(1) Generalities

If you can excuse the pun, it is wise to be nosy about the nose. In fact, examination of this important facial appendix may reveal unsuspected abnormalities that lead to a diagnosis of either systemic diseases or capital sins (such as cocaine abuse).

(2) The External Nose

1 What are the normal structures of the external nose?

They are shown in Fig. 6-1:

Bridge: Located superomedially and representing the bony upper third of the nose

Alae (wings in Latin): Cartilages that make up the inferior, medial, and lateral two thirds of the nose

Nares: The paired orifices (i.e., the nostrils)

Tip and columella

Figure 6-1 The external nose.

(From Epstein O, Perkin CD, de Buono DP, Cookson J: Clinical Examination, 2nd ed. St. Louis, Mosby, 1998.)

2 What is rhinophyma?

From the Greek rhino (nose) and phyma (tumor), this is a variety of acne rosacea characterized by a bulbous and rather prominent nose. It is also referred to as copper-, hammer-, or potato-nose since the skin is thickened, erythematous, nontender, and often covered with multiple telangiectasias (rum or gin blossoms). In fact, other colorful lay terms for this condition include brandy nose, rum nose, and toper’s nose—all paying tribute to its alleged association with the bottle, which is actually rather loose. Pathology shows follicular dilation and sebaceous hyperplasia, with fibrosis and hypervascularity. Of note, rhynophima may degenerate into basal cell carcinoma.

3 What are the causes of rhinophyma?

The ones conventionally blamed are climatic exposure and alcohol, with the best example of gin blossoms being those of the great comedian W.C. Fields, a man whose nose was directly proportional to his affinity for liquor. Rhinophyma is also rather common among politicians, with an early phase of it noted in the 42nd U.S. president, Bill Clinton. If this prompts you to wonder whether Pinocchio had rhinophyma, too, the answer is no. Pinocchio had variable rhinomegaly, a peculiarly reversible condition related to his telling lies.

4 Is there any scientific basis for the “Pinocchio effect”?

Yes. Recent evidence indicates that liars may indeed experience nasal changes, resulting in a telltale itch that eventually prompts them to unconsciously touch their nose. To corroborate this phenomenon, Alan Hirsch, director of the Chicago-based Smell and Taste Research Foundation, gathered 23 giveaway signs (both verbal and nonverbal) of “mendacious speech” and recently used them to analyze Bill Clinton’s famous 1998 grand jury testimony on the Lewinsky affair. Overall, Clinton did 20 of the 23 signs, but whenever being particularly untruthful (or “legally accurate”), he consistently touched his nose, which brings us back to Collodi’s Pinocchio and science. The nose contains abundant vascular erectile tissue (an unfortunate property it shares with the penis), which involuntarily dilates whenever a person lies, thus making the node redder, bigger, and itchy. Hence, the repetitive nose-touching of liars. Hirsch honored Collodi’s insight by naming this phenomenon the “Pinocchio effect.” His observation has been confirmed in other famous cases. For example, even O.J. Simpson touched his nose rather frequently during trial when describing Nicole Brown Simpson’s murder. Hence, simple observation might allow policemen, attorneys, psychiatrists, and everyone else to tell whether someone is lying. Or, as Yogi Berra used to say, “You can observe a lot by watching.”

5 What is a saddle nose? Does it really exist outside of board questions?

A saddle nose is the congenital (or acquired) erosive indentation of the nasal bone, turning the distal tip of the nose upward and outward. A true saddle nose (caused by destruction of the bony portion of the nose) is typical of congenital lues, but actually more frequent in Wegener’s granulomatosis. Given the increasing availability of good therapy for both these conditions, a saddle nose has now become less common. A pseudo-saddle nose is instead a feature of relapsing polychondritis, although the destruction in this case involves cartilage and not bone.

6 What are nasal fractures?

They are the most common trauma-related disorders of the nose. They present with severe pain and anterior epistaxis, often from both nares. Periorbital ecchymoses invariably develop 24 hours after trauma, along with significant sequelae, such as septal hematoma or septal deviation. Because these fractures are open, antibiotics are necessary to prevent osteomyelitis.

7 What is a septal hematoma? How does it differ from septal deviation?

A hematoma is a purple and painful nodule in the nasal septum, easily spottable through the nostril. Conversely, traumatic displacement of the nasal septum (i.e., septal deviation) may be difficult to see until later, since edema of the early posttraumatic stages makes physical exam difficult to perform. Both of these complications require referral to an ear-nose-throat (ENT) specialist for drainage or reduction. If undrained, the hematoma may cause the septal cartilage to become ischemic and necrotic, with a resulting permanent nasal deformity.

8 What is lupus pernio?

It is a chronic, nonblanching, diffuse, and purple skin discoloration of the external nose, in the absence of true nasal enlargement (Fig. 6-2). Hence, it differs from rhinophyma. A sign of active sarcoid, it may occur with uveitis, erythema nodosum, and pulmonary involvement. It may also coexist with lesions of the ears, cheeks, hands, and fingers. The term lupus refers to any disfiguring skin condition that, like a wolf (lupus in Latin) “devours” the patient’s facial features. It is thus used with modifying terms to designate various disfiguring skin diseases, such as lupus verrucosus, lupus erythematosus, lupus tuberculosis, lupus vulgaris, and, of course, lupus pernio. Pernio is Latin for frostbite and refers to the peculiar violet-bluish hue of the condition (see Chapter 3, The Skin, question 265).

Figure 6-2 Lupus pernio.

(From Fitzpatrick JE, Aeling JL: Dermatology Secrets. Philadelphia, Hanley & Belfus, 1996.)

9 What did Rudolph of the reindeer story really have?

Probably rhinophyma, but that begs the question: Did Santa spill the grog while feeding his reindeer?

(3) The Internal Nose

10 What are the normal structures of the internal nose?

The normal internal structures are shown in Fig. 6-3:

1. The vestibules. As indicated by the term, these are paired internal widenings, immediately beyond each naris. They are delimited:

Medially by the septum. Like the external nose, this is partly bony and partly cartilaginous. The word septum is an anglicized adaptation of the Latin saepire, “to erect a hedgerow.” Indeed, the function of the septum is to provide a medial boundary to each vestibule.

Laterally by a wall of cartilage

2. Deeply beyond the vestibules are the turbinates, or conchae. These are curving bony structures that project into the internal nose. There are three turbinates (and three corresponding meatuses) in each nasal cavity: superior, middle, and inferior. Their main function is to increase the nasal surface for humidification, temperature control, and filtering of inhaled air. To do so, they are covered by a well-vascularized and erectile mucosa.

Figure 6-3 The internal nose.

(From Epstein O, Perkin CD, de Buono DP, Cookson J: Clinical Examination, 2nd ed. St. Louis, Mosby, 1998.)

Pearl:

On routine examination by either otoscope or Vienna speculum, one can only inspect the vestibule, anterior portion of the septum, and the inferior and middle turbinates.

11 What are paranasal sinuses?

They are the frontal, maxillary, ethmoid, and sphenoid sinuses: four hollow and air-filled paired cavities that open through small ostia into recesses of the nasal cavities called meatuses. These are covered by bony shelves lined by erectile soft tissue (the turbinates)—three on each side.

12 And what about the adenoids?

They are aggregates of lymphatic tissue located on the roof of the nasopharynx, just below the sphenoid sinus. They typically regress with puberty and so in adults are usually absent. Yet in infants and children, they may enlarge considerably and cause nasal obstruction, nasal voice, snoring, restless sleep, and mouth breathing. Since mouth breathing in times of facial formation may result in bony changes, affected children often develop an adenoid facies, with a high, arched palate; prominent upper teeth; pinched-in nose; shortened upper lip; a staring expression of the eyes; and a slightly elongated and dumb-looking face. Adenoidal hypertrophy also may obstruct the eustachian tubes and thus result in recurrent middle ear effusions and otitis media.

13 What is the significance of flaring of the nostrils?

Flaring of the nostrils (i.e., of the alae of the nose) is a sign of increased work of breathing, typical of impending respiratory failure. It is often associated with other findings of distress, such as respiratory alternans and abdominal paradox (see Chapter 13, Chest Inspection, Palpation, and Percussion, questions 52–58). It also can occur in peritonitis as a result of impaired and painful excursion of the diaphragm.

14 What are the best tools for inspecting nares and internal nose?

Figure 6-4 Hand-held Vienna speculum.

(Courtesy Chosmic Surgical, Inc., Ellicott City,MD.)

In the absence of these tools, you may simply use fingers and penlight. Either way, always instruct the patient to first blow the nose (gently but forcibly) to expel any mucus.

15 Is inspection of nasal secretions useful?

Yes. In fact, there is quite some value in snot, the colloquial term for excessive flow of nasal mucosa. Although the butt of vulgar jokes, snot is actually noble in origin, going all the way back to the Old English gesnot. It also retains diagnostic value, since different diseases tend to produce different snots:

16 What is an abscess of the nasal vestibule?

It is a superficial abscess of hair follicles (furunculosis), usually caused by Staphylococcus aureus and not uncommonly located in the nasal vestibule or septum. Quite painful, it presents as an erythematous and fluctuant nodule in the septal mucosa. Usually treated with antibiotics and warm compresses, it may require incision and drainage to avoid cavernous sinus thrombosis.

17 What are the causes of swelling/bumps in the nasal septum?

All require ENT referral, since an untreated hematoma (or abscess) may result in septal perforation.

18 What are the most common causes of airflow obstruction in one or both nares?

In addition to the conditions previously listed, other causes include nasal mucosa edema, septal deviation, and foreign bodies—all diagnosable by exam. Foreign bodies are especially common in children, given their unique penchant for inserting rocks, twigs, and crayons into nares and various body orifices.

19 What are nasal polyps?

They are pedunculated, fleshy, and friable structures that hang from the lateral or septal mucosa. Polyps originate from localized swellings of either sinus or nasal mucosa, initially small, but eventually growing with each recurrence of submucosal edema until they may even protrude from the vestibule and cause nasal obstruction. They are often multiple, clearly visible, easy to move back and forth, and not tender (which differentiates them from other internal nasal structures). They are common in chronic (atopic) rhinitis and aspirin sensitivity (often in association with asthma) and can be easily removed through endoscopy.

20 What is a papilloma of the nasal vestibule?

It is a wart of the inner nose. In contrast to the more common polyp, papillomas are jagged in appearance and more likely to bleed. Like polyps, they can interfere with the sense of smell and cause obstruction. They are easily visible on exam and must all be removed since they can undergo neoplastic degeneration. Like warts elsewhere, they often recur.

21 What is a nasopharyngeal carcinoma (lymphoepithelioma)?

It is a sequela of Epstein-Barr virus (EBV) infection, rare in Europe but frequent in Southeast Asia, where it represents the third most common cancer. Tumor growth is often asymptomatic, and presentation is late, typically with cervical lymphadenopathy. Hence, the prognosis is poor, even though screening for anti-EBV antibodies may help detect early and treatable disease.

22 What does a nasal septal perforation look like?

Like a hole in the septum. This can be demonstrated on inspection or by shining a light into one nostril and seeing it transilluminate both sides.

23 What are the common causes of a septal perforation?

The traditional four are:

24 What are the less-common causes of perforation?

25 What are the nasal manifestations of a basilar skull fracture?

In addition to the direct facial trauma, patients often show evidence of nasal fracture, such as periorbital ecchymoses, swelling/tenderness of the nasal bridge, and anterior epistaxis. There also may be cerebrospinal fluid rhinorrhea (leakage of cerebrospinal fluid [CSF] through the fracture site). This is a risk factor for the development of meningitis and thus necessitates prompt surgical attention.

26 How do you recognize CSF rhinorrhea?

By placing a drop of nasal secretions over a paper tissue. In CSF rhinorrhea, this will serve as a “poor man’s” paper chromatography, showing a clear halo around “nasal” secretions that represent instead spinal fluid leakage. Alternatively, the glucose content of secretions may be measured at the bedside by using a Chemstrip. In patients with CSF rhinorrhea, this will reveal a high glucose concentration, close to spinal fluid levels of 40–80   mg/dL.

27 What is a cold? What are its nasal manifestations?

The common cold, one of humankind’s most frequent afflictions, has a plethora of nasal manifestations: swollen mucosa (to the point of obstruction), stuffy feeling, and serous or purulent nasal discharge. Since it represents a viral infection of the upper respiratory tract, there may be concomitant serous otitis media, nonexudative pharyngitis, and shotty nodes.

28 What results in swelling of the nasal mucosa?

One of three causes:

29 Can you diagnose the cause of GI bleeding by peeking into the patient’s nose?

Yes, bleeding in the gut may indeed be linked to the nose. The most common reason is simple epistaxis, wherein patients swallow nasal blood, resulting in guaiac-positive stools and even melena. More rare are the multiple nasal telangiectasias of Rendu-Osler-Weber syndrome, an autosomal dominant disorder characterized by multiple (and often bleeding) vascular lesions of the gut, mouth, face, extremities, and chest. The tongue and lips also may have telangiectasias.

30 Who was Rendu?

Henry J.L. Rendu (1844–1902) was the grandson of a distinguished Parisian painter and the son of an agricultural inspector. An art lover, he was so fascinated by his father’s profession as to pursue a medical career only after a stint in agriculture, geology, and botany. Still, he never lost his passion for plants and eagerly maintained it as a lifelong hobby. At age 43, he finally joined the staff of the Necker Hospital in Paris (the same one where Laënnec had been chief of chest medicine), rapidly gaining fame as a charismatic lecturer and gifted clinician.

31 Who was Weber?

Frederick P. Weber (1863–1962) was a British physician, already encountered in the ear chapter because of Sturge-Weber disease. Educated in Cambridge, Vienna, and Paris, Weber cultivated throughout his life an interest in medical philosophy, the arts, and numismatics, which he then expressed in many books and articles. His father was Herman D. Weber (1823–1918), himself a famous and long-lived physician (he is the same Weber who described the midbrain syndrome that still carries his name). Weber père was a charming man with many interests, who taught himself English so that he could read Shakespeare and befriend, among others, Addison, Carlyle, and several Waterloo veterans (including the famous Sir Peregrine Maitland of Wellington’s cry: “Now it’s your time, Maitland, now it’s your time!”). Increasingly fascinated by England, Weber senior eventually moved there in 1854, married an Englishwoman, and became member of the Royal College of Physicians. Both father and son were avid climbers and advocates of physical exercise as key to long and productive lives (which served them well, since both lived well into their 90s). The older Weber climbed several mountains in the Italian Alps (including one for his 80th birthday) and walked 40–50 miles/week.

32 Who was Osler?

Sir William Osler (1849–1919) is such a legend that a few lines in this chapter will do him a disservice. Born in the backwoods of Canada as son of a missionary, Osler was so spiritual that early in life he even considered joining the clergy. A charming and compassionate man with a prankish twist, he was a charismatic teacher, a superb bedside diagnostician, and a good person who never lost his respect for patients as fellow humans in need of help. After teaching in Canada and the United States, he moved to England, where he became regius professor of Medicine at Oxford. The last part of his life was unfortunately quite sad, tormented by the memory of his only son, who had died in Flanders toward the end of World War I.

33 What is anosmia?

It is the congenital or acquired absence of smell (from the Greek an, lack of, and osme, smell).

34 Do smell and taste interact?

Yes. Patients whose olfaction is weakened or absent (hyposmia or anosmia) can only taste the five fundamental sensations of sweet, sour, bitter, salty, and umami (i.e., the taste of glutamate). This is because flavor results from oral combination of the five basic tastes plus the foodstuff’s odor and various chemical characteristics, such as texture, temperature, and other sensations. Hence, flavor is typically absent when olfaction is also absent. Overall, smell disorders are more common than isolated taste disorders (such as hypogeusia and ageusia). Perversion of taste can also occur, with misreadings and distortions, such as foul tastes from otherwise pleasant substances.

35 Is perception of alcohol odor an indication that the sense of smell is intact?

No. Alcohol is an irritant. Hence, it stimulates the trigeminal rather than the olfactory endings of the nasal mucosa. That is why even patients without olfactory lobes (such as those with Kallmann’s syndrome) can “feel” an alcohol sponge. Same is true for other irritants, such as ammonia and pepper. To test the sense of smell, you should use nonirritating substances with strong odors. Coffee and spices (such as cinnamon, cloves, nutmeg) are excellent choices.

(1) Generalities

If it is true that you should not look a gift horse in the mouth, it is also true that patients are not horses. Hence, always do a good inspection of the oropharynx, since mouth and tongue lesions may provide important clues to systemic disorders. Even the lowly teeth, which represent important risk factors for serious anaerobic infections of the respiratory tract, can hint at an otherwise unsuspected systemic or psychiatric disorder. In fact, lead poisoning, congenital syphilis, and bulimia can all be recognized by an astute dental examination. Unfortunately, far too many patients have gone undiagnosed because of a poor or incomplete mouth exam.

(2) Posterior Pharynx and Tonsils

36 What are the two main structures of the posterior pharynx?

The hard and the soft palate (Fig. 6-5). These are supported by the anterior and posterior pillars.

Figure 6-5 Anatomy of the oropharynx.

(From Epstein O, Perkin CD, de Buono DP, Cookson J: Clinical Examination, 2nd ed. St. Louis, Mosby, 1998.)

37 What is a cleft palate?

A congenital deformity that is usually corrected in infancy but may persist into adulthood. It is quite common (1 case in 1000 live births, with or without cleft lip), with greater prevalence in Native Americans (3.6 cases per 1000 live births), and lower in African Americans (0.3 cases per 1000 live births). Of all cases, 20% are an isolated cleft lip; 50% are a cleft lip and palate, and 30% are a cleft palate alone. Cleft lip and palate together are more common in males, whereas isolated cleft palate is more common in females. Bifid uvula occurs in 1 of 80 patients, often in isolation (see question 38).

38 What is the uvula? What disease processes may affect it?

The uvula (little grape in Latin) is the midline structure that projects from the roof of the posterior pharynx, and whose main function is probably to prevent fluids from entering the nasopharynx upon swallowing. Interesting presentations include:

39 What is uvulomegaly? What are its causes?

Uvulomegaly is a swollen and elongated uvula. Causes are mostly two: one quite common (pharyngitis), and the other exceptionally rare (gamma-heavy chain disease). Uvulomegaly of pharyngitis is often associated with oral manifestations, whereas that of heavy chain disease is associated instead with pancytopenia and “B” symptoms of lymphoproliferative disorders. In both conditions, the uvula may become large enough to cause coughing, snoring, and even gagging.

40 What is a localized reddening of both anterior pharyngeal pillars? What are its causes?

It is a condition that is different from diffuse inflammation of the oropharynx. It was first described by Cunha in association with chronic fatigue syndrome (CFS) and dubbed the crimson crescents. As many as 80% of CFS patients may indeed present with a peculiar purplish discoloration of the two anterior pharyngeal pillars. These crescents are always bilateral, of a vivid crimson color, and quite briskly demarcated from the rest of the pharynx. There is no pain, no sore throat, and no other evidence of pharyngitis. Crescents last for months and gradually fade as disease goes into remission. During exacerbations, however, they may redden again. Although present in 3–5% of nonchronic fatigue patients with nonspecific sore throats, crimson crescents are typically absent in pharyngitis due to group A streptococcus, mononucleosis, cytomegalovirus, or the common viral upper respiratory tract infection.

41 What are the causes of a diffuse reddening of the oropharynx?

The most common are viral and bacterial infections:

42 How common is sore throat?

Very common. In fact, it is the third most frequent presenting complaint in office-based practice, accounting for 4.3% of all visits. Identifying patients with group A beta-hemolytic streptococcal pharyngitis (strep throat) is often difficult.

43 What are the causes of an exudate (i.e., pus) on the posterior pharynx?

Many agents can cause exudative pharyngitis (Table 6-1), the most important being upper respiratory tract viruses, group A beta-hemolytic streptococci, and the EBV.

Table 6-1 Causes of exudative posterior pharyngitis

(Data from Ebell M, et al: Does this patient have strep throat? JAMA 284:2912–2918, 2000.)

44 What are the clinical features of viral upper respiratory tract infections?

Pharyngeal vesicles and ulcers. These are so typical as to argue against group A streptococci being the cause of the patient’s sore throat (see herpangina, questions 87 and 89).

45 What are the clinical features of group A beta-hemolytic streptococcal infection?

Marked and diffuse pharyngeal swelling and redness, with coating of lymphoid tissue by a punctuated or confluent gray exudate. This eventually causes whitish tonsillar spots (follicles), thus giving the disease its name of follicular tonsillitis. Even though the beefy red color of the pharynx typically ends at the soft palate with just a few scattered petechiae, there are often erythema and swelling of the surrounding structures (faucial pillars, uvula, and base of the tongue). Cough and rhinorrhea are usually minimal, but high fever, chills, and mild nausea can be present. Enlarged (and tender) jugulodigastric and anterior cervical lymph nodes are typically palpable, especially at the angle of the jaw. This is particularly true in the early phase of the disease. Throat pain is persistent, often radiating to the ear upon swallowing. In fact, mouth opening is painful and at times difficult. Tongue coating and halitosis can occur too. Local suppurative complications include peritonsillar abscess (<1% of patients treated with antibiotics), retropharyngeal abscess, suppurative cervical lymphadenitis, otitis media, sinusitis, and mastoiditis. More serious complications (such as meningitis, pneumonia, bacteremia, rheumatic fever, and scarlatina) are instead less common.

46 What is scarlatina (scarlet fever)?

It is a typical scarlatiniform rash, characterized by fine scarlet-like papules that start on the trunk, spread to the extremities, and spare palms and soles. The tongue is initially coated (and with enlarged papillae), but later may become denuded (“strawberry tongue”). There are also circumoral pallor and rash accentuation in skin folds, especially in the antecubital fossae (Pastia sign). In very young children, there may even be excoriations around the nares. The rash typically blanches to pressure, has a sandpapery feel, and eventually subsides in 6–9 days, to be then followed by desquamation of palms and soles.

47 When should you think of gonococcal pharyngitis?

When confronted with an exudative and ulcerative pharyngitis that is refractory to standard therapy. Inquire about the patient’s sexual activities, and do a Thayer-Martin culture of the throat.

48 What is infectious mononucleosis? What are its features?

Infectious mononucleosis, the clinical illness caused by EBV, presents after an incubation of 30–50 days with:

49 What are the glandular fever–like syndromes?

They are infections presenting with illnesses clinically indistinguishable from glandular fever (i.e., infectious mononucleosis). These include:

All of these infections share the same nonspecific clinical manifestations of EBV, with severity ranging from a flu-like illness to a very debilitating disease. Acute symptoms include sore throat, fever, tender lymphadenopathy, erythematous rash involving the trunk, and various constitutional symptoms (such as malaise, headache, myalgias). Most symptoms only last a few weeks, but lymphadenopathy and malaise may persist for months.

50 Can strep throat be diagnosed by history and physical examination?

Not really. Although its various findings have good interobserver reliability (with the possible exception of adenopathy), no single element of history or physical exam is powerful enough to confirm the diagnosis of streptococcal pharyngitis. Findings with the highest positive likelihood ratio (LR) (and thus best at ruling-in the disease) are:

No finding, if absent, can rule out the disease. The ones with lowest negative LR are:

Routine use of throat cultures or rapid antigen test may lead to overtreatment of low-risk patients (due to false positive results) and undertreatment of high-risk patients (due to false negative results). Hence, you should rely on a combination of clinical findings. Those that can best separate patients with and without strep throat are:

In addition, strep throat will not present with rhinorrhea or earache, but may instead occur with nausea, vomiting, headaches, and moderate to severe sore throat. Still, the pharyngitis of mono can closely resemble “strep-throat,” with fever, exudates, and adenopathy.

51 What are the causes of a nodule in the posterior pharynx?

52 What is Vincent’s angina of the tonsil?

It is an acute necrotizing infection of the pharynx caused by the same organisms that cause “trench mouth” gingivostomatitis (i.e., fusiform bacilli and the Borrelia vincentii spirochete). Patients present with a few days of rapidly worsening unilateral sore throat, ipsilateral referred earache, and fetid bad breath/bad taste. Exam reveals submandibular lymphadenopathy and an ulcerated tonsil, with a deep, well-circumscribed, and grayish base that easily bleeds upon swabbing. A smear of the exudate confirms the presence of fusobacteria and spirochetes.

(3) Oral Mucosa

54 What are the best sound and tongue positions for the task?

There are three schools of thought: (1) the traditional falsetto “Ahhhh,” with tongue protruded; (2) “Ae” rather than “Ahhhh”; and (3) “Ha,” with the tongue maximally pulled in. Although no studies have assessed the predictive values of these sounds, the controversy is best settled by the universal rule: use whatever works best for you, and make sure that by doing so you can visualize the patient’s tonsils and oral mucosa. Yet, proper examination of the throat remains challenging. It requires elevation of the soft palate and uvula and depression of the posterior tongue. Although the tongue blade does help, it also can induce gagging, coughing, and even biting. An alternative consists in asking the patient to pant, or in cases of small children, to imitate a puppy.

55 What is the descriptive nomenclature of lesions in the oral mucosa?

One akin to that of dermatology (see Chapter 3, question 2), similarly relying on lesions’ size and characteristics to classify them as:

Other terms, such as vesicles and bullae for fluid-filled lesions, are similarly used.

56 What are the colors of oral lesions?

It depends on the lesion. Colors range from flesh to white, black, and red (Table 6-2).

Table 6.2 Oral Lesions*

* See text for further discussion.

57 What causes flesh-covered palpable lesions in the oral mucosa?

The most common are normal anatomic structures, such as Wharton’s or Stensen’s ducts, which drain, respectively, the submaxillary and parotid salivary glands.

58 What is a ranula?

Latin for small frog, a ranula is a unilateral, painful, dome-shaped fluctuant nodule on the floor of the mouth. It is caused by the salivary duct obstruction of a sublingual or submandibular gland, resulting in mucus retention. It may require surgery.

59 What is a torus?

It is a benign and nontender exostosis (i.e., a cartilage-capped and mucosa-lined bony spur). Based on its origin, a torus may be mandibularis or palatinus. The mandibularis is smaller and located on the lingual surface of the mandible, whereas the palatinus is larger and originates from the midline of the hard palate. The term torus is Latin for protuberance, used most commonly to indicate the bony structures of the skull. Tori are benign and require only clinical recognition.

60 Who were Wharton and Stensen?

61 What is a buccal exostosis?

It is a benign and painless bony spur (which is the literal meaning of the term “exostosis”), very much like the torus (previously discussed), except that its location is different: on the facial surface of either the upper, or less commonly, lower jaw. It originates in the alveolar bone during early adulthood and may slowly enlarge over the years. Yet, it is more commonly self-limited, never undergoes neoplastic degeneration, and usually requires no treatment, other than a differentiation with other mucosal-colored lesions.

62 What are the two most common causes of white spots in the oral mucosa?

Figure 6-6 Squamous cell carcinoma presenting as leukoplakia with erythematous and verrucous areas.

(From Sonis ST: Dental Secrets, 2nd ed. Philadelphia, Hanley & Belfus, 1999.)

Less common causes of white spots in the oral mucosa include:

63 What is hairy leukoplakia?

A distinctive lesion of the lateral aspects of the tongue and, occasionally, of the buccal mucosa of the cheeks (see also question 100).

64 What is oral thrush?

Candidal infection of oropharyngeal mucosa. This presents as multiple whitish papules and plaques, often surrounded by an erythematous rim. Unlike hairy leukoplakia (which is part of the mucosa, and not an overlay), candidal lesions are easily scraped off with a tongue blade, leaving an underlying mucosa that is highly inflamed and often bleeding. Diagnosis is confirmed by potassium hydroxide (KOH) preparation. Oral thrush patients are either immunocompromised (as a result of AIDS, high-dose steroids, chemotherapy) or on inhaled corticosteroids.

65 What are Koplik’s spots?

They are less-common causes of white oral lesions, presenting as a cluster of tiny white macules on the buccal mucosa, near the first and second molars. Consistent with early rubeola, they precede the skin rash by a day.

66 Are Koplik’s spots specific for rubeola?

No. They also may be seen in echovirus and adenovirus infections. Hence, they are an interesting, albeit minor, feature of systemic viral infection.

67 Who was Koplik anyway?

Henry Koplik (1858–1927) was an American pediatrician. Born in New York and trained in Berlin, Vienna, and Prague, he eventually practiced at the Mt. Sinai Hospital of New York. In addition to being one of the founding fathers of the American Pediatric Society, Koplik also was instrumental in developing the first sterilized milk deposit for American infants.

68 What are Fordyce’s spots?

They are tiny, whitish (or more often yellowish) dots, 1   mm in size. They are found on lips, cheeks, or tongue and represent normal mucosal sebaceous cysts. They were described in 1896 by the American dermatologists John Fordyce.

69 What is Wickham’s sign?

Wickham’s sign (or Wickham’s striae) is a lacy, white, reticulated pattern on the surface of lesions in patients with lichen planus. Lesions are flat topped, shiny, pruritic, whitish/grayish, streaky, and with a violaceous background. They are located not only on the buccal mucosa but also on flexor surfaces and male genitalia. At times, they may form linear groups and thus give a patterned configuration that resembles lichens on rocks.

70 Who was Wickham?

Louis F. Wickham (1860–1913) was a French dermatologist and one of the early promoters of radium as treatment of skin cancer. His name also is linked to a special knife that he designed for the scarification of lesions in lupus vulgaris.

71 Why is leukoplakia a “garbage can diagnosis” that should be abolished?

All white lesions used to be termed leukoplakia, since the word, quite conveniently, means white lesions in Greek (leukos, white, and plax, patch). Subsequently, the term was unjustly elevated to the rank of diagnosis. Since it is absolutely impossible to differentiate benign from malignant white lesions solely on the basis of inspection and palpation, the term leukoplakia should be returned to its original descriptive meaning. Hence, suspicious white lesion must be biopsied.

72 What features of a white lesion increase its chance of being malignant?

73 List the causes of pigmented spots in the oral mucosa.

74 What is Peutz-Jeghers syndrome?

Named after the Dutch John Peutz and the American Harold Jeghers, this is an autosomal dominant disease characterized by pigmented and hamartomatous intestinal polyps. It is associated with multiple melanin deposits on the mucocutaneous junctions of the mouth and, occasionally, anus. Pigmented spots (1–5   mm in diameter) appear shortly after birth or in very early childhood. They also may be seen on the lips, oral mucosa, and dorsal aspects of fingers and toes. Perioral lesions usually fade with age, whereas lesions on fingers, toes, and oral mucosa become more prominent. Peutz-Jeghers carries a slightly higher risk of gastrointestinal malignancies, albeit not as high as Gardner’s syndrome.

75 What is smokers’ melanosis?

A benign focal pigmentation that presents as multiple, irregularly shaped, flat, and brownish macules, <1   cm in diameter, and mostly localized over the maxillary (and mandibular) anterior labial gum, buccal mucosa, and floor of the mouth and soft palate. Smoker’s melanosis requires prolonged exposure to cigarette smoke and thus occurs only after the third decade of life. It is not due to local stains, but to a benign increase in melanocytic activity. Since melanocytes are stimulated by estrogens and progesterone, smoker’s melanosis is much more common in women. It is also associated with yellow staining of the teeth and fingernails and with an increased risk of oral carcinoma. Differential diagnosis includes physiologic pigmentation (usually in dark-skinned individuals), Peutz-Jeghers syndrome, Addison’s disease, and melanoma.

76 How are skin and mucosae in Addison’s disease? Who was Addison?

Skin and mucosae are hypergmented. Buccal mucosa (as well as lips, tongue, and gingiva) may also have a few scattered melanotic spots. The disease is named after Thomas Addison (1793–1860), a contemporary of Bright and Hodgkin. Born in Newcastle and educated in Edinburgh, Addison taught and practiced at Guy’s Hospital in London, gaining a reputation as a brilliant teacher and an astute clinician. Yet his shy and introverted personality, plus his emphasis on diagnosis more than treatment, adversely affected his popularity. Even his work on primary adrenal insufficiency (published in London in 1855) was almost discounted as fiction. Plagued by recurrent bouts of depression, Addison eventually jumped to his death at age 67.

77 How do you distinguish Peutz-Jeghers syndrome from plain freckling?

The pigmented spots of Peutz-Jeghers are not only more prominent on the lips than the surrounding skin but also are present in the buccal mucosa. This is not the case with freckling (see question 113).

78 List the common causes of red spots in the oral mucosa.

79 What does pyogenic granuloma look like?

As a red, small, well-defined, and rounded nodule composed of highly vascular granulation tissue. This projects from the buccal mucosa and frequently ulcerates. Histologically, it resembles a capillary hemangioma.

80 Describe the lesions of erythema migrans.

They are multiple, flat, irregularly shaped red patches with raised white rims, usually located on the buccal mucosa, ventral tongue, and gum. Erythema migrans is often associated with a geographic tongue, which is in fact also referred to as erythema migrans lingualis (i.e., benign migratory glossitis, geographic tongue. See question 97).

81 What are palatal petechiae?

They are scattered lesions near the border of the hard and soft palate. These are highly suggestive (but not pathognomonic) of infectious mononucleosis, where they may be seen in two thirds of patients toward the end of the first week of illness.

82 What do the oral lesions of Kaposi’s sarcoma look like?

As raised or flat purplish lesions. These typically affect the palate of AIDS patients, while instead sparing the elderly, nonimmunocompromised patients of Mediterranean origin who have the classic form of the disease.

83 What are the causes of ulcers and erosions in the oral mucosa?

The most common are (1) thermal injuries (such as burns from hot coffee), and (2) aphthous ulcers (canker sore, from the Greek aphthae, ulcerations). Less common (but more ominous) causes include (1) autoimmune gingivostomatitis (pemphigus, pemphigoid, and Stevens-Johnson syndrome), which causes a tender, painful, inflammatory sloughing of mucosa, usually preceded by vesicles or bullae; (2) carcinoma or primary syphilis, both of which produce a painless and solitary ulcer; and (3) viral gingivostomatitis (from either herpes or coxsackievirus).

84 What are aphthous ulcers?

They are among the most painful mucosal erosions: round or oval, with a whitish-yellowish color and a reddened rim. Aphthous ulcers come in three different types: minor, major, and herpetiform:

Patients with benign aphthous ulcers should have no fever, adenopathy, gastrointestinal symptoms, arthritis, or other skin or mucous membrane involvement (such as uveitis, conjunctivitis, or genital ulcerations). If present, these manifestations suggest an underlying systemic disease and thus should always prompt a thorough diagnostic search. Otherwise, minor aphthae are benign, idiopathic, and spontaneously healing, albeit often recurring.

85 How do you differentiate between a canker and a chancre?

Although both may result in oral mucosal ulcers, there is considerable difference between these two terms:

Both terms actually derive from the Latin cancer (crab), or the Sanskrit karkata (crab) and karkara (hard). Their gloomy connotation reflects the time-honored and ominous significance of having a mouth ulcer, often the first manifestation of the “French disease”: syphilis. Note that the link between syphilis and France was initiated by the Italian physician, astronomer, wine connoisseur, and philosopher extraordinaire, Girolamo Fracastoro, who in 1530 wrote a poem titled: Syphilis, sive Morbus Gallicus (“Syphilis, or the French Disease”). Ironically, the French had acquired syphilis during their 1494–1515 invasion of Italy (and, indeed, tried to dub it the Italian disease, a term that never took). The Italians, in turn, had acquired it from the Spanish sailors who had visited their ports after returning from America. Considering where syphilis probably originated, a more appropriate term would have been the American disease. As for the poem that started it all, its protagonist was indeed Syphilis, a shepherd and, presumably, the first victim of the disease. Fracastoro used the term syphilis again in his medical treatise De Contagione, published in 1546—a true landmark in the history of infectious disease, since it proposed a scientific germ theory that predated Pasteur and Koch by more than 300 years. The term syphilis was eventually adopted into English in 1718.

86 Can the vermilion border of the lip identify the cause of oral mucosal ulcers and vesicles?

Yes. Lesions that cross the vermilion border of the lip and involve the skin are due invariably to herpes simplex. Conversely, lesions that do not cross the border (and are thus limited to the lip) are more likely due to coxsackievirus infection or an autoimmune disease.

87 Where is Coxsackie? Who there has the disease?

Coxsackie is a city in New York state, the proud hometown of patients in whom the virus of herpangina (infection of the oropharynx) was first isolated. This virus is also responsible for aseptic meningitis, pericarditis, myocarditis, and pleurodynia. Of course, coxsackie viruses are not limited to Coxsackie, New York, but cross both interstate and international borders.

88 What is Bornholm and why is it in geographic competition with Coxsackie?

Bornholm is a Danish island in the Baltic Sea, where the syndrome of epidemic pleurodynia (aptly called Bornholm disease) was first described. The intriguing aspect of this syndrome (characterized by sore throat, cough, and paroxysms of pain, usually pleuritic but also abdominal) is that it is caused by a virus named after another geographic location, Coxsackie, New York.

89 Why should you examine the palms and soles of patients with oropharyngeal vesicles/erosions?

Because these patients (especially children with coxsackie herpangina) may indeed present with vesicles on palms and soles, both important clues for explaining a particularly vexing sore throat.

90 Describe the anatomy of the tongue.

It consists of skeletal muscle covered with mucosa. On its dorsum are many exophytic structures (the papillae) that increase surface area and, more importantly, contain taste buds for gustatory sensation. These come in different types: filiform, fungiform, and circumvallate. Filiform and fungiform papillae are small and cover the entire dorsal surface of the organ; circumvallate papillae are instead larger and only located on the posterior dorsum, in semicircular arrangement.

91 What is dysgeusia?

It is the altered perception of taste (from the Greek dys, abnormal, and geusis, taste). It may reflect either local (i.e., involving the tongue) or central abnormalities (involving the nervous system).

92 What is the best way to inspect the tongue?

By achieving its effective protrusion. This is best accomplished by asking the patient to say the infamous “Ahhhh” (or “Aeee,” but probably not “Ha”—as previously discussed) while at the same time protruding and curling the tongue upward, which allows access to the sublingual surface of the organ. Examination of the far interior and lateral aspect can be accomplished by placing gauze on the tip of the tongue, gently grasping it, and pulling it out. Note that a unilateral paralysis of cranial nerve XII (hypoglossal) is associated with asymmetric protrusion of the tongue.

93 Summarize the abnormalities of the tongue.

See Table 6-3.

Table 6-3 Tongue Abnormalities^*

* See text for further discussion.

94 What is macroglossia? What are its causes?

Macroglossia (large tongue in Greek) is a rare finding. The patient presents with indentations on the sides of the tongue (caused by pressure from the lateral teeth), and may also have a history of thickened speech, snoring, or full-blown sleep apnea. Although politicians are at greater risk for developing an occupational variety of this condition, macroglossia is often associated with systemic disorders, such as acromegaly, hypothyroidism, Down syndrome, amyloidosis, and various thesaurismoses. In all these conditions, the enlargement of the tongue is caused by either proteinaceous infiltration or hypertrophy of the muscle. The exception, of course, is politicians (whose macroglossia is due to idiopathic tongue-in-cheek), and some normal people, who present instead with simple lateral indentations, without clear-cut macroglossia or systemic illness.

95 What is a scrotal tongue?

A relatively common finding in the elderly. The tongue has many ugly-looking fissures (hence, the colorful term, scrotal) of otherwise little or no clinical significance.

96 What is a hairy tongue?

Another common condition, characterized by an abnormal desquamation of the filiform papillae,which, instead of being 1   mm long, can become 15   mm in length, thus giving the tongue its characteristic “hairy” coating, plus a brownish-to-blackish discoloration (lingua villosa nigra, or “black hairy tongue”). Note that a hairy tongue also may appear brown, white, green, or pinkish, depending on its etiology and secondary factors (such as the use of colored mouthwashes, breath mints, candies). Common causes include radiation therapy to the head and neck and certain medications, especially broad-spectrum antibiotics. The condition, however, may often be idiopathic, and in this case usually results from inadequate tooth brushing, or a diet with too little roughage to mechanically débride the dorsum of the tongue. Prevalence is high, and usually higher with age (from 8.3% in children and young adults to 57% in IV drug abusers and prison inmates), probably because of the high frequency among older subjects of practices that predispose to the condition. Although there is no racial predilection, a hairy tongue is more prevalent in males. It is also more prevalent in HIV patients, smokers, and tea/coffee drinkers. It is usually asymptomatic, although patients may complain of tickling (and at times gagging) upon swallowing. Overgrowth of Candida sp. may result in a burning feeling (glossopyrosis), while retention of oral debris between the elongated papillae (and its associated bacterial and fungal overgrowth) may cause halitosis. Yet, like the scrotal tongue, a hairy tongue is usually of little clinical significance. Differential diagnosis includes oral candidiasis and the much more ominous hairy leukoplakia. Treatment consists in using a tongue scraper to remove elongated papillae and retard the growth of additional ones.

97 What is a geographic tongue?

A benign inflammatory condition, often referred to as benign migratory glossitis (i.e., erythema migrans lingualis; see also question 80). This is characterized by multiple, smooth, red, and glossy patches of glossitis, each surrounded by a serpiginous rim of a whitish/hyperkeratotic border (Fig. 6-7). The patches resemble the islands of an archipelago (hence, the nickname of geographic), and primarily affect the tongue’s dorsum, even though they may often extend to the lateral borders. Histologically, they are caused by atrophy of the filiform papillae and may even wax and wane with time. Hence, the adjective of migratory. Eventually, they resolve spontaneously only to reappear at different sites (if lesions occur in other mucosae, the condition is instead termed erythema migrans). A geographic tongue often runs in families and is relatively common, being present in up to 3% of the general population. It has no racial or ethnic predilection, but does affect adults more than children and women more than males (2:1). In fact, exacerbations have often been linked to hormonal factors. Still, unlike atrophic glossitis, a geographic tongue is not associated with nutritional deficiency, but is instead idiopathic. A psychosomatic relation has even been suggested. Histologically, lesions are quite similar to those of psoriasis, or to the mucocutaneous presentations of Reiter’s syndrome. In fact, a geographic tongue is four times more prevalent in psoriatics. It remains, however, asymptomatic (although some patients report increased sensitivity to hot and spicy foods), quite benign, and usually self-limited. Differential diagnosis includes candidiasis, contact stomatitis, chemical burns, lichen planus, and psoriasis. Given the typical clinical presentation, reassurance (and not biopsy) is the best management.

Figure 6-7 Geographic tongue.

(From Sonis ST: Dental Secrets, 2nd ed. Philadelphia, Hanley & Belfus, 1999.)

98 What is a median rhomboid glossitis (MRG)?

It is another benign involvement of the dorsum of the tongue, inflammatory or infectious in nature, and often mistaken for cancer. Rather uncommon (estimated prevalence <1% of adults), it presents as a rhomboidal patch of reddened mucosa on the midline of the dorsum, just anterior to the “V” region of the circumvallate papillae (sulcus terminalis). This patch is sharply circumscribed, flat or raised, and with a firm texture. It is either asymptomatic or associated with a slightly burning sensation after spicy foods. The etiology is unknown, although candidiasis has been implicated, especially given the frequency of positive cultures and histologic examinations.

99 Can the tongue be white?

Yes. Although it may often appear whitish as a result of foodstuffs ingested, several entities may result in a tongue that is really white—the same entities causing white oral lesions.

100 What is a white hairy tongue (hairy leukoplakia)?

A serious condition characterized by multiple white, warty, corrugated, and painless plaques, full of hair-like projections of keratin growth (Fig. 6-8). These are usually on the lateral margins of the tongue, but can occasionally involve the buccal mucosa of the cheeks and other oral sites. Unlike thrush, hairy leukoplakia cannot be scraped off. The lesion is typically associated with HIV infection, even though it also can occur in severely immunocompromised organ transplants. Caused by the Epstein-Barr virus, it is neither painful nor dangerous. In fact, most patients are unaware of it. May even regress in response to antiviral therapy, yet it does carry a worse prognosis for HIV progression. Clinical appearance is distinctive enough to yield a diagnosis. When in doubt, biopsy.

Figure 6-8 Oral hairy leukoplakia.

(From Fitzpatrick JE, Aeling JL: Dermatology Secrets. Philadelphia, Hanley & Belfus, 1996.)

101 What is the cause of a smooth, red tongue?

The most common is atrophic glossitis, the final stage of glossitis. This is an entity characterized initially by papillary hypertrophy, then by papillary flattening, and finally by loss of all but the circumvallate papillae. As a result, the initially shiny red color (beefy tongue) changes to a paler hue, in a tongue that is often smooth and sore (because of atrophy).

102 What causes atrophic glossitis?

Usually, a profound deficiency of B-complex vitamins, such as niacin, pyridoxine, thiamine, riboflavin, folate, and B₁₂. Physical examination may help differentiating folate from B₁₂ deficiency by testing of proprioceptive sensation. In folate deficiency, the patient has glossitis but normal proprioception; in B₁₂ deficiency (and, therefore, in pernicious anemia), the glossitis is instead accompanied by abnormal proprioception. Other causes of glossitis include regional enteritis, iron-deficiency anemia, alcoholism, severe malnutrition (protein-calorie), and malabsorption. Glossitis often presents with cheilitis (see question 108).

103 What causes palpable lingual nodules and papules?

Many entities, with most being variants of normalcy, but some being harbingers of malignancy.

104 Is an indurated tongue ulcer neoplastic?

Not necessarily. A midline, indurated ulcer of the dorsum of the tongue is unlikely to represent cancer, but suggests instead a granulomatous disorder (tuberculosis or histoplasmosis). Conversely, an ulcer located on the lateral or inferior surface of the tongue suggests a diagnosis of Behçet syndrome (first described by the Turkish dermatologist Hulusi Behçet in 1937, and consisting of orogenital ulcers plus joint and ocular manifestations). Finally, a nonindurated peripheral ulcer unassociated with systemic manifestations is a simple aphtha.

105 What is a tongue-tie?

Not what happens to shy people when out on a date, but a congenital condition characterized by a short lingual frenulum. This prevents protrusion of the tongue (ankyloglossia) and may occasionally interfere with breast-feeding. Usually requires surgery.

106 What are sublingual varicosities? What is their significance?

They are enlarged and purplish veins of the tongue’s undersurface. They resemble little drops of purple-black caviar, and thus are often referred to as caviar lesions. Varicosities of this type tend to be an entirely normal by-product of age, due to loss of elasticity in the venous wall, resulting in venodilation and tortuosity, often resembling a hemangioma. Still, in some patients they may indicate a chronic increase in right-sided cardiac pressure, and thus suggest a diagnosis of either superior vena cava syndrome or congestive heart failure.

107 What is the significance of tongue-biting?

In patients presenting with a history of syncope, it represents an insensitive but highly specific clue to the diagnosis of generalized tonic-clonic seizures, especially when the biting involves the side of the tongue. In a study of 106 consecutive patients admitted to an epilepsy monitoring unit, tongue-biting had a sensitivity of 24% and a specificity of 99% for the diagnosis of generalized tonic-clonic seizures. Lateral tongue-biting had a specificity of 100%.

108 What is the difference between cheilosis and cheilitis?

Unfortunately, cheilosis and cheilitis are often used interchangeably (as in the hybrid term, “angular cheilosis”), thus generating a bit of confusion. They should be distinguished as follows:

109 What are the causes of lip ulcers or erosions?

The most common are squamous cell carcinoma and Herpes labialis. Carcinoma usually presents as a solitary, nontender, and firm ulcer involving the lip; Herpes labialis, on the other hand, results in a cluster (herpes means indeed “cluster” in Greek) of tender vesicles and erosions.

110 What causes a diffusely enlarged lip?

Other than trauma (i.e., “fat-lip”), the most common cause is angioedema.

111 What is angioedema (angioneurotic edema)?

It is a painless, nonpruritic, nonpitting, and well-circumscribed edema caused by increased vascular permeability. This may come and go rather quickly (over a period of hours), typically involving the head and neck (the face, lips, floor of the mouth, tongue, and larynx), but also other regions of the body. In fact, it may involve the gastrointestinal tract, causing intestinal wall edema with colicky abdominal pain, nausea, vomiting, and diarrhea. In more serious cases, it may even cause life-threatening laryngeal edema, with stridor, upper airway obstruction, and respiratory failure. Although nonpruritic, angioedema is usually allergic in origin, triggered by medications, foods (berries, shellfish, fish, nuts, eggs, and milk), pollen, animal dander, insect bites, environmental exposure (water, sunlight, cold or heat),and emotional stress. It may even follow infectious illnesses or be associated with autoimmune disorders and leukemia.

112 What is hereditary angioedema?

A more rare (and serious) genetic condition that affects up to 1/10,000 individuals. It is characterized by recurrent episodes of edema, involving the intestinal wall (and thus causing abdominal pain, nausea, and vomiting), but also the hands, feet, face, and upper airways.

113 What is the cause of pigmented areas on the lips?

The most esoteric, of course, is Peutz-Jeghers syndrome (previously discussed). Yet, a much more common occurrence is simple ephelides (i.e., freckles). These are pigmented macules, 2–3   mm in diameter, that may indeed involve the lips as solitary or multiple lesions. Ephelides are benign but should always be excised if changes occur.

114 What lip lesion may result in an ophthalmologic emergency?

Herpes keratitis. In fact, any red and painful eye in a patient with antecedent or concurrent herpes labialis should indeed suggest the possibility of ocular extension. Diagnosis is confirmed by a positive corneal uptake of fluorescein with a characteristic dendritic pattern.

115 What is a parulis?

A sessile nodule on the gingiva at the site of drainage of a fistulous tract originating from a tooth infection.

116 What is an epulis fissuratum (denture-induced hyperplasia)?

It is an exuberant response of the gum to recurrent trauma (epulis, gumboil in Greek), usually from ill-fitting dentures. It presents as folds of hyperplastic mucosa that encompass the border of the denture flange, and usually has a normal mucosal color. At times, however, it may also present as a sessile or pedunculated nodule, purplish-brown in color, and with more of a pyogenic granuloma-like appearance. This is due to capillary proliferation, and may result in easy bleeding. Since the epulis is due to trauma from denture flanges, it is usually observed in the maxillary or mandibular vestibule, typically in the anterior portion of the jaws. It is more common in women than men, Caucasians than African Americans, and older than younger individuals—probably because of greater use of dentures in these three groups. It is typically slow growing and asymptomatic. It must be differentiated from squamous cell carcinoma and pyogenic granuloma.

117 What is a pyogenic granuloma?

A rather common and benign vascular lesion of the skin of the head, neck, digits, and upper trunk, but also of the various mucosae, including gums and lips, gastrointestinal tract, nose, larynx, conjunctiva, and cornea. Despite its name, it is neither infectious (hence, no “pyogenic”) nor granulomatous. Instead, it has unknown etiology, although it can present as a “pregnancy tumor” in 5% of all pregnancies (or more rarely after use of oral contraceptives). The lesion typically presents in children and young adults as a solitary and shiny, bright red nodule, friable and polypoid, slowly evolving over a period of a few weeks. This often bleeds spontaneously, may ulcerate, and can even be associated with bony erosion. Surgical excision may be indicated for control of local symptoms. If untreated, lesions eventually atrophy into a soft fibroma.

118 What is the most common cause of a diffuse thickening of the gums? What are the other possible causes?

The most common cause is gingivitis vulgaris, usually associated with periodontal disease. This represents not only a local problem, but also an important clue to the possible presence of coronary artery disease (CAD). In fact, patients with periodontal infections are twice as likely to have CAD, probably because of increased plasma levels of inflammatory mediators, such as fibrinogen, C-reactive protein, and several cytokines. Periodontal pathogens also may cause atherosclerosis by entering the bloodstream and invading the blood vessel wall. Other causes of gum thickening include:

119 What is scurvy?

The result of vitamin C deficiency, and an important cause of gum hypertrophy and bleeding. It is also an important (albeit rare) cause of morbidity and even mortality. Scorbutic gums are diffusely swollen, friable, thickened, and bleeding. There also may be concurrent petechiae in the perifollicular areas and dysmorphic, corkscrew-like hair. All these manifestations can be prevented (and reversed) by vitamin C—something well known to the British sailors of old, whose fondness for citrus fruits even earned them the nickname of “limeys.”

120 What is the most ominous cause of gum hypertrophy and bleeding?

Leukemic infiltration. This is often due to acute monomyelocytic leukemia, where gum disease may even be the presenting manifestation.

121 What are the local complications of gingivitis vulgaris?

The most common is tooth loss. The patient may also develop recurrent aspiration (with anaerobic pneumonias and abscesses) and severe gingival infections, with pain, fever, gum erosions (acute necrotizing ulcerative gingivitis or trench mouth), and halitosis “paramaligna.”

122 What does “long of tooth” mean?

It refers to the observation that teeth tend to look longer over the years. This used to be viewed as a normal feature of aging but is actually due not to teeth lengthening (as in sharks) but to gum regression (as in gingivitis). Hence, anyone long of tooth may rapidly become short of teeth.

123 What causes tooth loss?

Not so much tooth extraction (or fracture) but rather:

124 If you plumb a sulcus and it is normal, can the patient still have plumbism?

Yes. A dentist plumbs a gingival sulcus to detect the severity of gingivitis. An inappropriately deep sulcus indicates moderate to severe gum disease, but certainly not plumbism, which is chronic lead intoxication. Although rarer than gingivitis, plumbism can be diagnosed by examining the tooth gingival margin: chronically and markedly elevated serum levels of lead will cause lead lines (also called Burton’s lines from Henry Burton, a physician at St. Thomas Hospital in London and a victim of the great cholera epidemic of 1849). These lines are dark blue in color and formed by a series of tiny dots circling the tooth at its point of gum insertion. They are produced by tartar bacteria synthesizing lead sulfide (which is bluish black). Hence, they are absent in patients with no concomitant gingival infection (such as edentulous subjects). Note that similar dark lines also may be seen with chronic exposure to bismuth. Other manifestations of plumbism include renal insufficiency, peripheral neuropathy, saturnine gout (monoarticular arthritis), and, in younger individuals, a cognitive delay that may be quite profound.

125 What are Hutchinson’s teeth?

They are part of Hutchinson’s triad of congenital syphilis (interstitial keratitis, labyrinthine deafness, and Hutchinson’s teeth). The upper incisors are smaller than normal and notched.

126 What is halitosis?

It is bad breath (halitus is Latin for breath, and osis is a Greek suffix indicating an abnormal condition). In the olden days, physicians used to differentiate “fetor oris” (a smell originating from the rhinopharynx or oropharynx, including the paranasal sinuses) from true halitosis, intended as a systemic odor exhaled from the lungs. This difference, however, is entirely disregarded today.

127 What is the diagnostic importance of halitosis?

Aside from its social and psychologic implications, halitosis is an important sign of underlying disease awaiting recognition and treatment. Although usually unrecognized by the patient, it is rarely missed by the unfortunate innocent bystander. Hence, unless you are blessed with Kallmann’s syndrome (previously discussed), you cannot escape it—both medically and socially.

128 What nonpathologic factors may cause halitosis?

129 What are the pathologic causes of halitosis?

Pathologic causes may be either local or systemic. The most common local causes include:

Systemic conditions presenting with a particular odor of the breath include:

130 What about psychiatric conditions that may be related to halitosis?

In psychiatric conditions, the “bad smell” is not real, insofar as it is only felt by the patient and not by others. Psychiatric patients may perceive bad odors as emanating from either an external source or themselves. Causes of extrinsic olfactory hallucinations include schizophrenia and temporal lobe epilepsy. Conversely, a common cause of intrinsic olfactory hallucinations is the olfactory reference syndrome (ORS). This is a hypochondriacal psychosis characterized by excessive preoccupation with body image. Patients with ORS are sensitive, insecure, mildly paranoid, compulsive, and depressive. They also are convinced of smelling badly (especially of having bad breath). In fact, they are so obsessed with this idea that they eventually isolate themselves. Providing reassurance is usually not enough, since patients often seek confirmation of their smells from a different doctor.

Acknowledgment

The author gratefully acknowledges the contributions of Dale Berg, MD, and Katherine Worzala, MD, MPH, to this chapter in the first edition of Physical Diagnosis Secrets.