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3 Mouth and Pharynx

3.1 Applied Anatomy and Physiology

3.1.1 Basic Anatomy

3.1.1.1 Oral Cavity

The oral cavity is bounded anteriorly by the lips, posteriorly by the anterior faucial arch, inferiorly by the floor of the mouth, and superiorly by the hard and soft palates. It is continuous with the oropharynx through the anterior faucial arch ( ▶ Fig. 3.1 and ▶ Fig. 3.2a).

The faucial arch and the base of the tongue form the faucial isthmus. The oral cavity is divided into two parts by the upper and lower alveolar process and the teeth: first, the vestibule of the mouth, lying between the lip and cheek on one side and the teeth and the alveolar process on the other, and second, the oral cavity proper, limited externally by the alveolar process and the teeth.

The vestibule of the mouth communicates directly with the oral cavity proper on both sides, even when the teeth are in apposition, between the ascending ramus of the mandible and the last molar tooth.

This is of practical importance: in intermaxillary wiring, the patient is able to ingest a fluid diet using this route, even when the teeth are fixed in occlusion.

The Tongue

The tongue fills the oral cavity almost completely when the mouth is closed ( ▶ Fig. 3.2b, c). The surface tension force ensures that the tongue adheres to the hard and soft palate, thus maintaining closure of the mouth.

The following parts of the tongue are distinguished: the tip, the margins, the body, the base, the dorsum, and the ventral surface.

The dorsum of the tongue is covered with a modified epithelium containing the filiform papillae at the tip, the fungiform papillae at the tip and margins, the foliate papillae on the posterolateral part of the tongue, and the vallate papillae on the dorsum. The boundary between the body of the tongue and the base of the tongue is formed by the V-shaped terminal sulcus, the central point of which is the foramen cecum, a remnant of the thyroglossal duct.

The base of the tongue contains the lingual tonsil, which can be a site of inflammation and abscess due to an impacted foreign body and can cause mechanical difficulty in swallowing when it is hypertrophic. The base of the tongue is limited inferiorly by the edge of the epiglottis. The two valleculae lie in the angle between the epiglottis and the base of the tongue. They are sometimes difficult to inspect and may be a site for cysts, foreign bodies, and malignant tumors. In supine unconscious patients or patients under general anesthesia, the base of the tongue may fall backward to occlude the entrance to the larynx, and together with the epiglottis may lead to respiratory obstruction. This is prevented by pulling the tongue forward and by introducing an oropharyngeal airway.

The arrangement of the musculature of the tongue provides it with extreme mobility. Two groups of muscles can be distinguished: first, those without any bony attachments, running free in the body of the tongue, i.e., the transverse, superior, and inferior longitudinal muscles, and the vertical muscles; and second, muscles that are attached to fixed points, i.e., the styloglossus, the genioglossus, the hyoglossus, and the palatoglossus muscles ( ▶ Fig. 3.3).

The floor of the mouth is formed mainly by the mylohyoid muscle, which is stretched between the U-shaped mandible like a diaphragm and which is inserted into the hyoid bone and the median raphe. On the oral surface, with the tip of the tongue elevated, the plica sublingualis with the sublingual caruncle can be found on both sides of the lingual frenulum.

In the caruncle and the immediate vicinity lie the efferent ducts of the submandibular gland, the submandibular duct (Wharton duct), and the sublingual gland and sublingual duct (Bartholin duct). The efferent duct of the parotid gland (Stensen duct) opens into the cheek at the level of the second upper molar, and that of the anterior lingual gland (Blandin gland) in the region of the fimbriated fold on the ventral surface of the tongue.

The mandible consists of two separate bones at birth, but these consolidate to form one bone during the first year of life. ▶ Fig. 3.4a shows the most important anatomic details and the typical sites of fracture. The third branch of the trigeminal nerve runs in the body of the mandible, together with the blood vessels that supply the lower teeth. The mandibular nerve enters the mandible at the mandibular foramen and exits at the mental foramen.

The temporomandibular joint is of considerable clinical interest, as it may be involved in dental diseases, in trauma of the facial skeleton and skull, in otologic diseases, and in generalized arthropathies. In addition, it may be the cause of headache in Costen syndrome. ▶ Fig. 3.4b shows the anatomic relationships. Its proximity to the auditory meatus and mastoid, the lateral part of the base of the skull, the parotid gland, and the lateral wall of the oropharynx and nasopharynx should be noted.

The epithelial lining of the oral cavity consists of nonkeratinized stratified squamous epithelium that is thickened in certain points such as the alveolar edges and hard palate, where it unites with the underlying periosteum to form a mucoperiosteum. Subepithelial collections of minor salivary glands are found all over the oral cavity, and are more common in some parts than others (see also ▶ Fig. 9.2).

Vascular supply: The external carotid artery supplies the tongue via the lingual artery; the floor of the mouth via the sublingual artery; the cheek via the facial artery; and the palate via the ascending pharyngeal artery and descending palatine artery. The latter arises from the internal maxillary artery. Venous drainage is through the veins of the same names to the facial vein, the pterygoid venous plexus, and the internal jugular vein. There is also a connection to the cavernous sinuses via the pterygoid plexus.

The lymph drains via the regional submental, submandibular, and parotid nodes to the internal jugular chain. The lymph drainage of the base of the tongue and the floor of the mouth is to the same side and to the opposite side ( ▶ Fig. 3.5a, b). This is important for the development of contralateral lymph-node metastases (see ▶ p. 454).

Nerve supply: The tongue derives its motor supply from the hypoglossal nerve. Its sensory supply comes from the lingual nerve and the vagus nerve, which innervates the posterior part of the base of the tongue. Taste fibers come from the glossopharyngeal nerve to the base of the tongue and from the chorda tympani fibers of cranial nerve VII, accompanying the lingual nerve for the anterior two-thirds of the tongue (see also ▶ Fig. 3.2c).

The floor of the mouth derives its motor supply from the mylohyoid branch of the mandibular nerve and its sensory supply from the trigeminal nerve. Parasympathetic secretory fibers from the salivary glands are supplied from the chorda tympani and branches of the submandibular ganglion. Sympathetic fibers for blood vessels of the glands come from the carotid plexus.

The masticatory muscles derive their motor supply from the mandibular branch of the trigeminal nerve, but the buccinator muscle is supplied from the facial nerve.

The teeth of the upper jaw receive their sensory supply from the maxillary nerve and those of the lower jaw from the mandibular. These are both branches of cranial nerve V.

The temporomandibular joint derives its nerve supply from the auriculotemporal branch of the mandibular nerve.

The soft palate derives its motor innervation from the glossopharyngeal, vagus, and trigeminal nerves, and probably the facial nerve as well.

3.1.1.2 Nasopharynx, Oropharynx, and Hypopharynx

The pharynx is a muscular tube, 12 to 13 cm long in the adult; it narrows from above downward, is covered with mucosa, and is divided into three compartments, each of which has an anterior opening ( ▶ Fig. 3.6).

The nasopharynx is limited superiorly by the base of the skull and inferiorly by an imaginary plane through the soft palate, and it opens into the nasal cavity. The most important anatomic structures are as follows: anteriorly, the choanae; superiorly, the floor of the sphenoid sinus; posterosuperiorly, the adenoid; laterally, the pharyngeal ostium of the eustachian tube and the cartilaginous torus tubarius, immediately posterior to which is the Rosenmüller fossa (pharyngeal recess) and the tubal tonsil; and anteriorly and inferiorly, the soft palate. The embryonic pharyngeal bursa ( ▶ Fig. 3.7) may persist in the posterior wall of the nasopharynx, causing chronic inflammation and retention of secretions. The posterior wall of the nasopharynx is separated from the spinal column by the tough prevertebral fascia, which lies on the longus capitis muscles, the deep muscles of the neck, and the arch of the first cervical vertebra.

The shape and width of the nasopharynx show marked individual variation. The epithelial lining consists of respiratory ciliated and stratified squamous epithelium, with transitional epithelium at the junction with the oropharynx.

The oropharynx extends from the horizontal plane through the soft palate described above to the superior edge of the epiglottis ( ▶ Fig. 3.7) and is continuous with the oral cavity through the faucial isthmus. It contains the following important structures: the posterior wall, consisting of the prevertebral fascia and the bodies of the second and third cervical vertebrae; the lateral wall, containing the palatine tonsil with the anterior and posterior faucial pillars; and the supratonsillar fossa, lying above the tonsil between the anterior and posterior faucial arches.

The valleculae (see also ▶ Fig. 3.1), the base of the tongue, the anterior surface of the soft palate, and the lingual surface of the epiglottis are usually described as being part of the oropharynx.

The epithelial lining consists of nonkeratinizing stratified squamous epithelium.

The hypopharynx extends from the upper edge of the epiglottis superiorly to the inferior edge of the cricoid cartilage (see also ▶ Fig. 3.6). It opens anteriorly into the larynx. On each side of the larynx lie the funnel-shaped piriform sinuses. Important anatomic structures and relationships include: on the anterior wall, the marginal structures of the laryngeal inlet and the posterior surface of the larynx; on the lateral wall, the inferior constrictor muscle and the piriform sinus, the latter being bounded medially by the aryepiglottic fold and laterally by the internal surface of the thyroid cartilage and the thyrohyoid membrane. Immediate relationships of the hypopharynx at the level of the larynx include the common carotid artery, the internal jugular vein, and the vagus nerve. Relationships of the posterior wall, apart from the pharyngeal constrictor muscle, include the prevertebral fascia and the bodies of the third to the sixth cervical vertebrae. Inferiorly, the hypopharynx opens into the esophagus, the boundary being the superior sphincter of the esophagus. The epithelial lining consists of nonkeratinized stratified squamous epithelium.

The muscular tube of the entire pharynx consists of two layers with different functions:

1. 
   

   A circular muscle layer consisting of the three pharyngeal constrictor muscles: the superior constrictor, inserted into the base of the skull; the middle constrictor, inserted into the hyoid bone; and the inferior constrictor, inserted into the cricoid cartilage (see also ▶ Fig. 3.3 and ▶ Fig. 3.7). Each of these funnel-shaped muscular segments is overlapped at its lower end by the segment below. All of the segments are inserted posteriorly into a tendinous median raphe.

   
   
2. 
   

   The inferior constrictor muscle is of particular clinical importance. It is divided into a superior thyropharyngeal part and an inferior cricopharyngeal part. ▶ Fig. 3.7 shows how the triangular dehiscence (Killian triangle) is formed from the posterior wall of the hypopharynx between the superior oblique and the inferior horizontal fibers. A pharyngoesophageal pouch (Zenker diverticulum) may develop at this weak point in the hypopharyngeal wall.

   
   
3. 
   

   Raising and lowering of the pharynx are also carried out by three paired muscles radiating into the pharyngeal wall from outside. These are the stylopharyngeus, the salpingopharyngeus, and the palatopharyngeus muscles. The stylohyoid and styloglossus muscles are also responsible for elevation. A true longitudinal muscle does not occur in the pharynx and only begins at the mouth of the esophagus. The ability of the pharynx to slide over a distance of several centimeters is due to the existence of fascial spaces (parapharyngeal and retropharyngeal) filled with loose connective tissue. The importance of these tissue spaces in the spread of infection is described on ▶ p. 298 and in ▶ Fig. 3.44a, b.

Vascular supply of the pharynx: The arterial supply is provided by the ascending pharyngeal artery, the ascending palatine artery, the tonsillar branches of the facial artery, branches of the maxillary artery (i.e., the descending palatine artery), and branches of the lingual artery. These all arise from the external carotid artery. Venous drainage is via the facial vein and the pterygoid plexus to the internal jugular vein.

The lymphatic drainage is either via an inconstant retropharyngeal lymph node and then to the deep jugular lymph nodes, or directly to the latter group. The inferior part of the pharynx also drains to the paratracheal lymph nodes and is thus connected to the lymphatic system of the thorax (see also ▶ p. 257).

Nerve supply of the pharynx: The individual pharyngeal muscles gain their motor supply from the glossopharyngeal (IX), vagus (X), hypoglossal (XII), and facial (VII) nerves. The nasopharynx derives its sensory nerve supply from the maxillary division of the trigeminal nerve (V), the oropharynx from the glossopharyngeal nerve (IX), and the hypopharynx from the vagus nerve (X) (see ▶ p. 257).

3.1.1.3 Lymphoepithelial System of the Pharynx

The epithelial and subepithelial tissue is loosely arranged so that lymphatic cells can enter it in large numbers (“reticulated epithelium”). The reticulohistiocytic system, more commonly known as the reticuloendothelial system (RES), with its storage cells, is strongly represented in lymphoepithelial tissue. ▶ Fig. 3.8 shows the principle of a lymphoepithelial unit. Solitary units of this type, solitary follicles, are found in all parts of the mucosa. The epithelium is also diffusely interspersed with lymphocytes.

A very distinct collection of lymphoepithelial tissue, the Waldeyer ring, lies at the opening of the upper aerodigestive tracts.

The lymphoepithelial organs are called tonsils. From above downward, the following distinguished:

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  The pharyngeal tonsil, the adenoids, which is single and lies on the roof and posterior wall of the nasopharynx.

  
  
• 
  

  The tubal tonsil, which is paired and lies around the ostium of the eustachian tube in the Rosen-müller fossa.

  
  
• 
  

  The paired palatine tonsil, lying between the anterior and posterior faucial pillars.

  
  
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  The lingual tonsil, which is single and lies in the base of the tongue.

Less constant and obvious are:

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  The tubopharyngeal plicae, lateral bands, which run almost vertically at the junction of the lateral and posterior walls of the oropharynx and nasopharynx.

  
  
• 
  

  Lymphoepithelial collections in the laryngeal ventricle.

Unlike lymph nodes, lymphoepithelial organs only have efferent lymph vessels and do not have afferent vessels. Differences in the pathology and physiology of the individual collections of lymphoid tissue are due to their different structures. ▶ Fig. 3.9 shows the structure of a palatine tonsil and of the adenoids.

The fine structure of a tonsil ( ▶ Fig. 3.8 and ▶ Fig. 3.9) is in principle as follows: the soft tissue lamellae or septa arise from a basal connective-tissue capsule. These serve as a supporting framework in which blood vessels, lymphatics, and nerves run. This fan-shaped supporting framework considerably increases the active surface of the tonsil, as it holds the actual lymphoepithelial parenchyma. In the palatine tonsil, the active surface is sunk into the mucosa, whereas in the adenoids, it projects above the surface. The broad flat niches opening into the oral cavity caused by infolding are called lacunae, and the branching clefts running throughout the entire substance of the tonsil are called crypts. The actual tonsil tissue consists of a collection of a very large number of the lymphoepithelial units described above (see also ▶ Fig. 3.8). The crypts usually contain cell debris and round cells, but may also contain bacteria and colonies of fungi, collections of pus, and encapsulated microabscesses. (See ▶ Fig. 3.9b for the description of chronic tonsillitis.)

The tonsils of the Waldeyer ring are present at the embryonic stage, but they only acquire their typical structure with secondary nodes during the postnatal period, i.e., after direct contact with environmental pathogens. They begin increasing rapidly in size between the first and third years of life, with peaks in the third and seventh years.

They involute slowly as of early puberty. Like the rest of the lymphatic system, they atrophy with increasing age.

The arterial blood supply to the pharyngeal tonsil is provided by various branches of the external carotid artery, including the facial artery and/or the ascending palatine artery, the ascending pharyngeal and lingual arteries, and possibly direct tonsillar branches.

The veins of the pharyngeal tonsil usually drain via the palatal vein to the facial vein, and from there to the jugulofacial venous angle of the internal jugular vein. There is also drainage via the pterygoid venous plexus to the internal jugular vein. This route provides a possible pathway of spread for infection from the tonsils to the cavernous sinus (see also ▶ Fig. 3.44b and ▶ Fig. 3.46).

3.1.2 Physiologic and Pathophysiologic Principles

Several functional systems are collected in the mouth and pharynx, including the masticatory system, the swallowing apparatus (see Chapter 7 Swallowing), the taste organs, the lymphoepithelial ring, pregastric digestion, and articulation. In addition, the respiratory and digestive tracts cross in this area (see also ▶ Fig. 3.6). This requires a reliable reflex protective system. An important prerequisite for this is a well-functioning autonomic and voluntary nervous supply to this region, and a mucosa adapted to this dual function. The mouth is only involved in respiration as a supplementary measure (see ▶ pp. 257–259); continuous mouth breathing causes considerable local damage and can also affect the entire body.

3.1.2.1 Eating, Preparation of Food, and Swallowing

Normal feeding requires a normal masticatory apparatus and teeth, masticatory muscles, and temporomandibular joint. The function of the cranial nerves also has to be normal (see ▶ Table 7.3 ). The preparation of food serves to reduce the size of the food bolus by chewing and to moisten the food with saliva, of which 1.0 to 1.5 L are produced daily. The saliva lubricates the mucosa and makes the food capable of being swallowed. In addition, the enzymes contained in saliva prepare the food by partial chemical decomposition for further digestion in the gastrointestinal tract.

The results of quantitative or qualitative defects of saliva are summarized on ▶ p. 473. Satisfactory moistening of the mucosa of the oral cavity and pharynx by saliva is also necessary for normal speech and for normal taste (see discussion of salivary function on ▶ p. 474).

The act of swallowing: This is an extremely complex sequence of events that is controlled by several cranial nerves (trigeminal nerve, facial nerve with chorda tympani, glossopharyngeal nerve, vagus nerve, superior and inferior laryngeal nerves, hypoglossal nerve) and cervical nerves (cervical plexus, C 1–C 4). Central coordination is performed in the motoric cortex of the precentral gyrus, the amygdaloid body, nuclear regions of the hypothalamus, and the ventral tegmentum of the midbrain. The deglutition centers are located in the rhombencephalon of the reticular formation and in the medulla oblongata. The “pattern generator” coordinating the interactions of the nerves and muscles is inborn.

Phases of swallowing: Oral preparation phase: Food is chewed and mixed with saliva. The lips close, round off, and are retracted. The mandible and the tongue move in all directions, the cheeks tauten, and the soft palate faces anteriorly.

Oral phase: The bolus is pressed along the back of the tongue into the oropharynx, eliciting the swallowing reflex. The corresponding receptors are located in the palatoglossal arch and the base of the tongue.

Pharyngeal phase: This phase of the swallowing reflex consists of a succession of movements that include closure of the larynx and further transportation of the bolus through the pharynx to the esophagus.

Esophageal phase: This phase comprises transportation of the bolus by peristaltic waves through the esophagus and into the stomach.

3.1.2.2 Taste

Taste is dependent on the stimulation of taste receptors within the oral cavity, together with a significant stimulatory component from smell receptors in the olfactory clefts.

Taste receptors are distributed within the oral cavity, but they are concentrated in the taste buds on the dorsal surface of the tongue. There are two families of taste receptors, type 1 (sweet) and type 2 (bitter), and five recognized basic taste domains, namely sweet, salty, bitter, sour, and umami (savory). Umami is tasted by specific receptors that are stimulated by glutamate (ionized salts of glutamic acid) found in many foods, such as fish, mushrooms, vegetables, cheese, and cured meats. Many texts describe the taste domains as being distributed in a specific pattern on the dorsum of the tongue, but this is a misconception, and an oversimplification that does not really exist in nature.

The sensory organs for taste are the taste buds lying in the circumvallate (or vallate; dome-shaped) papillae, foliate papillae, and fungiform (club-shaped) papillae on the tongue and on the hard palate ( ▶ Fig. 3.10), the anterior faucial pillar, the tonsil, the posterior pharyngeal wall, the esophageal orifice, and the buccal mucosa. The filiform (cone-shaped) papillae do not contain taste receptors.

The fine gustatory hair cells have to be bathed in saliva or other fluids to allow the sense of taste to be evoked. The sensory nerve supply is provided peripherally by two nerves in particular: the chorda tympani, arising from cranial nerve VII and accompanying the lingual nerve from cranial nerve V, and the glossopharyngeal nerve, arising from cranial nerve IX.

The perception of taste is often portrayed as simple, but it is highly complex and dependent on input from visual, olfactory, trigeminal, and tactile stimulation. Spicy and hot-tasting foods stimulate pure sensory nerve fibers from the tongue and oral mucosa as well as taste receptors.

The boundary of the area supplied by each individual nerve in the mouth and pharynx is still not fully agreed upon, but the following is generally accepted (see ▶ Fig. 1.22). The anterior half of the tongue is supplied by the ipsilateral chorda tympani via the nervus intermedius, with synapses in the sensory geniculate ganglion. The posterior third of the tongue and the walls of the oral pharynx receive their sensory supply from the glossopharyngeal nerve. It is probable that the vagus nerve also has sensory contributions to the epiglottis, the laryngeal inlet (aditus), the upper part of the esophagus, and possibly also a small part of the center of the base of the tongue. Gustatory sensations from the soft palate are transmitted by the palatine nerves via the pterygopalatine ganglion, the greater petrosal nerve, the geniculate ganglion, and the nervus intermedius to the medulla oblongata.

The boundary between the area supplied by the lingual nerve and the accompanying chorda tympani and the glossopharyngeal nerve is still not generally agreed on.

Reflex reactions may affect the sense of taste, as they do the sense of smell. These include alterations in the quantity and quality of salivary secretion, the production of gastric juice, and interference with the course of the swallowing act.

Basic pathophysiology: Taste perception may change due to a general change in the threshold level or taste domains becoming dissociated.

With the advent of Covid, primary taste disorders became quite common due to a direct effect on taste receptors by SARS-Cov-2.

Taste disorders may be primary due to radiation therapy, local trauma or infection, or secondary to medication, neurological disease, endocrine disease or hyposalivation ( ▶ Table 3.1  and ▶ Table 3.2 ). Pregnancy may alter taste and sometimes cause a metallic taste. Taste alteration is a common side effect of many medications, including antibiotics, antidepressants, antihypertensive medications.

3.1.2.3 Function of the Tonsils

The tonsils have an immune-specific defense function. They send immunologically marked lymphocytes and immunoglobulins from the organism’s “front line” to the various stations in the immune system. This is made possible by the way in which the tonsils are structured. In the crypts and reticular epithelium, intensive contact with the widest variety of antigens in the oral cavity is ensured. The tonsils form lymphocytes and plasma cells; T lymphocytes serve specifically for cellular immune defense, while immunoglobulins (e.g., IgA, IgE, IgM) and B lymphocytes are formed for humoral immunological reactions. At the same time, lymphocytes and immunoglobulins are released directly from the tonsillar crypts into the oral cavity. The tonsils thus have both local and systemic immunological functions.

Basic pathophysiology: The increase in lymphoepithelial tissue during the early years of childhood development is explained by immunobiologic requirements. The increase in tonsil size during early childhood is an expression of an active immunological defense system to environmental antigenic substances. During this period, tonsillar hyperplasia is therefore a welcome condition and in no way suggests excess inflammation. Since the tonsils lie at a narrow point in the respiratory and digestive tract, the nasopharynx and the faucial isthmus, an increase in their volume beyond a certain point leads to increased narrowing of the diameter of this essential airflow pathway ( ▶ Fig. 3.11). Obstructive sleep apnea (OSA) may develop in extreme cases. Removal of the tonsils and adenoids is therefore justified in these circumstances, despite potential immunologic disadvantages. The palatine tonsils alone have slitlike, branching, poorly drained crypts permeating their entire substance. As long as these clefts drain freely into the oral cavity, the function of the tonsil is not endangered. However, if the physiologic content of the crypt stagnates due to anatomic or infective stenosis, an ideal culture medium is set up for microorganisms. Colonies of bacteria or fungi become established, leading to chronic suppuration (cryptitis), small abscesses in the crypts, and superficial ulceration of the surface of the crypts. In anatomicopathologic terms, this represents chronic tonsillitis. This is in no way related to the size of the tonsil. ▶ Fig. 3.8 shows how the superficial tonsillar capillaries are unprotected and course close to the lumen of the crypt, allowing relatively unhindered access for infective or toxic materials to the general circulation.

3.1.2.4 Formation of Sound and Speech

The oral cavity and pharynx make an important contribution to the timbre of the speech and voice, due to their action as a variable resonating space. In addition, the tongue, along with the palate, is necessary for the formation of consonants and vowels. Despite this, experience with tumor surgery shows that large parts of the tongue can be removed without loss of comprehensible speech.

With regard to nasality, it is still unclear whether closure of the nasopharynx during the articulation of consonants functions according to an “all or nothing” rule or whether it involves a graded mechanism of muscular obstruction by the soft palate.

3.2 Methods of Investigation

3.2.1 Inspection, Palpation, and Examination

The examination is carried out, with good illumination from a head lamp, using two tongue depressors (see also ▶ Fig. 2.14b, c; ▶ Fig. 3.12 and ▶ Fig. 3.13). The following should be observed:

• 
  

  The color and the normal symmetrical mobility of the lips, the condition of the skin and mucosa, and changes in the surface, ulcerations, induration, and tenderness of the lips are inspected.

  
  
• 
  

  The arrangement of the teeth and the occlusion are examined with the lips open. The symmetry of the contour of the jaws, the mobility of the mandible, and the function of the temporomandibular joint are also examined.

  
  
• 
  

  The shape and mobility of the tongue is examined with the mouth open. In hypoglossal paresis, the tongue deviates slightly to the paralyzed side. The floor of the mouth and the two caruncles are examined using a tongue depressor, with the tongue elevated. The surface and consistency of the tongue and articulation are also assessed.

  
  
• 
  

  The properties of the mucosa of the mouth and cheeks are assessed, with particular attention to color, moisture, dryness, membranes, ulceration, tumors, and disorders of sensation.

  
  
• 
  

  The condition of the hard and soft palate is examined. The innervation of the two sides is compared. In paralysis of the palate, the uvula deviates to the healthy side. The innervation of the pharyngeal musculature is tested.

  
  
• 
  

  The upper and lower vestibules of the oral cavity are examined with a tongue depressor.

  
  
• 
  

  The parotid duct in the cheek opposite the upper second molar tooth is inspected.

  
  
• 
  

  The palatine tonsils, lingual tonsil, and mucosa of the posterior wall of the pharynx are examined using two tongue depressors ( ▶ Fig. 3.13e). Normally, these structures should be pale yellow to pale pink, moist, and shiny. Dryness, coating, glazed crusts, and yellow streams of pus may be noted.

For the examination of the tonsils: A tongue depressor is laid carefully with the left hand on the lateral part of the posterior part of the tongue, and the tongue is pressed gently downward. The spatula should not be placed on the base of the tongue, since this elicits the gag reflex. As soon as the tonsillar cleft can be seen, the other hand is used to introduce the second tongue depressor between the ascending ramus of the mandible and the tonsil, and the edge of the tongue depressor is placed gently on the anterior faucial pillar, lateral to the tonsil, to dislocate it from its fossa into the oral cavity. An attempt is made to press material out of the visible crypt opening. The size of the tonsil and its connective-tissue fixation to the tonsillar fossa, the color and properties of the surrounding mucosa on the faucial pillars, and the color and properties of the surface of the tonsil, including any exudate and the expressed contents of the crypt, are noted. Differences between the two sides are also looked for. Palpation of the lymph nodes now follows, with particular attention being paid to the nodes at the angle of the jaw and in the submandibular and submental areas (see also ▶ Fig. 8.13).

Suspect areas in the oral cavity and base of the tongue should always also be palpated. The index finger, enclosed in a finger cot or glove, is used to palpate the suspicious area carefully for induration, infiltration, ulceration, and tender areas. Most patients tolerate careful examination. In patients with an exaggerated gag reflex, the oral and pharyngeal mucosa—particularly that of the soft palate, the base of the tongue, and the posterior wall of the pharynx—can be rendered insensitive first by applying a spray or a cotton applicator saturated with 1% tetracaine or lidocaine (Xylocaine). Local anesthesia of the pharynx is also recommended if satisfactory examination of the nasopharynx, hypopharynx, or larynx is not possible due to a marked gag reflex.

The nasopharynx, hypopharynx, and larynx can be examined with the mirror, but these techniques have been superseded by flexible nasendoscopy ( ▶ Fig. 3.14). Indirect mirror examination of the hypopharynx/larynx is particularly difficult in patients with a sensitive gag reflex or a prominent, infiltrated, tender tongue base.

The techniques of posterior rhinoscopy and indirect laryngoscopy are included for completeness (please refer to ▶ pp. 148 and ▶ 331).

3.2.2 Endoscopy

The nasopharynx, oropharynx, and hypopharynx are best examined by flexible transnasal endoscopy with local nasal anesthesia in the outpatient clinic setting.

Examination in theater is best performed under general anesthesia with suspension laryngohypopharyngoscopy and rigid endoscopy (see also ▶ Fig. 4.8). The nasopharynx is best viewed directly with a transnasal rigid endoscope.

Rigid endoscopy is an important diagnostic method in oncologic patients for evaluating the size, extension, and precise location of a tumor and for obtaining biopsies from margins of the lesion. The results are important for decision-making regarding the operability of a tumor, the surgical approach, and defect repair.

3.2.3 Imaging Studies

Plain radiographs of the nasopharynx were once commonplace for assessing the size of the adenoids in children, but with the advent of endoscopy and the radiation dose, there is little justification for these views anymore.

Tumors of the pharynx are best displayed by a combination of CT and MRI ( ▶ Fig. 3.15). Full radiological imaging assessment often includes positron emission tomography (PET-CT) scans either prior to surgery or during postoperative follow-up.

Vascular tumors are normally assessed by CT carotid angiography or magnetic resonance angiography (MRA).

Patients with juvenile nasopharyngeal angiofibromas normally undergo superselective angiography to identify the vascular supply from the external and internal carotid arteries. Feeding vessels can then be selectively catheterized and embolized prior to surgery ( ▶ Fig. 3.16; see also ▶ p. 318).

The hypopharynx is best demonstrated after administration of a contrast agent such as Gastrografin or barium. The swallow with contrast is very useful for diagnosing a pharyngeal pouch, stenoses, and swallowing disorders.

Lateral views of the neck and the upper thoracic region can be used to localize the site of radiopaque foreign bodies in the hypopharynx and upper esophagus. This projection is also of great value in inflammatory soft tissue swelling and surgical emphysema of the parapharyngeal tissues due to pharyngeal injuries, pharyngeal abscess, mediastinal abscess, etc.

Radiographic demonstration of the salivary glands using sialography and scanning is described on ▶ p. 477.

3.2.4 Examination of the Saliva

See ▶ p. 478.

3.2.5 Gustometry

Taste can be tested by applying substances to the tongue that represent four taste qualities—sweet, salty, sour, and bitter—at increasing concentrations, to assess the lowest concentration that can be recognized.

In normal ENT practice, objective gustometry is performed infrequently, and is probably now restricted to specialist units with a research interest.

Examination of overall taste sensation: The three-drop method makes it possible to evaluate the threshold of recognition for the qualities sweet, sour, salty, and bitter. Börnstein concentrations are used for testing. These are as follows: glucose 4%, 10%, 40%; sodium chloride 2.5%, 7.5%, 15%; citric acid 1%, 5%, 10%; quinine 0.075%, 0.5%, 1% (stale solutions should not be used). The sensation of taste is observed 0.5 to 4.0 seconds later, depending on the site tested, the temperature of the solution, and the size of the area tested. The test solution is applied alternately to the right and left sides of the tongue with a pipette, or better with a small piece of blotting paper ≈1 cm² in size. Confirming the threshold of recognition is usually satisfactory in ordinary practice.

Alternatively, test solutions of substances at concentrations slightly below or above the taste threshold can be administered in a defined sequence as one-drop tests. The sum of the recognized concentration levels of all four taste qualities is taken as a gustatory index. This test has high test-retest reliability (i.e., it is highly reproducible).

Assessing the ability to identify taste qualities: Oral application of sweet, sour, salty, and bitter test solutions, each at a concentration above the threshold that the patient is supposed to identify, is suitable for screening purposes. The test substances can be applied in solid form (known as tasties, taste strips, or wafers) or as fluids (drops, sprays). The patient is asked to identify each taste quality immediately after application.

Electrogustometry: Electric current can also be used to stimulate the taste receptors instead of test solutions. An anode current is used, with a normal threshold in adults between 2 and 7 μA. Electrogustometry has numerous advantages, but it is usually only used in specialist practices or hospital departments.

Reflex changes in the respiratory resistance of the nose or the electrical resistance of the skin are additional parameters that can be recorded simultaneously in response to a taste stimulus.

▶ Table 3.1  shows the most frequent causes of disorders of taste.

3.2.6 Specific Diagnostic Procedures

Bacteriologic, mycologic, and virologic culture: Microbiological culture and sensitivity should be considered for infective conditions prior to prescribing antibiotics.

Biopsy: Tissue biopsies are essential for tumors or suspected malignancy. Tumors and lesions in the mouth and pharynx are easily accessible.

Oropharyngeal biopsies may be combined with fine needle aspiration if a lesion is accompanied by an enlarge lymph node or neck mass.

3.3 Clinical Aspects of Diseases of the Mouth and Pharynx

The main symptoms and disorders that indicate disease of the mouth and pharynx include:

• 
  

  Pain on eating, chewing, or swallowing.

  
  
• 
  

  Dysphagia (see ▶ Table 7.3 ).

  
  
• 
  

  Globus symptoms (see ▶ p. 304 and ▶ Table 7.3 ).

  
  
• 
  

  Burning of the tongue (see ▶ Table 3.6 ).

  
  
• 
  

  Blood in the sputum.

  
  
• 
  

  Oral fetor (see ▶ Table 3.4 ).

  
  
• 
  

  Disorders of salivary secretion (see ▶ p. 478).

  
  
• 
  

  Disorders of taste (see ▶ Table 3.1 ).

  
  
• 
  

  Respiratory obstruction (see ▶ Table 6.2 ).

  
  
• 
  

  Disorders of speech.

  
  
• 
  

  Swellings on the head, neck, mouth, floor of the mouth, and swelling of the lymph nodes at the angle of the jaw (see ▶ p. 454).

3.3.1 Hyperplasia of the Lymphoepithelial Organs

The adenoid, the tonsil, and occasionally the lingual tonsil cause symptoms due to their size.

Hyperplasia of these organs is not in itself a disease, but only the morphologic expression of marked immunobiologic activity. A marked increase in the size of the tonsil produces primary mechanical obstruction of the aerodigestive tract and has detrimental effects on the entire body. Inflammation of neighboring organs is secondary. For this reason, tonsillar hyperplasia is here discussed separately from inflammation.

3.3.1.1 

Adenoid Hyperplasia

Clinical features: This is primarily a condition of childhood. Symptoms include nasal obstruction; nasal discharge; mouth breathing; feeding difficulty/slow eating, especially in small children; noisy breathing; loud snoring. The child may also have large tonsils and palpable lymph nodes near the angle of the jaw.

Secondary effects of large adenoids:

• 
  

  Chronic rhinitis, rhinosinusitis, and chronic/recurrent infection with mucopurulent nasal discharge.

  
  
• 
  

  Poor sleep quality, obstructive sleep apnea, daytime tiredness.

  
  
• 
  

  Eustachian tube obstruction, otitis media with effusion, recurrent acute otitis media (see ▶ p. 65).

Historically, children were described as having a typical adenoid face—i.e., dull facial expression, open mouth, dilated and flattened nasolabial folds, indrawn nasal alae, protruding upper incisor teeth, and hyponasal speech (rhinolalia clausa). These features are now rarely seen due to an improvement in children’s’ health care.

Pathogenesis: The condition is caused by above-average hyperplasia of the immunobiologically active lymphoepithelial tissue of the pharyngeal ring in children.

Diagnosis: The main symptoms include chronic mouth breathing, snoring, and susceptibility to infection. Examination by transnasal endoscopy or posterior rhinoscopy shows the enlarged adenoid ( ▶ Fig. 3.11).

Differential diagnosis: The main differential diagnosis is rhinitis that is often allergic. Rare causes of nasopharyngeal obstruction are a juvenile angiofibroma and unsuspected malignant tumors. Lymphoma is rare, but can masquerade as adenotonsillar hyperplasia leading to diagnostic delay.

Treatment: The options of managing enlarged adenoids include observation, topical steroid nasal sprays, and adenoidectomy. The adenoid is largest relative to the nasopharynx at about 7 years of age, and spontaneous improvement often occurs with natural growth after this age. There is some evidence that adenoid size decreases with a long-term topical steroid nasal spray.

Adenoidectomy remains a common operation in children, often combined with tonsillectomy. Blind curettage with an adenotome is still widespread practice. More recent techniques facilitate adenoidectomy under direct vision and include the use of suction diathermy coagulation, microdebriders, and coblation, each facilitating controlled removal of adenoid tissue and minimizing the risk of bleeding. The lower risk of operative bleeding together with the advent of the laryngeal mask facilitates surgery without an endotracheal tube ( ▶ Fig. 3.17 and ▶ Fig. 3.18).

Contraindications:

• 
  

  Recent infection of the upper respiratory tract or chest.

  
  
• 
  

  Known bleeding disorder.

Cleft palate or previous cleft palate repair: All children must have an assessment of the soft palate to exclude a submucous cleft prior to adenoidectomy. A bifid uvula may be a marker for a submucous cleft. Adenoidectomy could lead to palatal dysfunction/velopharyngeal insufficiency. Partial adenoidectomy under direct vision is an option in this situation.

Children with Down syndrome are at risk of atlantoaxial subluxation.

Tonsillar Hyperplasia

Clinical features: Tonsil hyperplasia can result in considerable respiratory obstruction, both with and without adenoidal hyperplasia (see above). In addition, there is increased difficulty in swallowing and eating because of obstruction of the faucial isthmus.

Diagnosis: See the section on adenoid hyperplasia ( ▶ p. 268). The local findings are obvious.

The tonsil size can be graded as follows:

• + Visible.

• + Halfway between the tonsillar pillars and the uvula.

• + Tonsils touching the uvula.

• + Tonsils touching each other.

Differential diagnosis: This is similar to that for adenoid hyperplasia. It is important to determine whether the tonsils alone are hyperplastic, or whether there is coexisting adenoid hyperplasia.

Treatment: Cold steel dissection is still the standard main technique for tonsillectomy. However, there are now several different techniques for performing tonsillectomy: bipolar diathermy dissection; laser tonsillectomy; radiofrequency/coblation surgery; ultrasonic dissection with the harmonic scalpel (Ultracision). The old operation of guillotine tonsillectomy is now obsolete.

An alternative to tonsillectomy is tonsillotomy in which the bulk of the tonsil is removed but a margin is left adjacent to the tonsillar fossa.

Course and prognosis: The symptoms usually resolve rapidly after removal of the mechanical obstruction. The child usually returns surprisingly rapidly to normal physical, psychological, and intellectual health. The prognosis is very good and recurrent adenoidal hyperplasia is unusual.

Complications: The main complications of adenotonsillectomy are bleeding and infection. All postoperative bleeding must be consistently observed and surgically stopped promptly. Infection becomes apparent a few days after surgery with the advent of fever, halitosis, and increased pain and morbidity. Postoperative infection can lead to delayed hemorrhage up to 10 to 14 days later.

Other postoperative complications include lip and dental trauma; temporomandibular joint strain or dislocation; aspiration from loose adenoidal tissue; altered taste following tongue depression; a change in the sound of the voice, which is usually only temporary.

Rare complications include hypernasal speech (rhinolalia aperta) adhesions in the nasopharynx, injuries to the ostium of the eustachian tube, and, very rarely, injuries to the glossopharyngeal nerve or the cervical spine. Nontraumatic atlantoaxial subluxation of the cervical spine can occur secondary to an inflammatory/infective process in the neck (Grisel syndrome), but children with Down syndrome may be susceptible.

Relative contraindications include a cleft palate, either corrected or not. A speech therapist consultation must be obtained before a decision is made for surgery in cleft patients.

Hyperplasia of the lingual tonsil rarely occurs in children, but may occasionally be seen in adults. Symptoms include a feeling of pressure in the throat, especially on swallowing, and occasionally recurrent inflammation of the base of the tongue. If necessary, the lymphoepithelial tissue can be partially removed. The cryoprobe or the laser are particularly suitable for this.

3.3.2 Dysphagia

Diagnosis: The two mainstays of diagnosis are radiographic videography and video endoscopy. Radiographic evaluation of swallowing using fluoroscopy requires the administration of a contrast medium bolus (barium sulfate, provided there is no risk of aspiration). Phases and functional disorders can be visualized that elude identification by endoscopy (e.g., pumping movements of the base of the tongue, passage into the larynx, or peristaltic waves).

Etiology: A distinction is made between neurogenic and structural etiologies. Neurogenic dysphagias occur as sequelae to apoplexy, cerebrocranial trauma, hypoxia, neurosurgical operations, or degenerative disease. Structural dysphagias result from tumors or tumor resection in the aerodigestive tract (see also ▶ Table 7.3 , ▶ p. 415).

Pathophysiology: Dysphagia is defined as difficulty in swallowing and may be accompanied by the following symptoms:

• 
  

  Drooling: The bolus leaves the mouth through incompletely closed lips (e.g., due to lip defects or facial nerve paralysis).

  
  
• 
  

  Leaking: The bolus enters the pharynx during the oral preparation phase (e.g., due to tongue paralysis or soft palate impairments such as clefts or paralysis).

  
  
• 
  

  Larynx penetration: The bolus arrives at the entrance to the larynx. Aspiration is prevented only by the vestibular folds and the vocal folds.

  
  
• 
  

  Regurgitation: Larynx elevation, which plays an important role in opening the superior sphincter, may be impaired (e.g., after tracheotomy or excision of goiter), causing reflux into the mouth if the closing pressure in the superior sphincter is too high. Reflux to the epipharynx (e.g., in velopharyngeal insufficiency) is known as nasal regurgitation.

  
  
• 
  

  Odynophagia: Pain on swallowing (e.g., due to inflammation).

  
  
• 
  

  Bolus retention (e.g., in an epiglottic vallecula, the piriform sinus, or a diverticulum) is possible. Gastroesophageal reflux leads to aspiration at the end of the swallowing act (post deglutition).

Functional treatment: The goal of logopedics or speech therapy is to improve swallowing efficiency and prevent aspiration.

Exercises and facilitation techniques: Dysphagia is treated using techniques that facilitate the sequence of movements and inhibit undesired elevation of muscle tone. Sensibility is stimulated, and the coordination, force, and endurance of motor activity are improved by providing training in target-oriented movements and patterns of motion.

Pathologic reflexes are reduced and pharyngeal contractions improved.

Compensatory techniques: Instead of abolishing the causes, these techniques compensate for deglutition disorders. Their purpose is to facilitate swallowing and prevent aspiration. They include changing the posture of the head by inclination and rotation.

Adaptation methods: This term refers to adjustment of food consistency, positioning the food if there are transportation disorders within the oral cavity, and using special eating and drinking aids.

3.3.3 Inflammatory Diseases

3.3.3.1 Labial and Oral Mucosa

Internal or dermatologic diseases often present on the lips, oral mucosa, gingiva, and tongue. ▶ Table 3.3  provides an overview of the most common and most important of these disorders. Since changes in the mucosa of the lips, mouth, or pharynx can occur in many disorders, the following description will be confined to the most common ones.

Rhagades of the commissures, along with slight bleeding and pain in the commissures accompanying opening of the mouth. Causes include ill-fitting false teeth, mycotic infection, poor general resistance, diabetes, iron-deficiency anemia, nonspecific pyogenic infections, and syphilis. If possible, the cause should be confirmed and dealt with before treatment is attempted. Carcinoma of the commissure may also simulate rhagades in the early phases. Nonspecific local treatment includes topical corticosteroids, either as a cream or in a special base designed to adhere to mucosal surfaces. In addition, methylrosanilinium chloride in aqueous solution with concentrations of 0.1%, 0.3%, and 0.5% is available.

Cheilitis may be solitary and acute due to trauma, thermal injury (hot food), chemical injury (smoke), actinic damage (sunburn), or exposure to radiation.

Cheilitis granulomatosa, Miescher disease, is a chronic recurring disease which is usually ushered in with a complete Melkersson-Rosenthal syndrome of cheilitis, granulomatous glossitis, and facial paralysis. The pathogenesis of this triad is unknown, and the treatment is the same as that of idiopathic facial paralysis (see ▶ p. 127).

Although tuberculosis or syphilis, primary or secondary, may occur on the lips, a chronic or recurrent erosive or hyperkeratotic lesion of the labial mucosa must always be suspected of being premalignant (leukoplakia, Bowen disease). Numerous diseases affecting the oral mucosa also affect the lips.

Stomatitis, often combined with gingivitis or inflammation of the buccal mucosa, may be a primary disease of many different causes or may be secondary to other diseases. The clinical symptoms and prognosis are thus extremely variable.

Ulceromembranous Stomatitis

Clinical features: The disease usually begins on the gingival margins with redness, swelling, and sensitivity to pressure. Swelling of the buccal and lingual mucosa, stomatitis simplex, may also occur. The disease often progresses to ulceration with severe pain, presenting with superficial, and occasionally deep, mucosal ulcers with a dirty-gray fibrinous membrane. There are marked constitutional symptoms: oral fetor, sialorrhea, possibly cloudy or purulent saliva, loss of taste, difficulty in eating, and high fever in the initial stages. The disease may spread to the pharynx, and the regional lymph nodes may be enlarged and painful.

Pathogenesis: This includes poor oral hygiene, reduced general resistance, infections from cutlery, dental damage, virus infections with possible secondary bacterial infection, mucosal rhagades, gingival pockets, and dental calculus ( ▶ Fig. 3.19).

Diagnosis: Bacteriologic culture is necessary, and often shows spirochetes and fusiform rods as in Vincent angina (see ▶ p. 292).

Differential diagnosis: This consists of mucosal mycosis, excluded by culture, virus infection (herpes simplex, aphthous stomatitis, and herpes zoster), syphilis, tuberculosis, acquired immune deficiency syndrome (AIDS), hematologic diseases including agranulocytosis and leukemia, which can be excluded using a differential white blood count, and carcinoma, which requires a biopsy.

Treatment: This includes appropriate oral and dental hygiene or methylrosanilinium chloride in aqueous solution with a concentration of 0.3%. Antibiotics are given if indicated by culture and sensitivity tests. Local and general antimycotic therapy is given for fungal infections.

Course and prognosis: Both are good if the cause is treated appropriately.

Herpes Simplex Stomatitis and Gingivitis

Clinical features: These include a burning sensation in the mouth, difficulty in eating, a feeling of being unwell, fever in the early stages, and lentil-sized, clear vesicles at the mucocutaneous junctions of the lip and the nasal introitus, and also in the entire mouth. The vesicles may progress to superficial circular or oval ulcers with a red center. The disease often occurs in conjunction with febrile general infections or overexposure to sunlight. There is marked oral tenderness, oral fetor, sialorrhea, and painful regional lymphadenopathy. The disease is contagious. Serial crops of fresh vesicles may occur. Children are most at risk.

Pathogenesis: The cause is infection with the herpes simplex virus and usually occurs first in childhood. The first infection often causes no symptoms. The disease is very infectious: 90% of the population are said to be carriers of the virus, but clinical manifestations in the form of herpes labialis ( ▶ Fig. 3.20) or stomatitis herpetiformis only occur in 1%.

Diagnosis: This is made by exclusion. An attempt can be made to isolate the virus from the contents of the vesicle, if possible within the first 24 hours of the vesicular stage.

Differential diagnosis: Chronic recurrent aphthous stomatitis, varicella, acute infectious exanthema, herpangina, foot and mouth disease, Behçet disease, pemphigus, and mycoses must all be considered.

Treatment: Systemic antiviral therapy (acyclovir, valacyclovir, famciclovir) is effective and should be used for 72 hours for acute infections. A bland liquid diet and gentle rinsing is also recommended. Steroids must not be given. Treatment for recurrent herpetic infection may include topical anesthetics and/or early treatment with topical antiviral agents (acyclovir, penciclovir). Long-term systemic antiviral prophylaxis or treatment may be needed for resistant cases.

Course and prognosis: This disease is usually harmless and lasts 1 to 2 weeks. The vesicles heal to form crusts, but do not form scars. Recurrence is frequent, but herpetic sepsis and herpetic encephalitis are very rare.

Viruses of the Picornaviridae family (coxsackie-virus, echovirus) and rarely of the variola group may also cause small oral ulcers.

Metal stomatitis: A stomatitis with discoloration of the gingiva can be caused by either medical or occupational exposure to mercury or bismuth. The same also applies to workers handling lead. The use of gold in the treatment of arthritis can cause a gingival stomatitis. Finally, the mucosa can be damaged by arsenic, chlorine, chromium, fluoride, copper, manganese, nickel, sulfur, thallium, and zinc; by organic substances such as benzol, dimethyl sulfate, tetrachlorocarbons, tetrachloroethylene; and by mixed substances such as corrosive agents, synthetic resins, synthetic materials, enamels, etc., as well as by wood, dyes, hops, wool, and insecticides.

Stomatitis due to drugs: This may be observed particularly after the use of bromides, iodides, salicylates, antibiotics, and sulfonamides, psychoactive drugs that dry the mouth, and antiepileptic agents, and after pyramidone, barbiturates, laxatives such as phenolphthalein, and the contraceptive pill.

Allergic stomatitis: Hypersensitivity reactions on the oral mucosa and the lips, with varying severity, with or without angioneurotic edema, may be observed in response to almost all drugs, dental material, mouthwashes, toothpaste, cosmetics, chewing gum, and also to some foods such as fruit, fish, protein, and milk. The diagnosis can be established by testing, and if the allergen is found it should be withdrawn. Otherwise, antiallergic or local symptomatic treatment are given.

Candidal Stomatitis

Clinical features: Burning in the mouth and tongue, superficial white foci, and exudates on the mucosa are symptomatic. The exudate can be wiped off with mild pressure.

Pathogenesis: In normal individuals, almost all cases of oral yeast infections are caused by Candida albicans; rarely, other agents may be involved in severely immunosuppressed hosts. Candidiasis affect individuals with diabetes mellitus, reduced resistance, and after prolonged administration of antibiotics, chemotherapy, steroids, oral contraceptives, and after radiotherapy. Acute severe infection with ulceration can be a presenting sign of immune deficiency, human immunodeficiency virus (HIV) infection, or acute leukemia.

Diagnosis: This is made on the basis of the characteristic membranous white or gray exudates and very inflamed mucosa. Superficial ulceration occurs. A specimen is taken for culture for fungi.

Differential diagnosis: Diphtheria.

Treatment: The standard therapy is nystatin or fungistatic solutions. Options include methylrosanilinium chloride in aqueous solution with a concentration of 0.1% to 0.5% or borax-glycerin solution. Good oral hygiene is also crucial.

Course: The prognosis is good if the patient is relatively healthy. Prompt treatment for several weeks, with monitoring by culture, is advised in more severe cases. In immunosuppressed individuals, there is a risk of systemic spread if treatment is not adequate.

Herpes Zoster

Clinical features: Unilateral rapidly progressive vesicles are quickly followed by fibrinous superficial epithelial defects, affecting the segments of the face innervated by the second and third divisions of the trigeminal nerve. The disease is very painful. Mucosal lesions may occur in the same stage and may be partially confluent and arranged in groups.

Pathogenesis: This is a neurotropic infection with the varicella-zoster virus, which is morphologically identical to the herpes simplex virus.

Diagnosis: The diagnosis is established on the basis of the typical segmental arrangement of the vesicles, severe pain, and culture of the contents of the vesicle ( ▶ Fig. 3.21).

Differential diagnosis: This includes herpes simplex and recurrent aphthous stomatitis.

Treatment: Prompt institution of high-dose regimens of systemic antiviral agents (acyclovir, valaciclovir, famciclovir) within 48 hours has been shown to reduce the duration and severity of the acute disease and somewhat reduces the risk of postherpetic neuralgia. In severe cases or immunosuppressed patients, intravenous acyclovir should be considered. A prophylactic vaccine has recently been approved. Good oral hygiene, a bland liquid diet, and topical anesthetics or methylrosanilinium chloride in aqueous solution with a concentration of 0.1% can be used for symptomatic relief.

The disease is often followed by severe, therapy-resistant neuralgias, which may persist for months after resolution of the mucosal lesions. Occasionally, other regions and internal organs may be involved simultaneously. The generalized form in older patients suggests a systemic malignancy or immunosuppression.

Acquired Immune Deficiency Syndrome (AIDS)

Clinical features: Approximately 35% to 40% of HIV infections are associated with otorhinolaryngologic symptoms, including early symptoms such as angular cheilitis and Kaposi sarcoma ( ▶ Fig. 3.22 and ▶ Fig. 3.23). HIV infection has a relatively high association with cervical lymphadenopathies, candidiasis, herpes simplex, and herpes zoster. Other potential manifestations of HIV infection include sinusitis, tonsillitis, gingivitis, pharyngitis, esophagitis, tracheitis, sudden hearing loss, facial paralysis, and facial pain. General accompanying features are fever, anorexia, headache, muscle and joint pain, transient or persistent lymph-node enlargement, diarrhea, and profound weight loss.

Pathogenesis: HIV infection.

Diagnosis: HIV infection is diagnosed by the detection of HIV antibodies in the serum in a screening test (e.g., enzyme-linked immunosorbent assay, ELISA) followed by a confirmatory blot test.

Differential diagnosis: See the list of symptoms above. HIV infection should be suspected whenever a “classic” disease has an unusual location and presentation, runs an atypical course, and presents in an atypical age group, especially if the patient is in a high-risk group, such as intravenous drug users.

Treatment: The HIV virus cannot be eliminated by any of the current treatment regimens. In addition, no vaccine is available. However, highly active anti-retroviral therapy (HAART) using multiple drugs in different therapeutic classes designed to inhibit HIV in different ways has radically improved the outlook for infected patients and altered the spectrum of oral diseases seen. Oral Kaposi sarcoma has become uncommon again, and severe oral candidiasis, oral hairy leukoplakia, and recurrent herpetic infections are all suppressed with HAART.

Chronic Recurrent Aphthae

Aphthae are recurrent oral ulcerations, generally small with an erythematous base. Three types are observed:

1. 
   

   Minor type (Mikulicz): Only two to six oval aphthae in the oral mucosa; also known as canker sores.

   
   
2. 
   

   Major type (Sutton): Large mucosal aphtha (>1 cm), usually occurring on the soft palate, cheek mucosa, tongue, or lips.

   
   
3. 
   

   Herpetiform type (Cooke): Several very small and painful herpetiform ulcerations on the lateral border of the tongue.

Clinical features. Aphthae occur intermittently, affecting the buccal mucosa, the tongue, the palate, and the gingiva. They are very painful. The regional lymph nodes may be swollen, and concomitant stomatitis is possible.

Pathogenesis: The cause is unknown. The disease is not thought to be infectious, but instead to represent activation of intrinsic inflammation in susceptible individuals. Aphthae can be triggered by infections, hormonal factors such as menstruation, and certain foods.

Diagnosis: This is made on the basis of the long history of the condition and its tendency to recur. There is no sialorrhea, no oral fetor, and no fever.

Differential diagnosis: Herpes simplex, which occurs with fever, fetor, sialorrhea, a general malaise, and a large number of vesicles which are confluent and arranged in groups must be considered. Behçet disease can present with recurrent multiple aphthous ulcers.

Treatment: Causal or prophylactic treatment is not possible. Symptomatic treatment includes methylrosanilinium chloride in aqueous solution with a concentration of 0.1%, borax solution, chlorhexidine, and topical corticosteroids. The major type sometimes responds to antibiotics and oral tetracycline solution may be helpful.

Course: The lesions heal without scarring in 1 to 3 weeks, but early recurrence is possible. The course may extend over decades, and familial occurrences are known.

Behçet Disease

Clinical features: Aphthae occur in crops in the mouth and on the genitals. Eye symptoms are often monocular and typically wax and wane. They include hypopyon iritis, which is often fleeting, and later papilledema, involvement of the retina, and blindness. Rheumatic symptoms and renal involvement may also occur.

Pathogenesis: The cause is unknown. It may be generalized vasculitis, an autoimmune event, or a virus infection.

Diagnosis: The main, and often the first, symptom is involvement of the eye. Acute cochleovestibular disturbances may also occur.

Treatment: Oral mucosal lesions can be treated locally with topical corticosteroids, methylrosanilinium chloride in aqueous solution with a concentration of 0.1%, and gentle rinses.

Systemic treatment relies on immunosuppressive medication (cyclophosphamide, azathioprine, cyclosporine, methotrexate, mycophenolate) and long-term steroids. Biologics, such as rituximab, have been shown to be effective.

Course: With treatment, the symptoms can be eased, the mucosal infections can be reduced, and the disease can be controlled over a lifetime.

Tuberculosis

Clinical features: Mucosal lesions may take the form of a mucosal lupus or exudative ulcerative mucosal tuberculosis. Round nodules occur in groups in mucosal lupus, and they demonstrate yellowish-brown flecks in the oral mucosa on pressure with a glass spatula. They are not painful. Flat, dirty, exudative, painful ulceration with undermined edges and lymph-node involvement is found in ulcerative mucosal tuberculosis (see ▶ p. 291).

Pathogenesis: The oral cavity is nowadays almost never a primary site of manifestation of tuberculosis. The disease is usually due to hematogenous or intraluminal spread from the primary site, usually the lung.

Diagnosis: This is made by biopsy and culture, and chest radiography. Tuberculosis is a notifiable disease.

Differential diagnosis: Syphilis, mycoses, and carcinoma must be excluded.

Treatment: The original focus in the lung is treated by tuberculostatic drugs. Triple therapy consisting of isoniazid, rifampicin, and ethambutol is now usually given, supervised by a chest physician.

Course: This depends on the outcome of the primary lesion. However, the prognosis for mucosal lesions is good with general antituberculous therapy.

Syphilis

Clinical features: All stages of syphilis can occur in the mouth.

Stage I (primary syphilis): primary chancres occur on the lips, tonsil, anterior part of the tongue, commissure, gingiva, and buccal mucosa ( ▶ Fig. 3.24). A sharply delimited nodule 2 to 3 mm in diameter grows to the size of a penny. After a few days, a painless ulcer forms, with a very hard edge, and there is painless regional lymphadenopathy in the submandibular or jugulodigastric area. The primary lesion regresses spontaneously after 3 to 6 weeks.

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