


The tongue may be examined for myotonia by placing a tongue blade across the mandibular teeth, having the patient place his tongue on top of the tongue blade, and tapping on the relaxed tongue with a reflex hammer. The reflex hammer should be wrapped in a clean, disposable material. (See Chapter 25 for a description of myotonia as manifested in the hand.)


A Method

Ask the patient to count aloud from one to ten while you put your nose in the stream of exhaled air. If you have reasons to suspect a noxious odor, it is possible to turn your face away from the patient and still keep your nose in the stream.

Some patients have poor oral hygiene or have been vomiting so the breath odors are masked by those coming from the mouth. In that case, have the patient rinse out his mouth with a nonfragrant solution. With sufficient mouth care, one can reduce the odor sufficiently to be able to smell the breath that is actually emanating from the lungs.

Another method is to have the patient close his mouth. Place your nose where the steam would be if the patient were nose breathing on a cold day and smell the air as it exits from his nostrils. (To demonstrate to yourself that nose breathing decreases communication with the oral cavity, place a drop of peppermint oil on the tongue of a nose-breathing subject and see how well you can smell the peppermint with the subject’s mouth closed and then open.)

Specific findings are given later in this chapter.

Oral Aperture

Normally, the mouth should open sufficiently to permit the introduction of the tips of the patient’s three middle fingers, vertically aligned, without the fingers touching the lips. Three conditions in which the oral aperture is smaller are (a) tetanus (not usually a diagnostic problem); (b) various mechanical diseases of the jaw, especially disease of the temporomandibular joint; and (c) progressive systemic sclerosis (scleroderma). Dr Gerry Rodnan of the University of Pittsburgh charted the progress of systemic sclerosis by recording the patient’s maximum oral aperture. The patient’s mouth, opened as far as possible, was pressed against a piece of paper, such as a progress note sheet. Lipstick facilitated the measurement.


The most common deformity of the lips is seen in the cleft palate syndrome. Because of the resemblance to the lip of a rabbit, this was sometimes called hare lip, which has been absurdly transmogrified to “hair” lip. A hard lesion on the lip with a discrete edge could be molluscum contagiosum or a malignant epidermoid carcinoma. It usually requires a biopsy to make the distinction, although about 95% of labial epidermoid carcinomas occur on the lower lip.

A luetic chancre (a moist-centered ulceration) may occur on the lip. Such lesions are incorrectly stated to be confined to the upper lip. (If you suspect a luetic chancre, wear gloves and wash your hands carefully after touching it because the lesion will be teeming with live spirochetes, as can be seen by dark-field examination.)

The mucous patches of secondary syphilis may involve the lips, tongue, or cervix.

Leukoplakia (literally “white plate”) is often a precancerous lesion on the lips as on other mucosal surfaces.

Fever blisters (“cold sores”) are caused by the herpes simplex virus, usually type I. After the first infection, the virus inhabits the neural tissue in a latent form and recrudesces on the skin, usually at the vermilion border, sometimes triggered by another illness such as a pulmonary or upper respiratory infection. At first, there is a vesicle or vesicles containing clear fluid. In a few days, the vesicle ruptures, leaving a sore, inflamed, and infectious ulcer, which forms a crust and then heals without a scar. Primary herpes stomatitis involving the oral mucosa, especially the gingiva and tongue, is common in children but less so in adults. It may be quite severe.

Cheilitis is an inflammation of the lips characterized by vertical fissures. It may occur with regional enteritis; acrodermatitis enteropathica (inherited inability to absorb sufficient amounts of zinc from the diet); alcoholism; deficiency of pyridoxine, riboflavin, or folate; sprue; kwashiorkor; viral illness; oral candidiasis; hypervitaminosis A; actinic prurigo, an idiopathic photodermatitis of persons of American Indian ancestry (Lane, 1997); and iron deficiency anemia, with or without Plummer-Vinson syndrome (Beitman et al., 1981). The last may be associated with abnormalities of the nails (see Chapter 7).

Diffuse swelling of the upper and lower lips with mild discomfort is the most constant feature of the oral manifestations that occur in about 10% of cases of Crohn disease and that may precede systemic symptoms, sometimes by years. Granulomatous cheilitis signals the need for long-term surveillance (Eisen and Lynch, 1998).

Angular stomatitis, the reddening and cracking of the lateral corners of the mouth, may be seen as a benign condition in patients who drool. In children, it is given the specific name of perlèche. Although the condition has been stated to be diagnostic for riboflavin deficiency, the most common cause is Monilia (Candida). Angular stomatitis also occurs with anemia and lipstick allergy. I have seen it in upper respiratory viral syndromes in cold climates and been following the same regardless of climate.

Angular stomatitis must be differentiated from syphilitic rhagades (literally “cracks”); the latter are not just reddened and inflamed but are fully epithelized cracks, furrows, or ridges, radiating from the corners of the mouth, especially laterally. Rhagades, unlike angular stomatitis, are permanent. Formerly, a medical student could bet against rhagades and for angular stomatitis, but as we eat more wisely and love less so, rhagades may make a comeback.

In Peutz-Jeghers syndrome, adenomatous polyps of the intestine are associated with 10 to 20 pigmented maculae around the mouth and lips. The lesions are about 1 mm in size and like apple jelly in color. If the small, round, circumscribed lesions were red,
like senile hemangiomas or cherry-red spots, one would better diagnose Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia).

In Stevens-Johnson syndrome, the upper and lower lips are extremely swollen and sometimes hemorrhagic. The onset is sudden, and the lesions are nontender. The most common etiology is drug reaction, especially to sulfonamides. It may be accompanied by swelling of the tongue and buccal mucosa.



A great deal has been written about macroglossia, which simply means a large tongue. However, the diagnosis of macroglossia is a matter of opinion because no normal values are available for tongue size. The macroglossia reported in 22% of patients with primary systemic amyloidosis may also be associated with visible changes and palpable stiffness (Kyle and Greipp, 1983), but in Down syndrome and myxedema, it is difficult to be sure how much is macroglossia and how much is simple protrusion.

Some authors have suggested that lateral teeth indentations upon the tongue are presumptive evidence of macroglossia. However, I have seen that finding in a number of patients thought to have neither a disease of the tongue nor any of the known causes of macroglossia, which additionally include neonatal hypoglycemia syndrome (Combs et al., 1966), gargoylism, generalized gangliosidosis, glycogen storage disease, Beckwith-Wiedemann syndrome, acromegaly, and pemphigus vulgaris (Milgraum et al., 1985).


Glossitis means inflammation of the tongue. It can be confusing because the appearance of the tongue is different at different stages of the disease (Beitman et al., 1981). First, there is papillary hypertrophy, then flattening, followed by granular fusion, and finally atrophy. At first, the color of the tongue may be ruddy, “beefy,” or magenta, but when atrophy occurs, the tongue will become pale and smooth and shiny.

Causes of glossitis (some of which overlap) include regional enteritis; alcoholism; sprue; kwashiorkor; pernicious anemia; malabsorption syndromes; deficiencies of pyridoxine, thiamine, niacin, or riboflavin; amyloidosis; and (rarely) the carcinoid syndrome. In one study of patients with iron deficiency anemia, who had an average hemoglobin level of 8.7 g per dL, glossitis was seen in 17% (Kalra et al., 1986).

Haemophilus influenza type b (Hib) can cause an infective glossitis, a less serious condition than the epiglottitis caused by the same disease (vide infra). It is uncommon for other viruses or bacteria to involve the tongue (Schneiderman, 1990).

In geographic tongue, also called migratory glossitis, areas of denuded epithelium appear and are restored to normal, with the pattern changing over periods of a few days. The patient may suffer considerable anxiety from this otherwise harmless condition. Appearances similar to that of geographic tongue can occur in pustular psoriasis, in Reiter syndrome, and with the use of strong mouthwashes (Schneiderman, 1990). Chronic overgrowth of Monilia usually produces a white coating over the tongue but can in some cases have the appearance of a geographic tongue.

Black Tongue

A hairy black tongue secondary to broad-spectrum antibiotic administration is usually attributed to Aspergillus niger, a customarily harmless organism that quietly vacates this ecologic niche after antibiotic administration is stopped.

White Patches

Monilia spots, which look something like flecks of cottage cheese, can be scraped off, although that often leaves a denuded bleeding undersurface. Leukoplakia, by contrast, cannot be scraped off with a tongue blade because it is intrinsic. Candida or Monilia is the culprit in about 96% of chemotherapy-induced fungal infections and is a frequent presenting sign of human immunodeficiency virus (HIV) infection. Other sites commonly involved are the buccal, gingival, palatal, and pharyngeal mucosa, as well as the commissures of the lips.

Hairy leukoplakia is a distinctive lesion that occurs in persons seropositive for the acquired immunodeficiency syndrome (AIDS), who are at increased risk of developing frank AIDS (Centers for Disease Control, 1985; Hollander et al., 1986). It consists of white warty or corrugated projections, particularly on the lateral aspects of the tongue and cheeks (Mindel, 1987). Hairy leukoplakia also occurs in other immunosuppressed conditions, being about as common in kidney transplant recipients as in HIV-positive persons (Greenspan and Greenspan, 1996). It has been described in a patient with chronic renal failure (De Kaminsky et al., 1995) and in an HIV-negative asthmatic patient receiving systemic steroids (Zakrzewska et al., 1995).

Other Lesions

  • A smooth, round, red mass at the base of the tongue may be a lingual thyroid.

  • The tongue can become so red and inflamed that it resembles a strawberry. This appearance, due to the desquamation of the filiform papillae, may result from the erythrogenic toxin of scarlet fever or from other febrile illnesses, particularly in toxic shock and in Kawasaki disease in children.

  • Absence of the fungiform papillae has been associated with familial dysautonomia.

  • Mucosal neuromas, which may occur in Sipple syndrome (type II B or type III multiple endocrine neoplasia or adenomatosis syndrome), are illustrated in Fig. 13-1.

  • The location of indurated ulcers of the tongue can be diagnostically helpful. If they occur at the tip, in the midline, one should consider primary lues. Any midline-indurated ulcer, whether or not it is at the tip, could also be tuberculosis. Histoplasmosis is a rare cause of indurated midline tongue ulcers. An indurated ulcer located laterally is suggestive of cancer, but cancer almost never appears as a midline lesion. A ragged, painful lesion on the undersurface of the tongue suggests Behçet disease, although the lesions of this disease may also occur on the dorsal surface. Any collection of multiple indurated ulcers should suggest tuberculosis.

  • There are two types of tongue fissures, congenital and syphilitic. In the congenital case, most of the fissures are transverse. (They are of no clinical significance.) In syphilis, most of the fissures are longitudinal.

  • Mucous patches on the tongue frequently occur in secondary syphilis (Fig. 13-2).

  • Blanching of the tongue because of arterial insufficiency due to giant cell arteritis occurred for 5 to 10 minutes at a time in one unusual patient (Grahame et al., 1968). Emboli from bacterial endocarditis can cause portions of the tongue to blanch. Liebermeister syndrome is blanching of half of the tongue, as may occur in an air embolism.

  • Caviar lesions, resembling little globs of purple-black caviar (as from the sturgeon, not orange caviar from the salmon) or perhaps buckshot, occur under the tongue. These are varicosities in the superficial sublingual veins, and their only importance is that they may frighten patients who notice them while looking in the mirror (Bean, 1958).2

  • Erythematous candidiasis is less obvious than the white plaques of thrush or pseudomembranous candidiasis, but it is just as important as a marker of the progression of HIV infection. It manifests as smooth depapillated areas on the palate and dorsal surface of the tongue (Greenspan and Greenspan, 1996).

  • The tongue may also show the lesions of aphthous stomatitis, lichen planus, Peutz-Jeghers syndrome, and Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia). White reticulated lesions and erosions clinically identical to lichen planus are the most characteristic changes in chronic graft versus host (GVH) disease and occur in up to one third of such patients. Onset of chronic GVH disease is between 100 and 400 days after transplantation (Eisen and Lynch, 1998).

FIGURE 13-1 Mucosal neuromas are seen at the anterior edges of the tongue. Do not look for them at the base because the fungiform papillae might confuse you.

FIGURE 13-2 Mucous patch of tongue due to secondary syphilis. (From U.S. Public Health Service. Syphilis: A Synopsis. Public Health Service Publication No. 1660, January 1968, with permission.)

Other Findings

Examination of the sense of taste and of the motor function of the tongue is described in Chapter 26. Examination of the sublingual veins is covered in Chapter 19.



Children who have had neonatal jaundice may have biliverdin green teeth later in life. Tetracycline administration (during pregnancy or infancy) may cause brown teeth. Fluorosis may cause brown-and-black pits. Red teeth are seen in erythropoietic porphyria but not in the more common acute intermittent porphyria. Dead teeth become slightly darker than the others.


The teeth should be counted in any case in which a mysterious lesion appears in the jaw because it could be an odontoma. Dr Phil Bromberg of North Carolina first taught me the value of counting the teeth of a patient with a lung abscess—it is better if this is done before a tooth is found on the chest film.

Loose Teeth

Most cases of loose teeth result from tooth-and-gum disease but can result from jaw tumors or mercurialism. Periodontal disease
is characterized by gingival pyorrhea and gum recession, the latter being the origin of the term “long in the tooth” because it especially afflicts the senescent.

Dental Restorations

For more than a century, dental amalgam—a mixture of elemental mercury and a silver-dominated metal alloy—has been the most widely used dental-filling material. It has been a source of recurring controversy. Policy differences within Europe made dental amalgam a test case for the European Community’s medical device regulations (Gelband, 1998). Austria, Germany, and Sweden advise restriction of amalgam use or its removal in certain situations (as for children or pregnant women), and some other nations restrict its use through environmental regulations (Wahl, 2001). In the US, extracted amalgam fillings or amalgam-containing teeth must be disposed of as toxic waste.

According to the American Dental Association (ADA), “Dental amalgam (silver filling) is considered a safe, affordable, and durable material that has been used to restore the teeth of more than 100 million Americans…. Issued in late 1997, the FDI World Dental Federation and the World Health Organization consensus statement on dental amalgam stated, ‘No controlled studies have been published demonstrating systemic adverse effects from amalgam restorations’” (American Dental Association, 2002). The only side effects acknowledged by the ADA or the FDA are rare allergic or hypersensitivity reactions (U.S. Food and Drug Administration, 2002). Dentists are constrained against stating otherwise by the ADA code of ethics and the threat of sanctions by licensure boards. ADA Resolution 42H-1986 states: “the removal of amalgam restorations from the nonallergic patient for the alleged purpose of removing toxic substances from the body when such treatment is performed solely at the recommendation of the dentist is improper and unethical” (Odom, 1991).

Despite the widespread use of amalgam, there are no completed long-term large-scale studies of its health effects (Gelband, 1998). There are numerous case reports of severe systemic and neurologic symptoms that resolved upon removal of the fillings (Engel, 1998; Stock, 1926, 1939; Talbot, 1883). Additionally, oral and dental symptoms have been described, including loosened teeth, gingivitis, lichen planus, bleeding gums, and bone loss.

Quantitatively, dental restorations are the most significant non-occupational cumulative source of human exposure to mercury. Mercury exposure averages from 3.9 to 21 µg per day as elemental mercury from dental amalgam, 5.3 to 10.3 µg per day from food sources, 4.3 µg per day as inorganic mercury, and 1 to 6 µg per day as methylmercury from fish (Aposhian, 2004). Additionally, certain vaccines contain up to 25 µg Hg per dose as ethylmercury from thimerosal. Clearly, there are wide differences in individual susceptibilities to any potential untoward effects. Moreover, there are many difficulties in the accurate measurement of the absorbed dose of mercury from amalgams (Eley, 1997a,b).

Count the number of amalgam surfaces in your patients’ fillings. Be prepared to answer the questions of patients, especially those who frequent the Internet. Removal of fillings is not a procedure to be undertaken lightly.

Ask about and document the presence of endodontic restorations (root canals). These could serve as an asymptomatic nidus of infection, as nerves are destroyed in the procedure. Rare reported complications have included multiple liver abscesses (Schiff et al., 2003), precipitation of altitude sickness at a relatively low altitude (Finsterer, 1999), and recurrent pneumococcal bacteremia (Kragsbjerg and Rydman, 2001).

Other Findings

  • Lipstick adhering to the teeth suggests dry mucous membranes, for example, in the Sjögren syndrome (sicca syndrome).

  • Erosion of the enamel on the lingual, palatal, and posterior surfaces of the teeth because of frequent contact with gastric acid is a sign of bulimia (Mitchell et al., 1987).

  • Increased interdental spaces may be congenital or acquired, as in acromegaly.

  • Transverse ridging of the teeth may be seen in children with previous episodes of bone growth arrest due to deficiency of vitamin C or D.

  • Conditions of the teeth seen in congenital syphilis include the best-known Hutchinson teeth (Fig. 13-3). Hutchinson, an ophthalmologist, described the incisors as follows (Hutchinson, 1859):

    On looking at his teeth, all doubt as to the real nature of the case was dispelled. The lower incisors, just cut, were large but presented singularly irregular edges, being thin and unequally serrate. The upper incisors were all deeply notched.

    These teeth are sometimes called the notched teeth of congenital syphilis. Sometimes there is no notching of the incisors, but the teeth are still short and thin and tapered like the tip of a screwdriver; hence, they are called “screwdriver teeth.” The molars may also be involved in congenital syphilis. The crown may consist of an agglomerate of unusual enamel globules resembling a mulberry (Fig. 13-4), hence the name “mulberry molars.”

  • Rampant decay seen with methamphetamine abuse (“meth mouth”) is caused by the drug’s enamel-eroding hydrochloric acid as well as the user’s generally poor oral hygiene and consumption of sweet beverages owing to dehydration and sugar cravings.

  • Probing the area where the third molar should be can often lead to the detection of an impacted wisdom tooth, which can be the source of a low-grade fever of inapparent origin. The tooth is usually covered with a layer of gum under which bacteria feed on trapped food particles.

  • Fever of inapparent origin can also be due to an apical abscess. One may be able to find a single tooth that is sensitive to direct percussion. Alternately, one can screen all such patients with the Panorex, but the finding of tooth sensitivity is bound to increase the predictive value of this test if selectively ordered.

FIGURE 13-3 Congenital syphilis: Hutchinson teeth. Note the notched edges and “screwdriver” shape of the central incisors. (From U.S. Public Health Service. Syphilis: A Synopsis. Public Health Service Publication No. 1660, January 1968, with permission.)

FIGURE 13-4 Congenital syphilis: Moon’s “mulberry” sixth-year molar of late congenital syphilis. (From U.S. Public Health Service. Syphilis: A Synopsis. Public Health Service Publication No. 1660, January 1968, with permission.)

Gums (Gingiva)

All ulcerations of the mucosa may also affect the gums.

Hypertrophy of the gums in dentulous patients may be seen in chronic administration of phenytoin (diphenylhydantoin), leukemic infiltration (particularly monomyelocytic leukemia), scurvy, or (rarely) lues. Cyclosporine and any of the calcium-channel blockers may also induce gingival hyperplasia; the condition has most commonly been reported with nifedipine (Eisen and Lynch, 1998).

Bleeding of dentulous gums frequently results from periodontal disease. It also occurs in a variety of platelet defects, but it does not usually occur spontaneously with coagulation factor defects. Bleeding gums are seen in up to 93% of patients with scurvy but not in scorbutic patients who are edentulous (Vilter et al., 1946).

Periodontal conditions associated with the HIV infection include linear gingival erythema, possibly due to vasoactive cytokines; severe periodontal infections; and necrotizing ulcerative periodontitis (Greenspan and Greenspan, 1996).

The gingiva commonly appears healthy in periodontitis, giving no evidence of the destruction of the underlying supporting structures. Detection and diagnosis depend on a careful dental examination and radiographs. Bacterial growth and the consequent tissue destruction are facilitated by plaque and calculus on the teeth.

The possible role of periodontal disease in systemic conditions such as atherosclerosis and respiratory infections is a subject of investigation and controversy (Scannapieco and Genco, 1999). It could increase the risk of future cardiovascular disease by nearly 20%, with a 44% increased risk in persons aged 65 or under (Janket et al., 2003). Because about 30% of the American population has periodontal disease, the public health consequences could be significant (Slots and Kamma, 2001). It is worthy of note that about 50% of patients with coronary heart disease do not have one of the currently established risk factors, and there is increasing evidence of a role for inflammatory factors in atherogenesis (Armitage, 2000).

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Aug 10, 2020 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on The Oropharynx
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