Acute Orofacial 6 Yair Sharav, DMD, MS Rafael Benoliel, BDS

Acute is most frequently dental in origin, associated with the teeth and their support- ing structures—the periodontium. Dental pain is primarily due to dental caries. Other oral are periodontal or gingival in origin. Acute dental and periodontal pain is moderate to severe in intensity or ranges from 60 to 100 on a 100-mm visual analog scale.1 In about 60% of patients, pain is not localized but spreads into remote areas of the head and face and is reported in sites that differ from the pain source.1,2 Pain-referral patterns for maxillary and mandibular sources have considerable overlap, and the source of pain cannot be predicted from the pain location. Consequently, maps of facial pain-spread patterns are of no use diagnostically. Pain spread is correlated with pain intensity, and stronger pain tends to spread more (Fig 6-1), but neither duration nor quality of pain infl uences the incidence of referred pain.3 Pain spread is not dependent on the tissue affected by the patho- logic process, for example, dental or periodontal structures.1 The mechanisms responsible for pain spread are of central origin, resulting from interactions between primary nociceptive afferents and trigeminothalamic neurons. Factors that may be important for the extensive pain-spread patterns in the facial area include convergence of primary afferents from different areas, such as cutaneous, , visceral, neck, and muscle afferents, onto nociceptive and non-nociceptive neurons in the trigeminal subnucleus caudalis on common dorsal horn neurons; the large receptive fi elds of the wide dynamic range neurons; and the somatotopic organization.4,5 As pain intensity increases, neu- rons whose receptive fi eld center lies within the source of pain would increase their activity, thereby activating a larger receptive fi eld and somatotopically adjacent neurons.5

141 6 Acute Orofacial Pain

90

80

Visual analog scale 70

0123456 Pain spread (vectors)

Fig 6-1 Spread of acute dental pain as a function of pain intensity. Pain intensity is described on a 0- to 100-mm visual analog scale. Pain spread denotes the number of locations on the face to which the pain spreads (vectors). Pain spread is clearly a function of pain intensity. (Modified from Sharav et al1 with permission.)

a b c

Dentinal Pulpal Periapical

Fig 6-2 Acute dental pain presented at three progressive consecutive stages of car- ies penetration: (a) Dentinal pain is associated with caries penetrating into the ; (b) pulpal pain is associated with deep caries penetration approaching the dental pulp; (c) occurs when the inflammatory process invades the periapical area.

lasts longer. Finally, when the caries Caries and Symptom approaches the tooth pulp, a strong, spon- taneous, paroxysmal pain develops, which is Progression usually intermittent in nature. Microorganisms No pain is associated with caries confined to and products of tissue disintegration invade the enamel. As caries progresses to the su- the area around the root apex, and the tooth perficial layer of the dentin, however, pain is becomes very sensitive to chewing, touch, and evoked by various stimuli, such as change in percussion. Usually at that stage the parox- temperature and sweet substances. As the ysmal, intermittent pain has a continuous dull lesion penetrates deeper into the tooth, the nature, and the tooth is no longer sensitive to pain from these stimuli becomes stronger and changes in temperature. The development of

142 Epidemiology

Table 6-1 Anamnestic details of dental and periodontal pain Pain origin Localization Character Intensity Aggravated by Dental Dentinal Poor Evoked, does not Mild to moderate Hot, cold, sweet, or outlast stimulus sour foods Pulpal Very poor Spontaneous, Moderate to severe Hot, cold, sometimes paroxysmal, chewing intermittent Periodontal Periapical/lateral Good Continues for hours, Moderate to severe Chewing deep, boring

Table 6-2 Physical and radiographic signs of dental and periodontal pain Pain origin Associated signs Diagnostic findings Radiography Dental Dentinal Caries, exposed dentin, Sensitive to cold application, Proximal caries, defective defective restorations pain moderate, no overshoot restorations Pulpal Deep caries, extensive Strong pain to cold application Deep caries or restorations, restorations with overshoot, may be tender pulp exposure to percussion Periodontal Periapical Periapical tenderness, redness Very tender to percussion, Usually no periapical changes and swelling, vertical tooth nonvital tooth pulp at acute stage mobility Lateral Periodontal tenderness, Tender to percussion, deep Alveolar bone resorption redness and swelling, tooth pockets on probing mobility

symptoms follows the progression of pathol- dures, such as physical examination and radio- ogy and the dental structures involved: initial- graphs. The anamnestic details of dental and ly dentin, followed by pulp, and ultimately the periodontal pain are described in Table 6-1, periodontal tissues (Fig 6-2). In clinical prac- and the physical and radiographic signs are de- tice, the demarcation between these various scribed in Table 6-2. stages is sometimes indistinct; the tooth may be sensitive simultaneously to temperature changes and to chewing. Epidemiology Pain arising from the may be localized and associated with a detectable ero- Epidemiologic data on dental pain are sparse sive or ulcerative lesion or may be of a diffuse and of poor quality. The reported prevalence nature. Pain descriptors on their own are not of dental pain in community-dwelling adults sufficient for diagnosis, and orofacial diseases ranges from 12% to 40%, depending on the must be validated by other diagnostic proce- description used for dental pain.6–9

143 6 Acute Orofacial Pain

Pressure/ Probing percussion

F F E E

C C

P P a b

Fig 6-3 Detecting a crack in dentin by (a) oblique percussion or pressure on one cusp or (b) firm probing between filling and tooth with a sharp explorer to widen the crack. This will activate dentinal and/or pulpal nociceptive mechanisms. C, crack; E, enamel; F, filling; P, pulp chamber.

to evoke pain and locate its source. Not all ar- Dental Pain eas of exposed dentin are sensitive, and there- fore not all areas are a source of pain. Dentinal pain A bitewing dental radiograph (see Fig 6-4a) is Symptoms a useful diagnostic aid in these cases, especial- ly when the caries lesion is situated on a proxi- The pain originating in dentin is a sharp, deep mal tooth surface that is not easily visualized by sensation evoked by external stimuli that sub- direct observation or probing. A periapical den- sides within a few seconds. Hot, cold, and tal radiograph is useful for assessing processes sweet are among the external stimuli that may affecting the tooth root (see Fig 6-4b). produce pain. Pain is poorly localized, often only to an approximate area within two or three teeth adjacent to the affected tooth. Frequent- ly, the patient is unable to distinguish whether Symptoms. In addition to the symptoms typical the pain originates from the or the for dentinal pain, a patient may also complain maxilla. of a sharp pain, elicited by biting, that resolves immediately. Localization of the source of pain is not precise but aided by the biting location. Physical and radiographic signs Typically, the patient also complains of pain and Common associated with dentinal discomfort associated with cold and hot foods. pain are early dental caries, defective resto- These complaints indicate a crack in the dentin, rations, and areas of exposed dentin (due to known as cracked tooth syndrome.11,12 These or erosion of the enamel) and exposed incompletely fractured teeth may be associated roots (due to or periodontal with long-lasting diffuse orofacial pain and are therapy).10 Duplication of pain produced by difficult to diagnose.13 controlled application of cold or hot stimuli to various teeth in the suspected area as well Physical and radiographic signs. The main as direct observation and examination with a diagnostic challenge is localizing the affected sharp dental probe are useful in locating the tooth, especially because the crack is not read- affected tooth. Areas of exposed dentin, for ex- ily detected and radiographs are not helpful. ample, are scratched with a sharp dental probe Localization can be achieved by causing the

144 Dental Pain crack to widen, and thus duplicating the pain, precipitants.16,17 The use of CO and Nd:YAG 2 by the following techniques: lasers for cervical hypersensitivity were also found to be effective, as no damage to the • Using percussion or pressure on the cusps tooth pulp was recorded.18 A recent systematic of the suspected teeth at different angles review and network meta-analysis concluded (Fig 6-3a) that most active treatment options had a sig- • Asking the patient to bite on individual cusps nificantly better treatment outcome than the using a fine wooden stick or a predesigned placebo.19 bite stick (available commercially) • Probing firmly around the margins of fillings and in suspected fissures (Fig 6-3b) Pulpal pain Symptoms The bite test was found to be the most reli- able for reproducing symptoms.12 A similar but Pulpal pain is spontaneous, strong, often throb- distinct entity, a , may pro- bing, and exacerbated by changes in tempera- duce similar symptomatology and is discussed ture and pressure on the caries lesion. When under the periodontal pain section. evoked, pain outlasts the stimulus (unlike stimulus-induced dentinal pain) and can be excruciating for many minutes (see Table 6-1). Treatment of dentinal pain Similar to dentinal pain, localization is poor and Dentinal pain due to caries is best treated by becomes even poorer when pain is more in- removing the caries lesion and restoring the tense. Pain tends to radiate or refer to the ear, tooth. Sensitivity usually disappears within a temple, and cheek, but there are no definitive day or two, although when the caries lesion is pain-radiation patterns, and there is consid- deep the tooth may remain sensitive to cold erable overlap in pain reference locations of stimulation for a week or two. Treatment of the maxillary and mandibular teeth.1,3 Pain does not cracked tooth depends on the state of the tooth usually cross the midline. Patients may describe (existing restorations, periodontal condition) pain as a continuous dull ache that is periodical- and the extent of the fracture. Often, removal ly exacerbated (by stimulation or spontaneous- of an existing restoration allows the fracture to ly) for short (minutes) or long (hours) periods.20 be localized and its extent determined. Isolat- Pain may increase and throb when the pa- ed fractures of single cusps may be treated by tient lies down, and, in many instances, it wakes their removal and subsequent tooth restoration. the patient from sleep.1 Many believe that this In some cases, restoring the tooth is inevitable, throbbing is associated with arterial pulsations. but is usually not indicat- However, contrary to this accepted view, it was ed. Of 127 teeth that were restored because found that the throbbing rate (44 ± 3 beats per of a crack and specifically diagnosed with re- minute [mean ± SEM]) was much slower than versible , 100 did not require root canal the arterial pulsation rate (73 ± 2 beats per treatment within 6 years of follow-up. The re- minute [mean ± SEM]; P < .001) and that the searchers concluded, however, that about 20% two rhythms exhibited no underlying synchro- of the patients would need root canal treatment ny.21 Pain originating from the pulp is frequently within 6 months.14 not continuous and abates spontaneously; the Hypersensitive (exposed) dentin can be precise explanation for such abatement is un- treated by interventions that reduce dentinal clear. This episodic, sharp, paroxysmal, non- tubule permeability. Desensitizing toothpastes localized pain may lead to the misdiagnosis of with ingredients such as stannous fluoride or other conditions that mimic pain of pulpal origin nitrate will improve symptoms for (eg, cluster , trigeminal ; see most patients.15,16 Other tubule-blocking agents chapters 10 and 11). include resins; glass-ionomer cements and Although pain is the most common symp- bonding agents; strontium chloride or acetate; tom of a diseased pulp, no correlation exists aluminum, potassium, or ferric ; silica- between specific pain characteristics and the or calcium-containing materials; and protein histopathologic status of the pulp.22 Further-

145 6 Acute Orofacial Pain

Clinical characteristics to consider when deciding whether to preserve Table 6-3 (reversible) or extirpate (irreversible) the tooth pulp in cases of painful pulpitis Characteristics Reversible Irreversible Pain intensity Mild Severe History of spontaneous pain No Yes Pain duration Short Prolonged, recurrent Temperature sensitivity Mild, short-lasting Strong, overshoot Percussion Usually not tender Tender Caries removal Usually no exposure Very often clear pulp exposure Radiographs Early caries or shallow restoration, Deep caries or restoration with no recent tooth preparation secondary dentin

more, despite the fact that pain associated with or extracting the tooth. When pain is mild or pulpitis is severe, there are instances when a moderate and there is normal pulpal vitality, no diseased tooth pulp can progress directly to previous history of pain, and no pain on percus- without pain. Approximately 40% sion, the pulp is in the reversible category, and of 2,202 teeth that were treated endodontically the tooth pulp should be preserved by caries had no history of spontaneous pain or of pro- removal and indirect pulp capping.25 The suc- longed pain to thermal stimulation.23 cess rate of a calcium hydroxide–based direct capping agent in permanent teeth was 80.1% after 1 year, 68.0% after 5 years, and 58.7% Physical and radiographic signs after 9 years.26 Spontaneous, severe pain with a Localization of the affected tooth is the ini- history of previous pain and prolonged pain on tial aim of the diagnostic process, and it is cold stimuli was significantly more frequent in achieved through the same methods detailed patients with irreversible pulpitis.27 One should for dentinal pain (see Table 6-2). The applica- be aware, however, that these indications are tion of heat or cold to the teeth should be done under debate and some controversies exist.28 carefully because it can cause unbearable pain. Pulpal pain normally disappears immediately In reversible pulpitis, pain response outlasts the after treatment. Persistent pain, regardless of stimulus, usually by less than 10 seconds. In etiology, lasting 6 months or longer after en­ irreversible pulpitis, cold application results in dodontic treatment was estimated to be 5.3%, excruciating pain that outlasts the stimulus for though higher-quality studies suggested that it well beyond 10 seconds. Vital teeth requiring is greater than 7%,29 of which about half was endodontic treatment and painful on percus- thought to have a nonodontogenic origin.30 sion are common.24 Therefore, percussion is a Systemic penicillin administration clearly has quick test for localizing the affected tooth, as no effect on pain amelioration or prognosis of about 80% of teeth with painful pulpitis are ten- irreversible pulpitis.31,32 The anesthetic effica- der to percussion. The state of the pulp cannot cy of inferior alveolar nerve blocks in patients be judged from a single symptom, however; di- with irreversible pulpitis ranges between 26% agnosis should be based on the combination of and 56%. The rate of success can be improved several signs and symptoms20 (Table 6-3). by doubling the volume of anesthetics33 or, even better, by combining it with buccal infil- tration.34–36 The clinical characteristics that dic- Treatment tate treatment indications for teeth with painful Depending on the diagnosis, treatment may pulpitis are summarized in Table 6-3. Case 6-1 aim at conserving the pulp (reversible pulpi- demonstrates a patient with irreversible pulpitis tis), extirpating the pulp (irreversible pulpitis), (Fig 6-4).

146 Dental Pain

CASE A 22-year-old woman with acute pulpitis. 6-1 Primary complaint: For the past 2 days, the patient has suffered from strong, paroxysmal pain in the lower mandible. Pain radiates to the ear and wakes the patient from sleep. Findings: The bitewing radiograph (Fig 6-4a) exhibits more than one deep carious location and therefore presents diffi culty in locating the source of the spontaneous pain. The source of pain is detected by means of a physical examination. A periapical radiograph of the mandibular left fi rst molar (Fig 6-4b) demonstrates periapical radiolucency. Note that periapical radiolucency and tenderness to percussion coexist with strong pain to cold stimulation. Diagnosis and treatment: The diagnosis was irreversible pulpitis. The tooth pulp was extirpat- ed, resulting in complete subsequent pain relief. Comments: The history and type of pain indicate the diagnosis of acute pulpitis. Although the type of pain was typical for acute pulpitis, locating the affected tooth was somewhat problem- atic because there was more than one possible source. The source of the acute, spontaneous, severe pain was evident from the signs of the physical examination. Although the maxillary left second and the mandibular left fi rst molar both responded with strong pain to cold ap- plication, only the fi rst molar exhibited overshoot and tenderness to percussion. Note that peri- apical radiolucency and tenderness to percussion coexisted with strong pain to cold stimulation.

a b

Fig 6-4 Case 6-1. (a) Bitewing radiograph of the left side demonstrating multiple locations with deep caries, especially the maxillary second premolar and mandibular first molar. (b) Periapical radiograph of the mandibular left first molar demonstrating deep caries, widening of the periodontal ligament, and periapical radiolucency (especially at the mesial root).

Mechanisms of dental pain by applying various stimuli to exposed dentin, that is, drying by application of absorbent pa- Dentinal sensitivity per or a stream of air; mechanical stimulation (eg, cutting, scratching, probing); and changes The mechanisms of dentinal sensitivity and in osmotic pressure, pH, or temperature. How- pain have been extensively reviewed.37–40 Mor- ever, the application of well-established algesic phologically, nerve fibers may penetrate into substances, such as , acetyl- the dentin about halfway into the odontoblastic choline, 5-hydroxytryptamine, bradykinin, and process but certainly do not reach the dentino- histamine, to exposed dentin does not evoke enamel junction37,41 (Fig 6-5). Furthermore, the pain.43,44 All of these substances can produce concept that the has a role as a pain, however, when placed on a skin blister sensory receptor of the dentin has not been sub- base.45 The limited distribution of nerve fibers in stantiated.42 Experimental pain may be induced dentin and the fact that neuroactive chemicals

147 6 Acute Orofacial Pain

Enamel

Dentinal tubules

Odontoblastic process

Innervation

Fig 6-5 Diagram of dentinal innervation. Note that the intratubular odontoblastic pro- cess penetrates only about half of the dentinal tubule. Also, not all dentinal tubules are innervated. The percentage of innervated tubules decreases from the tip of the crown toward the root. (Modified with permission from Byers and Närhi.37)

fail to stimulate or anesthetize dentin led Brann- tinal tubules may account for the short latency strom46 to propose a hydrodynamic mecha- (< 1 second) activation of mechanosensitive nism. According to Brannstrom’s hypothesis, receptors after cooling. Long latency (> 10 sec- the movement of extracellular fluid that fills the onds) neural responses could be associated dentinal tubules will distort the pain-sensitive with the activation of thermosensitive recep- nervous structure in the pulp and predentinal tors.39 Facts and hypotheses regarding dental area and activate to pro- pain and are further discussed in duce pain. Several other theories have been a recent topical review.38 Immunohistochemical proposed, such as the so-called neural theory observation showed localization of transient re- and odontoblast transduction theory, but most ceptor potential vanilloid subfamily member 1 of the evidence supports the hydrodynamic (TRPV1) channel immunoreactions on the distal theory.47 The dentinal tubules seem to act as regions of odontoblast membranes, suggest- passive hydraulic links between the site of stim- ing that odontoblasts may directly respond to ulation and nerve endings sensitive to pressure noxious stimuli such as a thermal-heat stim- at the pulpal end in the underlying pulp. Analy- ulus.48 The expression of TRPV1 (heat) and sis of thermal-induced dentinal fluid flow and its TRPV2 (heat/mechanical) channels in the cell implications in dental thermal pain were exam- bodies and terminal arborizations of neurons ined by using a mathematic model to simulate that innervate the dental pulp and periodontal the temperature and thermal stress distribution tissues were recently evaluated.49 The TRPV1 in a tooth undergoing thermal stimulation.39 receptor was more extensively expressed in The researchers concluded that rapid fluid neurons innervating the periodontal ligament flow caused by thermal deformation of den- (26%), and about 50% of trigeminal ganglion

148 Periodontal Pain neurons retrogradely labeled from the dental the severity of clinical symptoms.55 Research- pulp expressed TRPV2.49 The cellular and mo- ers suspect that, unlike pulpal C fibers, A fibers lecular mechanisms of dental nociception were are relatively insensitive to inflammatory medi- recently reviewed40 in a study that discussed ators.56 On the other hand, it was found that three hypotheses proposed to explain dentinal leukotriene B4 (LTB4) can sensitize pulpal Aδ hypersensitivity: The first hypothesis emphasiz- fibers and may be a long-lasting hyperalgesic es the direct transduction of noxious tempera- factor that contributes to pain of pulpal origin.57 ture-sensitive transient receptor potential by Pulpal C nociceptors, however, seem to have a dental primary afferent neurons. The second, predominant role in transmitting pain from in- known as the hydrodynamic theory, attributes flamed pulp tissue.17 dental pain to fluid movement within dentinal Neurophysiologic and neurochemical cen- tubules. The third focuses on the potential sen- tral nervous system reactions occur as a result sory function of odontoblasts in the detection of local inflammatory changes in the dental of thermal or mechanical stimuli.40 pulp, some of which have been recorded in trigeminal nuclei. These responses include sig- nificant changes in mechanoreceptive fields, Pulpal pain altered response properties of brainstem neu- Pain mechanisms underlying pulpal pain are rons in the trigeminal nucleus, and neuroplastic related to inflammation and include a host changes involving N-methyl-d-aspartate recep- of mediators found in the pulp, such as cho- tor mechanisms.4 linergic and adrenergic neurotransmitters, prostaglandins, and cyclic adenosine mono- phosphate.17,50 Some substances, such as Differential diagnosis of odontalgia prostaglandins (particularly prostaglandin E Diagnosis of is challenging because 2 [PGE ]), serotonin, and bradykinin contribute to teeth often refer pain to other teeth and to other 2 tooth-pulp nerve excitability, and PGE enhanc- craniofacial locations.1,2 Other craniofacial pain 2 es bradykinin-evoked calcitonin gene-related disorders may refer pain to teeth and be ex- peptide release in bovine dental pulp.51 Brady- pressed as toothache, including pretrigeminal kinin released during may con- neuralgia, neurovascular orofacial pain, or atyp- tribute to the initiation of neurogenic inflam- ical pains associated with gustatory stimuli58–61 mation in dental pulp and may regulate pulpal (see chapters 10 and 12). One should consider response to injury or inflammation. The expres- that about half of all cases of persistent tooth sion of substance P, a neuropeptide with a ma- pain after root canal therapy were thought to jor role in nociception, significantly increases have a nonodontogenic origin.30 In this respect, with caries progression. Of clinical significance neurovascular orofacial pain is of great diag- was the fact that this increase in substance nostic importance62,63; it is discussed in more P was significantly greater in carious speci- detail in chapter 10. Other conditions mimick- mens that were painful than in asymptomatic ing odontalgia may refer from the maxillary si- carious specimens.52 Substance P increases nus or the ear (see chapter 6). Pain may also microvascular permeability, edema formation, be referred from more remote structures, such and subsequent plasma protein extravasation, as the carotid artery or heart and mimic the which underlie its powerful proinflammatory symptoms of a toothache64,65 (see chapter 14). properties.53 In endodontically affected teeth, Of particular importance is pain referred to the higher levels of endotoxin were detected in oral cavity that is associated with intracranial teeth with exudation, whereas elevated levels tumors66,67 (see chapter 12). of PGE were found in teeth with tenderness to 2 percussion and pain on palpation.54 Irreversible pulpitis (but not reversible pulpitis) is associat- Periodontal Pain ed with upregulation of tumor necrosis factor alpha (TNF-α) gene expression in human pulp, Periodontal pain is usually experienced in re- and this gene expression in inflamed human sponse to localized acute inflammation. Pain dental pulp tissue is positively associated with originating in the structures surrounding the

149 6 Acute Orofacial Pain

teeth is easily localized; the affected teeth are temperature changes.53 Regression analysis re- very tender on chewing and are readily local- vealed that a closed pulp chamber and caries ized by percussion. Etiologically, three clinical were highly associated with pulpal pain, and, conditions are possible: (1) acute periapical conversely, an open pulp chamber was associ- inflammation as a result of pulp and ated with periapical pain (P < .001).70 pulp necrosis, (2) acute periodontal infection In more severe, purulent cases, swelling of associated with deep pocket formation, and (3) the face associated with cellulitis is sometimes acute gingival bacterial or viral inflammation. present and can be associated with and Although the pain characteristics, ability to . The affected tooth may be extruded localize, and pain-producing situations are sim- and mobile, both vertically and horizontally. ilar for acute periapical and lateral periodontal When facial swelling appears, pain usually di- abscess (see Table 6-1), the physical and radio- minishes in intensity, probably because of rup- graphic signs differ (see Table 6-2). Treatment ture of the local periosteum and the decrease modalities are based on the etiology of each in tissue pressure caused by pus accumulation. condition and are entirely different. These cases are diagnosed as dentoalveolar abscess. Case 6-2 depicts a patient with peri- apical periodontitis that developed into a den- Acute periapical periodontitis toalveolar abscess (Fig 6-6). Symptoms Radiographs are of limited use in diagnos- ing acute periapical periodontitis because no Pain associated with acute periapical inflam- periapical radiographic changes are detect- mation is spontaneous, of moderate to severe able in the early stages. If a radiographic peri- intensity, and long lasting (hours). Pain is ex- apical rarefying osteitis is noticed in a tooth acerbated by biting on the affected tooth and, that is sensitive to touch and percussion, the in more advanced cases, even by closing the condition is then classified as re-acutization mouth and bringing the tooth into contact with of chronic periapical periodontitis (as in Case the opposing teeth. 6-2). Many times, however, such a rarefying os- Localization is usually precise, and the pa- teitis lesion is present in an otherwise asymp- tient is able to indicate the affected tooth. In tomatic situation. Furthermore, there is a lack this respect, periodontal pain differs from the of correlation between the radiographic picture poorly localized dentinal or pulpal pain. The im- and the microbiology or histology of the peri- proved localization of pain may be attributed to apical lesion.71,72 the proprioceptive and mechanoreceptive sen- sibility of the periodontium that is lacking in the pulp.68,69 Although localized, in approximately Pathophysiology 50% of patients the pain is diffuse and spreads The recent discovery of a new class of into the jaw on the affected side of the face.1 protease-activated receptors has shed light on enzyme-mediated sensory nerve acti- vation, especially on the important role of Physical and radiographic signs protease-activated receptor-2 in disease states The affected tooth is readily located by means associated with inflammation.73 Substance P of gentle tooth percussion, and the periapical immunoreactive nerve fibers have been found vestibular area may be tender to palpation. The in the vicinity of tryptase-positive mast cells pulp of the affected tooth is nonvital. However, (tryptase constitutes the major protein released in clinical practice pulpal and periapical pain during mast cell degranulation) in human peri- could occur at the same time. In these cases, apical .74 Of special interest is the it is thought that algesic substances, endoge- fact that the gingival crevicular fluid around nous from pulp tissue damage or neurogenic teeth with acute pain of pulpal origin demon- inflammation and exogenous from bacterial strated increased levels of substance P and toxins, invade the periapical area in spite of neurokinin-A compared with healthy teeth, and the fact that the pulp has not completely de- these levels decreased significantly 1 week generated and can still react to stimuli such as after pulpectomy.75 Painful stimulation of the

150 Periodontal Pain

CASE A 20-year-old man with periapical periodontitis and acute dentoalveolar abscess. 6-2 Primary complaint: The patient has experienced strong continuous pain on the left side of the face for the past 3 days. The maxillary left second premolar is very sensitive to chewing. Swelling of the left side of the face has developed rapidly since yesterday accompanied by marked relief in pain intensity. Findings: The left side of the face is swollen (Fig 6-6a). The maxillary left second premolar is sen- sitive to percussion, does not respond to cold application, and is slightly mobile; no periodontal pockets can be detected. A periapical radiograph (Fig 6-6b) demonstrates a deep disto-occlusal cavity in the maxillary left second premolar with a temporary fi lling and a periapical radiolucency with concentric condensing osteitis. Past history: Three months ago, the patient complained of discomfort on chewing and a sen- sitivity to cold foods on the left side of his mouth. A temporary fi lling of the maxillary left second premolar was performed. At fi rst the tooth was very sensitive to cold foods, but then it became comfortable until 3 days ago, when the strong pain started. Comments: This is a classic case that starts with discomfort and pain due to caries associated with dentinal and food impaction. Pulp irritation develops subsequent to cavity prepara- tion and placement of the temporary fi lling, which eventually leads to pulp necrosis. A periapical lesion develops asymptomatically, and some 3 months later an acute exacerbation with strong pain occurs because of acute periapical periodontitis.

a b

Fig 6-6 Case 6-2. (a) Note the acute swelling of the left side of the face (cellulitis) due to acute dentoalveolar abscess of the maxillary left second premolar. Note also the swelling of the left cheek, the left lower eyelid closing the eye, and the disappearance of the left nasolabial fold due to swelling. The left nostril and left upper are swollen, too. (b) Periapical radiograph demonstrating a deep disto-occlusal cavity in the maxillary left second premolar with a temporary filling and a periapical radiolucency with concentric condensing osteitis.

maxillary central incisor also caused signifi cant Treatment elevations of substance P levels in the gingi- val crevicular fl uid of the stimulated tooth; this Although pain originates from the periodontal supports the possibility of a local neurogenic periapical tissues, the source of insult and in- spread of infl ammatory reactions from intrapul- fection usually lies within the pulp chamber and pal to surrounding periodontal tissues.76 the root canal. To eliminate this source, the pulp

151 6 Acute Orofacial Pain

a b

Fig 6-7 (a) Lateral associated with pain, swelling, and a 10-mm periodontal pocket. (b) Intrabony periodontal pocket.

chamber is opened and the root canal cleansed Physical and radiographic signs and dressed in accordance with current en­ dodontic practice. Localized periapical pain or Swelling and redness of the gingiva may be no- swelling generally recovers quickly with local ticed and are located more frequently in coronal treatment, and there is no demonstrable ben- than in acute periapical . The swelling is efit from penicillin supplementation77 or amox- tender to palpation, and the affected tooth is icillin plus clavulanic acid.78 However, if cellu- sensitive to percussion and may be mobile and litis, fever, and malaise are present, systemic slightly extruded. In more severe cases, celluli- administration of antibiotics is recommended tis, fever, and malaise may occur. A deep peri- in addition to abscess drainage and tooth de- odontal pocket is usually located around the bridement. Amoxicillin, metronidazole, and clin- tooth (Fig 6-7a); once probed, pus exudation damycin are the antibiotics most widely used may occur, bringing occasional pain relief. Fre- and are recommended for patients suffering quently, probing is quite painful and has been from acute dentoalveolar who have correlated to the degree of the inflammatory become systemically unwell as a result of their process.80 The tooth pulp is usually vital but infection or for patients who are significantly may occasionally be slightly hyperalgesic. In a immunocompromised.79 Grinding the tooth to sample of 29 patients,81 more than 75% of the prevent contact with the opposing teeth helps abscesses demonstrated edema, redness, and to relieve pain. swelling, and 90% of the patients reported pain. Bleeding occurred in all abscesses, and suppu- ration on sampling was detected in 66%. Mean Lateral periodontal abscess associated pocket depth was 7.28 mm, and 79% of teeth presented some degree of mobili- Symptoms ty. Cervical lymphadenopathy was seen in 10% Pain characteristics of a lateral periodontal ab- of patients, and elevated leukocyte counts were scess are similar to those of acute periapical observed in 32%. Abscess formation usually re- periodontitis (see Tables 6-1 and 6-2). The pain sults from a blockage of drainage from a deep is continuous, moderate to severe in intensity, periodontal pocket, and it is frequently asso- well localized, and exacerbated by biting on the ciated with a deep intrabony pocket and teeth affected tooth. with root furcation involvement. A deep intra-

152 Periodontal Pain

a b

Fig 6-8 (a) A perio-endo lesion in which the mesial pocket is demonstrated with a gutta-percha point that approaches the apex of the mesiobuccal root of the maxillary second molar. In this case, the tooth pulp was vital. The patient com- plained of strong pain with hot and cold foods and sometimes strong spontaneous pain that lasted 10 to 15 minutes. (b) A perio-endo lesion in which a silver point was inserted into the pocket and a well-demarcated periapical radiolucent lesion was also demonstrated. The tooth pulp was nonvital and could be approached by drilling through the temporary acrylic crown without using any local anesthesia.

bony pocket may be present on the radiograph and malaise are present, systemic antibiotic (Fig 6-7b). Acute periodontal abscesses may administration may be recommended. As with also be associated with dental implants.82,83 periapical periodontitis, the need for antibiotic supplementation in addition to local treatment is unclear.85 Pain usually subsides within 24 Pathophysiology hours of treatment. A high prevalence of putative periodontal pathogens were found, including Fusobacte- rium nucleatum, Peptostreptococcus micros, Interrelationships between pulpal , Prevotella interme- and periodontal diseases: dia, and Bacteroides forsythus.81 Significant differences in the levels of PGE The “perio-endo” lesion 2 and LTB4 were found in patients with and with- The interrelationship between periodontal and out periodontitis. The levels of PGE and LTB4 endodontic disease may cause diagnostic con- 2 were correlated with clinical parameters and de- fusion and difficulty. A symptomatic tooth may creased markedly after phase one of periodon- have pain of periodontal and/or pulpal origin. tal treatment.84 Levels of PGE correlated with The nature of that pain is often the first clue 2 the severity of the periodontal status, and levels in determining the etiology, assisted by radio- of LTB4 correlated with gingival inflammation. graphic and clinical evaluation. In some cases, pulpal may create periodontal par- ticipation. In others, periodontal pathology may Treatment create pulpal involvement.86 Deep periodontal Gentle irrigation and curettage of the pock- pockets sometimes involve accessory canals et should be performed. A vertical incision for (in the furcation or laterally) and in extensive le- drainage is recommended when the abscess is sions may reach the root apex of the tooth and fluctuant but cannot be adequately approached cause retrograde pulp inflammation (Fig 6-8a). through the pocket. Acute lateral periodontal The major initial symptom is sensitivity to tem- abscess causes rapid alveolar bone destruc- perature changes, a situation that may prog- tion (see Fig 6-7b), hence the need for early ress to irreversible pulpitis. A second possibility and prompt intervention. Selective grinding of is an apical abscess that exudates through a the tooth should be performed to avoid con- periodontal pocket (Fig 6-8b). In this case, pain tact with the opposing teeth, reduce pain, and can be minimal due to the release of pressure restore tooth stability. When cellulitis, fever, through the pocket, or sometimes it may exac-

153 6 Acute Orofacial Pain

erbate into an acute dentoalveolar abscess. Fi- interdental contacts and may cause periodon- nally, the co-occurrence of symptomatic active tal disease.87 Remarkably, this loss of contact together with independent is highly prevalent (43%) between fixed implant endodontic pathology is a possibility that is prostheses and adjacent teeth, especially when termed a “true” combined lesion. the implant is distal to the adjacent tooth.88

Physical and radiographic signs. A faulty Treatment contact between two adjacent teeth is noticed Treatment for all these situations is initially en­ so that food is usually trapped between these dodontic, followed by conventional periodontal teeth; the gingival papilla is tender to touch and treatment. The prognosis of endodontic lesions bleeds easily. Food impaction should be treat- causing periodontal symptomatology is bet- ed promptly because it may cause cervical car- ter than in periodontal-initiated or combined ies and interdental alveolar bone resorption.89 lesions. Treatment. The cause of the faulty contact between the teeth is often a caries lesion, and Vertical root fracture restoring the tooth will eliminate pain. In some A fracture of the tooth that involves most of the cases, though the contacts are tight, food im- root will induce pain on biting. Root fractures are paction may occur, so creating anatomical es- more common in endodontically treated teeth cape grooves adjacent to the marginal ridge that have been restored with a post and core. may eliminate food impaction.90 Pain on biting in such cases is therefore of peri- odontal origin. Initially, there may be no clinical or radiographic signs. An isolated periodontal pocket in the area of the fracture is often found. Symptoms. Pain, which may be severe, is usu- Disease progression usually leads to a typical ally located at the distal end of the arch of teeth radiographic picture of a lengthwise rarefying in the mandible. Pain is spontaneous and may osteitis. If left untreated, infection and abscess be exacerbated by closing the mouth. In more may develop. Currently, the only treatment op- severe cases, pain is aggravated by swallow- tion for vertical root fractures is extraction. ing, and may occur. Acute pericoronal infections are common in teeth that are incom- pletely erupted and are partially covered by a Gingival pain flap or operculum of gingival tissue. Gingival pain may occur as a result of mechan- ical irritation, such as food impaction, acute in- Physical and radiographic signs. The oper- flammation associated with a partially erupted culum is acutely inflamed (red, edematous), tooth (pericoronitis), or acute inflammation as and an indentation of the opposing tooth is fre- a result of an acute bacterial or viral infection. quently seen on the swollen gingival flap. Oc- casionally, there is fever, malaise, and restricted mouth opening (trismus). Food impaction Symptoms. The patient typically complains Pathophysiology. Ten patients with pericoro- of a localized pain that develops between nitis and 10 healthy control subjects were inves- two teeth after meals, especially when food is tigated for the presence of TNF-α.91 TNF recep- fibrous. The pain is associated with a feeling of tors 1 and 2 were found in macrophage-like and pressure and discomfort that is annoying and fibroblast-like cells, vascular endothelial cells in sometimes severe.1 The patient may report that postcapillary venules, and basal epithelial cells pain gradually diminishes until evoked again at in pericoronitis, but they were only weakly ex- the next meal, or the pain may be relieved im- pressed in control subjects. The researchers mediately by removing the food impacted be- concluded that the potent proinflammatory cy- tween the teeth with a toothpick or dental floss. tokine TNF-α plays a role in the pain and inflam- Food impaction usually results from a loss in mation associated with pericoronitis.91 A study

154 Periodontal Pain of 2,151 patients with pericoronitis found that the peak age of occurrence was from 21 to 25 years, and the most frequent predisposing fac- tors were upper respiratory infection (38%) and stress (22%).90

Treatment. Irrigate debris between the oper- culum and the affected tooth with saline or antibacterial agent (eg, chlorhexidine 0.5%), and eliminate trauma by grinding or extract- ing the opposing tooth. Removal of the third molar, the affected tooth, positively influenced Fig 6-9 Acute necrotizing ulcerative . Note the quality-of-life outcomes in patients with mi- destruction of the gingival papillae and pseudomem- nor symptoms of pericoronitis.92 The risk of brane at the marginal border. seeding the infection into deeper spaces by performing immediate extraction is low. Sys- temic antibiotic administration is recommend- ed when trismus occurs or when the patient is is absent with herpetic infection, in which the febrile. Microbiologic cultures from 26 patients herpetic lesions typically create a punched-out with pericoronitis demonstrated that 9 of 26 appearance at the gingival margin. samples contained beta-lactamase-producing Relatively little is known about the epidemi- strains.93 The infection in pericoronitis is mul- ology of ANUG in healthy adolescent popula- timicrobial, predominantly caused strictly by tions. Most studies have focused on special beta-lactamase-producing anaerobic microor- target groups, such as military recruits, patients ganisms; the suggested first-line treatment is with human immunodeficiency virus, or sub- amoxicillin with clavulanic acid.94,95 jects who are severely malnourished.97 In 9,203 students aged 12 to 21 years in Santiago, Chile, the estimated prevalence of ANUG was 6.7%.98 Acute necrotizing ulcerative gingivitis Of 19,944 patients examined at a periodontal Symptoms. Soreness and pain are character- clinic in Cape Town, South Africa, less than istically felt at the margin of the gingiva and are 0.5% were found to have ANUG, and the study fairly well localized to the affected areas. Pain demonstrated significant seasonal variation in is intensified by eating and , and the occurrence of the disease.99 On the other both activities are usually accompanied by gin- hand, ANUG was found to be very prevalent (up gival bleeding. A metallic taste is sometimes to 37%) among boarding-school children in a experienced, and there is usually a fetid odor poor, developing country.100 from the mouth. Pathophysiology. ANUG is considered to Physical and radiographic signs. Necro- be an acute opportunistic gingival infection sis and ulceration are present on the marginal caused by bacterial plaque. The condition ap- gingiva accompanied by different degrees of pears more frequently in undernourished chil- gingival papillary destruction. This is an ulcer- dren and young adults as well as in patients ative characterized by pain, with immunodeficiency.101 The pathogenesis bleeding, and papillary necrosis.96 An adherent involves factors related to the oral microbiology grayish slough represents the so-called pseu- and its invasive ability as well as factors asso- domembrane that is present in the acute stage ciated with the host, including capillary and im- (Fig 6-9). Acute herpetic infection of the gingi- munologic disorders. va (herpetic gingivostomatitis) can sometimes resemble acute necrotizing ulcerative gingivitis Treatment. Treatment includes swabbing and (ANUG), but the clinical appearance and asso- gently irrigating the ulcerative lesions, prefer- ciated are different. The ably with chlorhexidine or an oxidizing agent papillary necrosis typical for ANUG (see Fig 6-9) (hydrogen peroxide), and then scaling and

155 6 Acute Orofacial Pain

cleaning the teeth. Systemic antibiotics are rec- classified as minor, major, or herpetiform on the ommended, especially when fever and malaise basis of ulcer size and number. are present.102 Local and systemic conditions, as well as genetic, immunologic, or microbial fac- tors, may all play a role in the pathogenesis Mucosal Pain of recurrent aphthous ulceration. No principal cause has been discovered, but an autoim- Pain originating from the oral mucosa can be mune pathophysiology is suspected. Because localized or have a more generalized, diffuse the etiology is unknown, diagnosis is entirely nature. Detailed descriptions of the various le- based on history and clinical criteria; there sions of the oral mucosa are beyond the scope are no laboratory procedures to confirm the of this chapter, and only the most common diagnosis.105 lesions—recurrent aphthous and acute herpetic gingivostomatitis—are briefly Treatment. Treatment for localized mucosal discussed here. pain is mostly symptomatic and includes the ap- plication of a topical protective emollient for the mild form and the use of topical cortico­steroids Localized mucosal pain and tetracycline to decrease healing time for the Localized pain is usually associated with a de- more severe form.106,107 Cyanoacrylate has been tectable erosive or ulcerative lesion that results used as an effective tissue adhesive for ster­ from physical, chemical, or thermal trauma; viral oids and tetracycline.107 The use of diclofenac, infection; or lesions of unknown origin. Pain is a topical nonsteroidal anti-inflammatory drug, usually mild to moderate but may become quite was also found to be effective.108 Patients who severe and last for some minutes when irritat- underwent a single, low-intensity, nonthermal ed, whether mechanically or by sour, spicy, or session of CO laser irradiation had significant- 2 hot foods.103 Pain is burning in quality and char- ly reduced pain from minor acterized by a higher degree of discomfort than compared with the placebo group and had no pain intensity. Additionally, the pain is more vis- visible side effects.109 ceral than cutaneous. In about 50% of patients, the pain wakes them from sleep, a feature that is correlated with the female sex and pain in- Acute herpetic gingivostomatitis tensity. Pain intensity or unpleasantness is not Oral infections caused by type 1 related to the size or number of the lesions.103 are widespread, even among otherwise healthy people.110 Although most of these herpetic in- fections are mildly symptomatic, young children Aphthous lesions are at risk for developing extensive oropharyn- Recurrent aphthous stomatitis is characterized geal vesicular eruptions when first infected with by a prodromal burning sensation 2 to 48 hours the virus. This initial outbreak is known as pri- before an ulcer appears. Although small in di- mary herpetic gingivostomatitis. The mean age ameter (0.3 to 1.0 cm), this type of lesion may of patients with acute herpetic stomatitis has be quite painful and induces a painful regional shown a general trend to increase, and, current- lymphadenopathy. In up to 80% of patients, the ly, most (> 50%) patients suffer their first attack pain is described as burning in quality followed during their third decade.111,112 Diagnosis can be by stabbing (33%) and throbbing (11%).103 In performed clinically and confirmed by labora- the mild form, healing occurs within 10 days, tory tests. Symptoms may persist for 2 weeks, and pain is usually mild to moderate in severity. causing significant mouth discomfort, fever, Recurrent aphthous ulcers represent a very lymphadenopathy, and difficulty eating and common but poorly understood mucosal disor- drinking. Pain is described by 71% of subjects der. They occur in men and women of all ages, as burning, followed by stabbing or throbbing races, and geographic regions. An estimated (28% each). More than half (57%) of patients are one in five persons has been afflicted with aph- awakened from sleep by the pain. No correlation thous ulcers at least once.104 The condition is has been found between pain and the size or

156 Pain from Salivary Glands number of lesions.103 The incidence of oral her- plain of a burning sensation in the mouth and pes simplex infection is particularly high in im- the tongue, though there are no observable munocompromised patients, and it occurs in up changes in the oral mucosa and no detectable to 50% of hospitalized patients with acute leu- underlying systemic changes. This group of pa- kemia.113 Cytology (Tzanck testing) may serve tients is usually diagnosed with burning mouth as a useful adjunct in diagnosis, but rapid and syndrome, which is discussed in chapter 11. highly specific detection of human herpes sim- plex type 1 in saliva is possible by in vitro ampli- fication using polymerase chain reaction.114 Pain from Salivary Glands Treatment. Antiviral agents such as acyclovir Pain from salivary glands is localized to the af- and famciclovir should be considered part of fected gland, is of moderate to severe intensity, early management of primary herpetic gingivo- and is usually associated with blockage of the stomatitis.115,116 A soft, bland diet preceded by duct. The salivary gland is swol- a local anesthetic mouthrinse is recommended. len and very tender to palpation, and salivary may be maintained by rinsing with flow is reduced and sometimes completely a mild bicarbonate or saline solution or a non- abolished. Pain is intensified by increased sali- alcoholic solution of 0.2% chlorhexidine. Pro- va production on starting meals or by applying viding supportive care and educating parents an acidic stimulant (citric acid is the standard about transmission of the virus are important.112 stimulant) to the tongue. Pus may secrete from the salivary duct when the gland is infected, and the condition may be associated with fever Diffuse mucosal pain and malaise. When generalized diffuse pain is felt in the oral Calcified may block the salivary mucosa, it usually has a burning nature and duct and is often identifiable on a radiograph. may be accompanied by a dysgeusia, predom- Ultrasound or sialography can aid in diagno- inantly of a bitter metallic quality. This pain may sis.120,121 The incidence of salivary calculi is 60 result from a direct insult to the tissues due to cases/million/year, and most stones are sit- bacterial, viral, or fungal infection, which can be uated in the middle or proximal portion of the identified by the characteristic appearance of duct.122 the oral mucosa. Diagnosis is aided by micro- In children, the most common blockage oc- biologic and other laboratory examinations. In curs with and acute recurrent . cases of chronic fungal infection (candidiasis), Recurrent parotitis of childhood is a rare condi- possible underlying etiologic factors such as tion of unknown etiology, though it is probably prolonged broad-spectrum antibiotic therapy, immunologically mediated. A clinical diagnosis immunodeficiencies, and other debilitating fac- can often be confirmed by ultrasound.123 Re- tors should be investigated.117 Radiation ther- cently, a new method that includes a salivary apy to the head and neck region may result in intraductal endoscopic technique was intro- acute mucositis with severe generalized muco- duced for diagnosis and treatment of these sal pain.118 Burning sensation of the oral muco- conditions.124 sa, particularly the tongue, may result from sys- temic diseases, such as chronic iron-deficiency anemia, and may be associated with atrophic Treatment .117 Atrophic glossitis and burning When a blockage is diagnosed, surgical or mouth sensations have also been associated endoscopic approaches are indicated.125 A with Helicobacter pylori colonization of tongue combined external lithotripsy/sialoendoscopy mucosa and nutritional deficiency.119 Mucosal method for advanced salivary gland sialolithi- pain associated with underlying systemic fac- asis was recently developed.126 In the acute tors is detailed in chapter 14. stage of bacterial infection, antibiotic therapy is A large proportion of patients, mostly wom- recommended. No antibiotics are recommend- en between the ages of 50 and 70 years, com- ed for mumps or recurrent parotitis, however.123

157 6 Acute Orofacial Pain

3. Falace DA, Reid K, Rayens MK. The influence of deep Conclusion (odontogenic) pain intensity, quality, and duration on the incidence and characteristics of referred orofacial pain. J Orofac Pain 1996;10:232–239. Diagnosis and treatment of acute orofacial 4. Sessle BJ. Peripheral and central mechanisms of pain is usually encountered in a first-aid situa- orofacial pain and their clinical correlates. Minerva tion. The task is complex, similar to that of any Anestesiol 2005;71:117–136. emergency treatment; the patient is anxious 5. Sessle BJ, Hu JW, Amano N, Zhong G. Convergence and seeks immediate relief, so the diagnosis of cutaneous, tooth pulp, visceral, neck and muscle afferents onto nociceptive and non-nociceptive neu- has to be reached under time pressure. Getting rones in trigeminal subnucleus caudalis (medullary a precise and full story is of utmost importance, dorsal horn) and its implications for referred pain. Pain as the pain history is usually the main lead for 1986;27:219–235. a diagnosis. As with most cases of acute pain, 6. Locker D, Grushka M. Prevalence of oral and fa- cial pain and discomfort: Preliminary results of the pain results from an acute inflammatory a mail survey. Community Dent Oral Epidemiol process that must be treated. Keep in mind, 1987;15:169–172. however, the possibility of misdiagnosis due to 7. Lipton JA, Ship JA, Larach-Robinson D. Estimat- nonodontogenic and, frequently, noninflamma- ed prevalence and distribution of reported orofa- tory causes. About half of all cases of persistent cial pain in the United States. J Am Dent Assoc 1993;124(10):115–121. tooth pain after root canal therapy were thought 8. Pau AK, Croucher R, Marcenes W. Prevalence esti- to have a nonodontogenic origin. Other cranio- mates and associated factors for dental pain: A re- facial pain disorders, mimicking odontalgia, view. Oral Health Prev Dent 2003;1:209–220. may refer from the maxillary sinus or the ear. 9. Goes PS, Watt R, Hardy RG, Sheiham A. The prev- alence and severity of dental pain in 14-15 year old Pain may also be referred from more remote Brazilian schoolchildren. Community Dent Health structures, such as the carotid artery or heart, 2007;24:217–224. and may resemble the symptoms of toothache. 10. von Troil B, Needleman I, Sanz M. A systematic re- Pretrigeminal neuralgia may be very misleading view of the prevalence of root sensitivity following and hard to diagnose. periodontal therapy. J Clin Periodontol 2002;29(3, suppl):173–177. Diagnosis and treatment of orofacial pain is 11. Goose DH. Cracked tooth syndrome. Br Dent a complex process compounded by the den- J 1981;150:224–225. sity of anatomical structures. Because of this 12. Seo DG, Yi YA, Shin SJ, Park JW. Analysis of fac- dense anatomy, management of orofacial pain tors associated with cracked teeth. J Endod 2012;38:288–292. calls for the services of clinicians from various 13. Brynjulfsen A, Fristad I, Grevstad T, Hals-Kvinnsland specialties, such as , otolaryngology, I. Incompletely fractured teeth associated with diffuse ophthalmology, and to name a few. longstanding orofacial pain: Diagnosis and treatment It has been the authors’ experience that pa- outcome. Int Endod J 2002;35:461–466. tients without a diagnosis are referred from one 14. Krell KV, Rivera EM. A six year evaluation of cracked teeth diagnosed with reversible pulpitis: Treatment specialist to another, trying to find help “some- and prognosis. J Endod 2007;33:1405–1407. where else.” Teamwork seems to be the ideal 15. Poulsen S, Errboe M, Hovgaard O, Worthington HW. solution, but ideals rarely exist. The right solu- Potassium nitrate toothpaste for dentine hypersensi- tion is to have clinicians who specialize in the tivity. Cochrane Database Syst Rev 2001;(2). 16. Brookfield JR, Addy M, Alexander DC, et al. Consensus- diagnosis and treatment of orofacial pain and based recommendations for the diagnosis and man- headache and can cross all specialties. agement of . J Can Dent Assoc 2003;69:221–226. 17. Hargreaves KM, Seltzer S. Pharmacologic control of dental pain. In: Hargreaves KM, Goodis HE (eds). References Seltzer and Bender’s Dental Pulp. Chicago: Quintes- sence, 2002:205–225. 1. Sharav Y, Leviner E, Tzukert A, McGrath PA. The spa- 18. Kimura Y, Wilder-Smith P, Yonaga K, Matsumoto K. tial distribution, intensity and unpleasantness of acute Treatment of dentine hypersensitivity by lasers: A re- dental pain. Pain 1984;20:363–370. view. J Clin Periodontol 2000;27:715–721. 2. Hashemipour MA, Borna R. Incidence and charac- 19. Lin PY, Cheng YW, Chu CY, Chien KL, Lin CP, Tu teristics of acute referred orofacial pain caused by a YK. In-office treatment for dentin hypersensitivity: A posterior single tooth pulpitis in an Iranian population. systematic review and network meta-analysis. J Clin Pain Pract 2014;14:151–157. Periodontol 2013;40:53–64. 20. Bender IB. Pulpal pain diagnosis–A review. J Endod 2000;26:175–179.

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Odontalgia in vas- Dent J 2009;206:357–362. cular orofacial pain. J Orofac Pain 1999;13:196–200. 80. Heft MW, Perelmuter SH, Cooper BY, Magnusson I, 64. Tzukert A, Hasin Y, Sharav Y. Orofacial pain of Clark WB. Relationship between gingival inflammation cardiac origin. Oral Surg Oral Med Oral Pathol and painfulness of periodontal probing. J Clin Peri- 1981;51:484–486. odontol 1991;18:213–215. 65. Roz TM, Schiffman LE, Schlossberg S. Spontaneous 81. Herrera D, Roldán S, González I, Sanz M. The peri- dissection of the internal carotid artery manifesting as odontal abscess (I). Clinical and microbiological find- pain in an endodontically treated molar. J Am Dent ings. J Clin Periodontol 2000;27:387–394. Assoc 2005;136:1556–1559. 82. Takeshita F, Iyama S, Ayukawa Y, Suetsugu T, Oishi M. 66. Aiken A. Facial pain—toothache or tumour? Int J Oral Abscess formation around a -coated Surg 1981;10(suppl 1):187–190. implant placed into the extraction socket with autoge- 67. Bullitt E, Tew JM, Boyd J. Intracranial tumors in pa- nous bone graft. A histological study using light mi- tients with facial pain. J Neurosurg 1986;64:865–871. croscopy, image processing, and confocal laser scan- 68. Griffin CJ, Harris R. Innervation of human periodon- ning microscopy. J Periodontol 1997;68:299–305. tium. I. Classification of periodontal receptors. Aust 83. Serino G, Ström C. Peri-implantitis in partially eden- Dent J 1974;19:51–56. tulous patients: Association with inadequate plaque 69. van Steenberghe D. The structure and function of control. Clin Oral Implants Res 2009;20:169–174. periodontal innervation. A review of the literature. 84. Tsai CC, Hong YC, Chen CC, Wu YM. Measurement J Periodontal Res 1979;14:185–203. of prostaglandin E2 and leukotriene B4 in the gingival 70. Estrela C, Guedes OA, Silva JA, Leles CR, Estrela crevicular fluid. J Dent 1998;26:97–103. CR, Pécora JD. Diagnostic and clinical factors as- 85. Herrera D, Roldán S, Sanz M. The periodontal ab- sociated with pulpal and periapical pain. Braz Dent scess: A review. J Clin Periodontol 2000;27:377–386. J 2011;22:306–311. 86. Shenoy N, Shenoy A. Endo-perio lesions: Diagno- 71. Block RM, Bushell A, Rodrigues H, Langeland K. A sis and clinical considerations. Indian J Dent Res histopathologic, histobacteriologic, and radiographic 2010;21:579–585. study of periapical endodontic surgical specimens. 87. Hancock EB, Mayo CV, Schwab RR, Wirthlin MR. In- Oral Surg Oral Med Oral Pathol 1976;42:656–678. fluence of interdental contacts on periodontal status. 72. Langeland K, Block RM, Grossman LI. A histo- J Periodontol 1980;51:445–449. pathologic and histobacteriologic study of 35 peri- 88. Koori H, Morimoto K, Tsukiyama Y, Koyano K. Sta- apical endodontic surgical specimens. J Endod tistical analysis of the diachronic loss of interproximal 1977;3:8–23. contact between fixed implant prostheses and adja- 73. Vergnolle N, Hollenberg MD, Sharkey KA, Wallace cent teeth. Int J Prosthodont 2010;23:535–540. JL. Characterization of the inflammatory response 89. Jernberg GR, Bakdash MB, Keenan KM. Relationship to proteinase-activated receptor-2 (PAR2)-activating between proximal tooth open contacts and periodon- peptides in the rat paw. Br J Pharmacol tal disease. J Periodontol 1983;54:529–533. 1999;127:1083–1090. 90. Newell DH, John V, Kim SJ. A technique of occlusal 74. Kabashima H, Nagata K, Maeda K, Iijima T. In- adjustment for food impaction in the presence of tight volvement of substance P, mast cells, TNF-alpha proximal contacts. Oper Dent 2002;27:95–100. and ICAM-1 in the infiltration of inflammatory cells 91. Beklen A, Laine M, Ventä I, Hyrkäs T, Konttinen YT. in human periapical granulomas. J Oral Pathol Med Role of TNF-alpha and its receptors in pericoronitis. 2002;31:175–180. J Dent Res 2005;84:1178–1182.­

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Oral mucosal pain characteristics: A prospective phy: A possible protocol. Clin Otolaryngol Allied Sci study. Poster, European Association of Oral Medicine, 1996;21:21–23. September 2014, Antalya, Turkey. 122. Iro H, Zenk J, Escudier MP, et al. Outcome of mini- 104. Kovac-Kovacic M, Skaleric U. The prevalence of oral mally invasive management of salivary calculi in 4,691 mucosal lesions in a population in Ljubljana, Slovenia. patients. Laryngoscope 2009;119:263–268. J Oral Pathol Med 2000;29:331–335. 123. Leerdam CM, Martin HC, Isaacs D. Recurrent 105. Natah SS, Konttinen YT, Enattah NS, Ashammakhi N, parotitis of childhood. J Paediatr Child Health Sharkey KA, Häyrinen-Immonen R. Recurrent aph- 2005;41:631–634. thous ulcers today: A review of the growing knowl- 124. Nahlieli O, Shacham R, Shlesinger M, Eliav E. Juvenile edge. Int J Oral Maxillofac Surg 2004;33:221–234. recurrent parotitis: A new method of diagnosis and 106. Lo Muzio L, della Valle A, Mignogna MD, et al. The treatment. Pediatrics 2004;114:9–12. treatment of oral aphthous ulceration or erosive lichen 125. Nahlieli O, Shacham R, Bar T, Eliav E. Endoscopic planus with topical clobetasol propionate in three mechanical retrieval of sialoliths. Oral Surg Oral Med preparations: A clinical and pilot study on 54 patients. Oral Pathol Oral Radiol Endod 2003;95:396–402. J Oral Pathol Med 2001;30:611–617. 126. Nahlieli O, Shacham R, Zaguri A. Combined exter- 107. Ylikontiola L, Sorsa T, Häyrinen-Immonen R, Salo T. nal lithotripsy and endoscopic techniques for ad- Doxymycine-cyanoacrylate treatment of recurrent vanced cases. J Oral Maxillofac Surg aphthous ulcers. Oral Surg Oral Med Oral Pathol Oral 2010;68:347–353. Radiol Endod 1997;83:329–333. 108. Saxen MA, Ambrosius WT, Rehemtula al-KF, Russell AL, Eckert GJ. Sustained relief of oral aphthous ulcer pain from topical diclofenac in hyaluronan: a random- ized, double-blind clinical trial. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;84:356–361.

161

Otolaryngologic Aspects of Orofacial Pain 7 Menachem Gross, MD Ron Eliashar, MD

Orofacial pain is a relatively common complaint in general medical and dental practice. The diagno- sis and management of orofacial pain originating from the ear, sinonasal area, oropharyngeal region, facial area, and neck has been a subject of great controversy over the years, and the controversy continues to date. This situation is unfortunate because there have been great advances in our un- derstanding of these conditions based on solid research over the past 25 years. Otolaryngologists are often involved when primary disorders of the ear, nose, and throat or the head and neck are the source of pain. This chapter deals with the differential diagnosis and management of common painful disorders affecting these areas. Different pitfalls may lead to misdiagnosis of orofacial pain. Therefore, it is important for clinicians to understand the following factors that can lead to misdiagnosis1:

• The complex regional anatomy of the head and neck often results in disparity between the site and the source of pain. • Symptoms of pain, limitation of mandibular movement, joint noise, tinnitus, and altered occlu- sion are not specifi c for the pathologic condition. Thus, these symptoms can be caused by local otologic and disorders or by infectious, neoplastic, neurologic, and sys- temic conditions. • Chronic tissue damage from trauma and/or multiple surgical procedures can lead to central sensi- tization of sensory nerve pathways, leading to neuropathic pain, allodynia (pain response to non- painful stimuli), and (excessive pain response to mildly painful stimuli). The presence of neuropathic pain can make accurate diagnosis extremely diffi cult because clinicians can be easily misled into believing that the source of the pain is localized when, in fact, there is a central nervous system–mediated component.

163 7 Otolaryngologic Aspects of Orofacial Pain

rect cause of earache). Because of the nature of (Otalgia) the ear’s sensory innervation, a wide variety of disorders can produce referred otalgia. Branch- Earache, or otalgia, is quite common among es of the trigeminal, facial, glossopharyngeal, children and adults. The pain can vary from mild and vagus cranial nerves all participate, as to excruciating, severe, dull, aching, or lanci- do the lesser occipital and the great auricular nating. Otalgia may be associated with such cervical nerve roots. The ear thus shares its sensations as a sense of fullness in the ear, sensory innervation with other head and neck burning, throbbing, tenderness, or itching. The structures, including the face, eyes, jaws, teeth, exact incidence of otalgia is not known. Adults , and larynx. tend to suffer from fewer ear problems and otal- The incidence of referred otalgia increases gia than children. Children are mostly affected with age. About half of otalgia cases are caused because acute (AOM), which is the by referred pain from non–ear-related prob- most common cause of otalgia, occurs mainly lems, and half these cases of referred otalgia in young people.2,3 are caused by dental disorders.1,6,7 Diseased According to the International Classification molars are the most common dental cause of of Headache Disorders, third edition (ICHD-3), secondary otalgia, which results in severe unre- headache attributed to disorder of the ears is mitting pain that often worsens when cold flu- headache caused by an inflammatory, neoplas- ids enter the oral cavity (see chapter 6). tic, or other disorder of one or both ears and Muscular pain originating in the muscles, associated with other symptoms and/or clinical tendons, or fascia of the head or neck, such signs of the disorder.4 The ICHD-3 criteria are as myofascial pain and tension-type headache described in Table 7-1. Because of nociceptive (see chapter 8), can also produce ear pain.1 The field overlap and convergence in the nocicep- pain is constant, dull, and aching and is usual- tive pathways of the head and neck, it seems ly not throbbing.8 Movement of the jaw or the clear that a painful disorder or lesion of the ear head worsens the pain. Prolonged clenching of may lead to headache. It is highly unlikely that the teeth, abnormal jaw movements, and den- headache in such conditions can occur in the tal disease may cause a type of muscle spasm absence of ear pain, the typical manifestation known as protective muscle splinting (see of otologic pathology. chapter 8). Otalgia may be caused by several different Pharyngeal and laryngeal diseases cause medical conditions. Detailed history and phys- referred otalgia via the glossopharyngeal nerve. ical examination, with directed studies as indi- Associated symptoms may include dysphagia, cated, can clarify the source of the pain. Based throat pain, and breathing difficulty. After ton- on the resultant findings, the disease is clas- sillectomy, patients almost always complain sified as primary (Table 7-2) or secondary (re- of postoperative otalgia.3,8 The pathologies of ferred) otalgia (Table 7-3). cervical vertebrae have also been identified as Primary otalgia is caused by a disease in the causing referred otalgia.9 ear itself (a direct cause of earache), and the Persistent earache with a normal ear exam- most serious problems are usually caused by ination increases the suspicion of carcinoma, infection (see Table 7-2). The areas most com- especially when associated with hemoptysis, monly involved in causing pain, or becoming in- weight loss, tooth pain, or difficulty in swallow- fected, are the external ear and the middle ear. ing. Otalgia is one of the earliest symptoms of Pain in the external ear radiates most often to carcinoma of the pyriform sinus, although neo- the vertex and to the temple, but it sometimes plasia producing otalgia may also be located spreads toward other areas of the head. Often in the larynx, esophagus, nasopharynx, lungs, patients cannot differentiate between pain orig- tonsils, or tongue.5,8,10,11 In patients suffering inating in the inner ear and pain originating in from carcinoma of the base of the tongue, the the external or middle ear.5 incidence of otalgia was found to be 33%.12 Secondary or referred otalgia (see Table 7-3) Amundson13 stressed that unilateral ear pain in is pain stemming from another region or loca- an adult who is a heavy smoker or a heavy drink- tion in the body and radiating to the ear (an indi- er is most likely a sign of cancer until ruled out.

164 Ear Pain (Otalgia)

Table 7-1 Diagnostic criteria for headache attributed to disorder of the ears* Diagnostic criteria A. Any headache fulfilling criterion C B. Clinical, laboratory, and/or imaging evidence of an infectious, neoplastic, or other irritative disorder or lesion of one or both ears, known to be able to cause headache C. Evidence of causation demonstrated by at least two of the following: 1. Headache has developed in temporal relation to the onset of the ear disorder or appearance of the ear lesion 2. Either or both of the following: a. Headache has significantly worsened in parallel with worsening or progression of the ear disorder or lesion b. Headache has significantly improved or resolved in parallel with improvement in or resolution of the ear disorder or lesion 3. Headache is exacerbated by pressure applied to the affected ear(s) or periauricular structures 4. In the case of a unilateral ear disorder or lesion, headache is localized ipsilateral to it D. Not better accounted for by another ICHD-3 diagnosis *Reproduced with permission from the International Headache Society.

Table 7-2 Causes of primary otalgia Classification Condition Comments for entities not covered in this chapter Auricular disorders Auricular cellulitis Auricular trauma Injury to the ear may cause hyperemia, abrasions, lacerations, and auricular hematoma in cases of blunt trauma. The hematoma should be drained to relieve pain and to prevent abscess formation and such auricular deformities as “cauliflower ear.” Relapsing polychondritis Disorders of the Impacted cerumen Wax may obstruct the ear canal and may cause pain, itching, external ear and temporary . Wax is removed by irrigation or by rolling it by a blunt curette or loop. Foreign object in the Children often insert foreign bodies such as beads, erasers, external ear and beans into the ear. Foreign bodies should be removed by raking them out with a blunt hook. Furuncle of the external ear canal Necrotizing otitis externa Ramsay Hunt syndrome (herpes zoster oticus) Disorders of the Otitis media middle ear Myringitis bullosa Traumatic tympanic The tympanic membrane may be perforated by objects placed membrane rupture in the external canal; by sudden overpressure, such as an explosion, a slap, or diving; or by sudden negative pressure. This results in sudden severe pain followed by bleeding from the ear. Spontaneous closure of the perforation is usual. Persistent perforation is indication for myringoplasty. Eustachian tube dysfunction Barotrauma

165 7 Otolaryngologic Aspects of Orofacial Pain

Table 7-3 Causes of secondary otalgia Classification Condition Comments Dental problems Infant , pain of See chapter 6. tooth eruption, impacted third molars (wisdom teeth), dental infections in the maxillary molars, fractured tooth, dry socket after , gingivitis and other periodontal disease Infections Upper respiratory tract An acute, usually viral infection of the respiratory tract with infection inflammation in the nose, throat, larynx, and trachea that is associated with watery nasal secretions, , , and referred otalgia through the glossopharyngeal nerve. See the Facial Pain section in this chapter. Infection of the throat: These conditions are covered in the Throat Pain section in tonsillitis, , and this chapter. peritonsillary abscess Laryngitis An acute viral inflammation of the larynx that is associated with unnatural change of voice, throat pain, and referred otalgia through the vagus nerve. Salivary gland infection See chapter 6. Diseases of the Masticatory muscle See chapter 8. joints and muscles disorders of the mandible Temporomandibular joint See chapter 8. dysfunction Head and neck See chapter 8. muscle spasms Removal of Post-tonsillectomy pain After tonsillectomy, patients have throat pain and may tonsils feel a referred pain in one or both ears through the glossopharyngeal nerve. The pain vanishes within a few weeks. Cervical spine See chapter 14. problems Inflammation of Temporal arteritis See chapter 14. the blood vessels in the temple Neuralgic disorders Trigeminal neuralgia See chapter 11. Glossopharyngeal neuralgia See chapter 12. Arnold’s nerve cough Reflex cough, caused by chronic irritation of auricular syndrome branch of the vagus (X) nerve. It is associated with an attack of suboccipital stabbing or burning pain and auricular pain. Cancer of the See chapter 14. head or neck

166 Ear Pain (Otalgia)

Common diseases causing by biopsy of the affected cartilaginous tissue in which infiltration of the cartilage and peri- primary otalgia chondrial tissues with neutrophils and lympho- Auricular cellulitis cytes as well as loss of cartilaginous matrix are demonstrated. Michet et al17 developed crite- Auricular cellulitis is a diffuse, spreading, acute ria for diagnosing relapsing polychondritis. An infection of the auricular skin or subcutaneous advantage of their criteria is that a biopsy does structures that is characterized by hyperemia not need to be obtained routinely. Although and edema with no cellular necrosis or suppu- not validated, these criteria are useful in clini- ration. The most common pathogen is Strep- cal practice. tococcus pyogenes (group A beta-hemolytic Mild cases may respond to symptomatic streptococci [GABHS]). Staphylococcus aureus treatment with aspirin, indomethacin, or other occasionally causes superficial auricular cellu- nonsteroidal anti-inflammatory drugs. Patients litis, which is less extensive than that of strep- with severe cases are initially treated with sys- tococcal origin. The infective process involves temic corticosteroids, and the dose is tapered the entire auricle, including the auricular lobule. in accordance with the clinical response. In The infection can occur spontaneously or after very severe cases, an immunosuppressive acute external otitis, chronic auricular dermati- agent, such as cyclophosphamide, is also tis, or trauma (such as auricular piercing). Pri- required. mary treatment includes parenteral antibiotic therapy, such as oxacillin or cefazolin, with top- ical antibiotic therapy. Furuncle of the external ear canal Furuncle of the external ear canal is an acute, tender, perifollicular inflammatory nodule result- Relapsing polychondritis ing from an S aureus infection. The initial nod- Relapsing polychondritis is an episodic inflam- ule evolves into a pustule with central necrosis, matory condition of the cartilaginous and non- which later discharges a sanguineous purulent cartilaginous tissues that causes progressive exudate. A furuncle causes localized pain with- destruction of the head and neck cartilages, in the external auditory meatus, which is in- predominantly those of the ear, nose, and la- tensified by local pressure. Treatment includes ryngotracheobronchial tree.14,15 Other affected surgical drainage of the furuncle; systemic anti- structures may include the eye, the cardio- biotic therapy with oxacillin or cefazolin may be vascular system, small and large peripheral added when required. joints, and the middle and inner ear.14–16 The etiology is unknown; however, the pathogen- esis of relapsing polychondritis involves an Acute otitis externa autoimmune response to as yet unidentified Acute otitis externa, an infective condition in- cartilage antigens, followed by cartilage matrix volving the external ear canal, is usually caused destruction by proteolytic enzymes.15 Signs by a gram-negative rod such as Pseudomonas and symptoms of relapsing polychondritis of aeruginosa or Escherichia coli; however, S au- the auricle include auricular cellulitis, typically reus or, rarely, a fungus, may also be a caus- with a sudden onset of unilateral or bilateral ative agent.18 This infection is often caused by auricular pain; tenderness; swelling; and red- moisture in the external ear canal, such as in ness with sparing of the lobules. The pain and warm, moist climates or after bathing. Injury redness usually disappear within 2 to 4 weeks caused by attempts to clean or to scratch an but may recur. Auricular chondritis is specific itching ear, as in patients suffering from con- to relapsing polychondritis once a local dis- tact dermatitis (from earrings or earphones), ease or infection has been ruled out. Auricular allergic dermatitis, or seborrheic dermatitis, is chondritis is found in 20% of patients at pre- another common cause.19 A variant of acute sentation and in 90% of patients at some point otitis externa is swimmer’s ear, a condition during the course of the disease.15 A definitive caused by a combination of external ear ca- diagnosis of relapsing polychondritis is made nal trauma and humidity during the swimming

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season. Signs and symptoms of acute otitis Ramsay Hunt syndrome externa include mild to severe otalgia associ- (herpes zoster oticus) ated with purulent discharge from the external ear canal. Auricular movement or pressure on Ramsay Hunt syndrome, also called herpes zos- the tragus intensifies the pain. The otalgia can ter oticus, is a herpesvirus 3 infection (varicella become extreme as the canal swells and be- zoster virus infection, which causes chickenpox comes blocked. and ) of the geniculate ganglion (facial Appropriate treatment includes topical ap- nerve ganglion). The virus spreads from the ge- plication of a combination of antibiotic and niculate ganglion to the facial nerve and to the corticosteroid eardrops instilled directly into the adjacent vestibulocochlear (XIII) nerve. The syn- ear canal. Irrigation of the ear canal with hydro- drome consists of unilateral facial paralysis, se- gen peroxide or 70% alcohol can temporarily vere ear pain on the same side of the infection, stop the pain and itching. tinnitus, vertigo, and herpetic blistering rash or vesicles on the pinna, external canal, and some- times the roof of the mouth, in the distribution Necrotizing otitis externa of the sensory branches of the facial nerve.21,22 Necrotizing external otitis usually starts as an Other cranial nerves may be involved, and some external otitis caused by P aeruginosa and pro- degree of meningeal inflammation may occur.23 gresses into an of the temporal Ramsay Hunt syndrome is usually more painful bone.18 This disease commonly occurs in el- than Bell’s palsy. The condition is rare in healthy derly patients with diabetes and occasionally people and occurs more commonly in people in patients who are immunocompromised.20 with a weakened immune system, such as the The disease spreads outside the external ear elderly and immunocompromised persons.24 Di- canal through the fissures of Santorini (two slits agnosis of Ramsay Hunt syndrome is based on located at the anterior cartilaginous external the clinical symptoms and signs. canal wall and the osseocartilaginous junction) Prompt treatment with corticosteroids and into the skull base. Necrotizing external otitis antiviral medications, such as acyclovir and is characterized by persistent severe otalgia, famcyclovir, reduces the symptoms and im- purulent otorrhea, and granulation tissue in proves recovery.25,26 A recent report recom- the external ear canal.20 Preauricular and tem- mends antiviral medication in combination with poromandibular joint pain, intensified by open- corticosteroids to improve the outcome for ing the mouth or by chewing, may be present. patients with Ramsay Hunt syndrome.27 Over- Severe headache in the temporal or occipital all, chances of recovery are better if treatment areas may accompany the earache. The sever- is started within 3 days of the onset of symp- ity of the pain can give a clue to the diagnosis. toms. Certain degrees of hearing loss or facial In severe cases, facial nerve involvement may paralysis may become permanent.26 Recovery occur, indicating an invasive infection. Other may be complicated if the nerve grows back to cranial nerve palsies, for example, in nerves IX, the wrong areas (synkinesis). This may cause X, XI, and XII, may also occur. Imaging evalu- inappropriate responses, such as tearing when ation by computed tomography (CT) usually laughing or chewing (crocodile tears). Some pa- demonstrates soft tissue infiltration and bone tients may start blinking when talking or eating. destruction. Technetium-99 bone scan is usual- ly positive and is highly sensitive to necrotizing external otitis. Acute otitis media Treatment includes good control of diabe- AOM is an infection of the middle ear cavity that tes and prolonged therapy with an antipseu- occurs most frequently in infants and children, domonal antibiotic such as ciprofloxacin for particularly between the ages of 3 months and at least 6 weeks, in addition to local therapy 3 years, although it may occur at any age. AOM for the otitis externa. Surgical debridement usually follows or accompanies an upper re- through a mastoidectomy approach is occa- spiratory infection (URI) or a reduced immune sionally required to control the spread of the response with no special reason.28 AOM is the infection. second most common childhood disease after

168 Ear Pain (Otalgia)

URI. The first complaint is usually persistent, the ear). Myringotomy (small incision of the TM) severe otalgia, which is often caused by an should be considered in cases of a bulging TM accumulation of fluid and pressure behind the or a persistent earache. tympanic membrane (TM). Other symptoms in- clude hearing loss, fever, chills, irritability, and a feeling of fullness and pressure in the affected Myringitis bullosa ear. Spontaneous drainage of pus or a clear or Myringitis bullosa is an inflammatory infec- bloody fluid from the middle ear is common and tion of the TM caused by a viral or bacterial may indicate perforation of the TM.29 Rupture of infection. Mycoplasma pneumoniae and S the eardrum usually results in a sudden, marked pneumoniae are the most common bacteria decrease in pain and defervescence of fever. responsible for myringitis bullosa. The disease Otoscopic examination reveals abnormal is characterized by very painful vesicles on the findings of the TM, including an erythematous TM, which may be full of serous or hemorrhag- and bulging TM, middle ear effusion, nondis- ic fluid. A URI can precede the ear manifesta- tinct anatomical middle ear landmarks, dis- tions. Pain is severe, starts suddenly, persists placed or absent TM light reflex, and decreased for 24 to 72 hours, and is caused by the TM TM mobility on . The most blisters, which appear between the richly inner- common bacterial pathogen in AOM is strepto- vated outer epithelium and the middle fibrous coccus pneumoniae, followed by Haemophilus layers of the TM. Bullae involving the TM may influenzae and Moraxella catarrhalis.29 These also extend toward portions of the external au- three organisms are responsible for more than ditory canal immediately adjacent to the TM. 95% of all AOM cases with a bacterial etiology. Objective cochlear and vestibular involvement The most important factors in the pathogenesis manifested by sensorineural or mixed-type of a middle ear infection are eustachian tube hearing loss and vertigo have been reported in dysfunction and direct extension of infectious patients suffering from myringitis bullosa.31,32 processes from the nasopharynx into the mid- Treatment includes analgesic and antibiotic dle ear cleft.29 therapy, such as azithromycin, which is applied AOM is treated with painkillers and oral against the major known pathogens causing amoxicillin systemic antibiotics.28 Topical anal- myringitis bullosa. gesics, such as tetracaine applied by eardrops, and oral decongestants, such as xylometazo- line, may be helpful. Antibiotic therapy relieves Eustachian tube dysfunction the symptoms, hastens resolution of the infec- The middle ear is connected to the nasophar- tion, and reduces the chance for developing ynx by the eustachian tube, which enables nor- complications (eg, or meningitis). mal fluids to drain from the middle ear and has However, the Cochrane Review of antibiotics an important role in equalizing the pressure in for AOM in children, representing a more cos- the middle ear when the atmospheric pressure mopolitan perspective, notes that antibiotic of ambient air shifts. Acute obstruction of the treatment slightly decreases pain at 24 hours eustachian tube, mainly in cases of URI, may and for a few days and that delayed antibiot- cause otalgia. This is especially common in ic prescribing works as well as immediately small children, in whom the eustachian tube prescribed antibiotics.30 The Cochrane Review is naturally shorter and more horizontal. Eu- also notes that antibiotics make no difference in stachian tube dysfunction (ETD) in adults also recurrence or in preventing more severe com- occurs when there is an increase of postnasal plications, such as temporary deafness, rupture drainage, allergy, rhinosinusitis, nasopharyn- of the TM, or mastoiditis. However, complica- geal mass, and adenoidal hypertrophy.33 tions from the antibiotic treatment (vomiting, Brunworth et al34 showed that ETD was diarrhea, and rash) were common (37%). The more likely to be associated with a higher num- Cochrane Review concludes that antibiotics ber of nasopharyngeal acid reflux events and a should not be used for most cases of AOM, higher acid reflux finding score. He concluded and they are appropriate only if there is bilater- that nasopharyngeal acid reflux may have a role al AOM or AOM with otorrhea (discharge from in the pathogenesis of ETD. As the postnasal

169 7 Otolaryngologic Aspects of Orofacial Pain

secretions drain posteriorly, or as acid reflux- Ear barotrauma es into the nasopharynx around the opening of the eustachian tube, the eustachian tube gets Barotitis media, also known as aerotitis, rep- irritated and swollen and eventually becomes resents damage to the middle ear and TM due blocked on one or both sides. When this hap- to ambient pressure changes. When ambient pens, surrounding tissue absorbs the air in the pressure suddenly increases, air must move affected tube, creating a vacuum, which causes from the nasopharynx into the middle ear to the differences in pressure to pull the TM in- maintain equilibrium on both sides of the TM. ward, the result being a sensation of fullness In cases of ETD, the pressure in the middle ear and pain. Hearing can be slightly impaired, and is below the ambient pressure, and the relative the ears can feel blocked or stuffed. negative pressure in the middle ear results in In isolated ETD, otoscopic examination will retraction of the TM and transudation of blood show a normal or retracted TM or, in more se- from vessels. Very severe and sudden pressure vere cases, middle ear effusion. Neck exam- differences may rupture the TM, causing bleed- ination and fiber-optic nasopharyngoscopy ing in the middle ear with severe earache and are important parts of the physical examina- conductive hearing loss. A perilymphatic fistula tion in patients with ETD to exclude cervical through the oval or round windows can occur, lymphadenopathy or a nasopharyngeal mass, causing sensorineural hearing loss and verti- which may be associated with nasopharyngeal go. Barotrauma commonly occurs with altitude carcinoma. changes, such as in the descent of an airplane, One-third of patients with ETD show sponta- deep sea diving, scuba diving, or driving in the neous improvement at the 6-month follow-up.35 mountains.38,39 Intranasal medications have no proven benefit Otalgia is the most common complaint of for symptomatic relief of ETD, although studies scuba divers and is experienced at some point are limited in number.35 However, topical na- by almost every diver. Some divers call it the sal decongestants may be used, but only for a ear squeeze. A person with an acute URI or al- maximum of 7 days because of the risk of a re- lergic rhinitis should be advised to abstain from bound rhinitis medicamentosa associated with diving. Topical application of a nasal vasocon- long-term use. Intranasal steroids are safe for strictor, such as xylometazoline, before any use on a longer-term basis than decongestants, activity associated with descent and pressure although the lowest possible dose should be changes can prevent barotrauma. prescribed, and the patient should be warned of local side effects, such as nasal crusting and dryness. Intranasal antihistamines may be used Facial Pain when an allergic cause of rhinitis is thought to have precipitated the ETD. Evidence suggests Sinus-related are located in the a benefit of autoinflation devices (eg, Otovent, forehead, behind the eye, or in the occiput. Oc- Abigo; Ear Popper, Summit Medical), which ap- casionally, they may radiate to the ears or to ply positive pressure through the nose during the temporal region. Headache related to the swallowing and improve tympanogram and au- paranasal sinuses is often associated with fa- diometry results at follow-up.36 These devices cial pain. Facial pain complaints are commonly can be bought over the counter and are rec- encountered and treated by primary care physi- ommended for use two or three times a day for cians. However, persistent or severe facial pain at least 2 weeks initially. Eustachain tuboplasty, should be referred to otolaryngology, dental, which is a balloon catheter used to dilate the ophthalmology, or neurology clinics because eustachian tube, is relatively novel and was as- the condition often requires multidisciplinary sessed by the National Institute for Health and evaluation and management.40 Care Excellence in 2011.37 Early data indicate Facial pain is located in the area between or that this technique is thought to be safe, has below the eyebrows, or the supraorbital rim, ex- the advantage over tympanostomy of being rel- tending along the course of one or more trigem- atively noninvasive, and may have greater lon- inal dermatomes. Facial pain may be caused by gevity of results. local disease of any of the major facial structures

170 Facial Pain

Table 7-4 Differential diagnosis of facial pain from an otolaryngologist’s viewpoint Classification Entity Comments for entities not covered in this chapter Sinonasal pain Rhinosinusitis Mucosal contact point headache Intranasal tumor Nasal obstruction and local nasal pain may occur as the intranasal tumor enlarges, especially is it invades nerves. Granulomatous diseases Granulomatosis with polyangiitis (Wegener granulomatosis) of the nose and sarcoidosis may affect the nasal cavity, causing congestion, nasal secretions, and local pain due to destructive lesions of soft tissue cartilage and bone. Midfacial segment pain Persistent Formerly called atypical See also chapter 12. idiopathic facial pain facial pain Scuba diving– Sinus pain caused pain Tension-type headache or muscle pain Carbon dioxide toxicity Decompression sickness headache Trigeminal See chapter 11. Sphenopalatine Primary headaches See chapter 8. See chapter 10. See chapter 11. Chronic paroxysmal See chapter 11. hemicrania

(eg, rhinosinusitis) or by a condition affecting However, many patients suffering from this so- their innervation (eg, neuralgia) (Table 7-4). The called sinusitis have no evidence of a sinona- latter can occur anywhere between the poste- sal disease. Awareness is increasing among rior cranial fossa and the distal ends of the tri- primary care physicians and otolaryngologists geminal nerve. The most common acute causes that other, non–sinus-related causes may be re- of pain are dental. The most common nondental sponsible for most of the suffering experienced pains are temporomandibular disorders, espe- by patients with facial pain or headache. The cially musculoskeletal disorders involving the gold standard in establishing a sinonasal etiol- muscles of mastication.40 The prevalence of fa- ogy for facial pain or headache is a diagnosis cial pain of paranasal sinus origin has probably made by obtaining a thorough personal history been overestimated. Patients’ expectations are and conducting a careful physical examination. often tempered by a prior diagnosis of sinus- Imaging studies, response to medical and sur- itis, guided by their knowledge of the location of gical treatment, and an extended follow-up pe- the sinuses or by their primary care physician. riod may help establish the diagnosis.41

171 7 Otolaryngologic Aspects of Orofacial Pain

Proposed International Headache Society diagnostic criteria for Box 7-1 mucosal contact point headache

A. Any headache fulfilling criterion C B. Clinical, nasal endoscopic, and/or imaging evidence of a hypertrophic or inflammatory process within the nasal cavity C. Evidence of causation demonstrated by at least two of the following: 1. Headache has developed in temporal relation to the onset of the intranasal lesion 2. Headache has significantly improved or significantly worsened in parallel with improvement in (with or without treatment) or worsening of the nasal lesion 3. Headache has significantly improved following local anesthesia of the mucosa in the region of the lesion 4. Headache is ipsilateral to the site of the lesion D. Not better accounted for by another ICHD-3 diagnosis

Common diseases causing facial pain mucosal contact points cause facial pain or headache, and that their removal is therapeu- Sinonasal disorders causing pain: The tic, concluded that most people with contact neurobiology of primary sinonasal pain points experience no facial pain, the presence of a contact point is not a good predictor of The trigeminal nerve is the main facial sensory facial pain, and the removal of a contact point supply. The ophthalmic (V1) and maxillary (V2) rarely results in the total elimination of facial divisions of the trigeminal nerve provide sen- pain, making the theory that a contact point is sation to the mucosa of the sinonasal cavity. responsible unlikely50 (Box 7-1). These nerve branches terminate as extensive According to the ICHD-3, headache attribut- uncovered nerve terminal endings next to the ed to disorder of the nose or sinuses is head- basal cells of the nasal epithelium.42 ache caused by a disorder of the nose and/or Nasal pain is mediated by Aδ fibers, the paranasal sinuses and associated with other fast-responding, primarily mechanoreceptive symptoms and/or clinical signs of the disorder.4 pain fibers, and by C fibers, the slower, unmy- The term sinus headache is considered outmod- elinated fibers associated with a duller pain ed by the ICHD-3, because it has been applied from mechanothermal and chemosensory both to primary headaches and to headache stimulation.42 supposedly attributed to various conditions in- Theories of sinonasal pain from contact volving the nasal or sinus structures. points or pressure from sinus inflammation are based on substance P release from trigeminal sensory neurons located in the nasal muco- Rhinosinusitis sa.43–46 This may be accompanied by the re- Rhinosinusitis is a group of disorders character- lease of various other neuropeptides, such as ized by inflammation of the mucosa of the nose calcitonin gene-related peptide and vasoactive and paranasal sinuses. The term rhinosinusitis intestinal peptide, which appear to be involved is used instead of sinusitis because the latter in the inflammatory cascade.42 The local stimu- is almost always accompanied by concurrent lation of the trigeminal fibers leads to a painful nasal airway inflammation, and, in many cases, orthodromic and an antidromic response typ- sinusitis is preceded by rhinitis. Rhinosinusitis ified by vasodilation and hypersecretion.42,43 has been estimated to affect approximately Despite this cited mechanism for contact-point 24 million patients in the United States each sinonasal pain, it is poorly documented and year.51 Total direct health care costs related to highly controversial.47–49 A systematic review recurrent acute rhinosinusitis (ARS), which af- aiming to analyze the evidence that intranasal fects approximately 1 in 3,000 adults per year,

172 Facial Pain average around $1,100/patient each year, and expected, the ICHD-3 classification relates to oral antibiotic and nasal prescriptions cost an diseases that may induce facial pain or head- average of $210 and $450 per year, respective- ache, whereas the AAO-HNS and EPOS clas- ly. Thus, rhinosinusitis has a significant direct sifications are concerned primarily with the dis- health care cost.52 ease process of sinusitis itself. Rhinosinusitis may be classified by duration Rhinosinusitis may be diagnosed clinically as acute (less than 4 weeks), subacute (4 to 12 in most patients based on history and physi- weeks), or chronic (more than 12 weeks, with or cal examination. Physical examination includes without acute exacerbations). otoscopy, anterior rhinoscopy, percussion over ARS may be classified further by symptom the areas of the paranasal sinuses, and oropha- pattern into viral rhinosinusitis or acute bacteri- ryngeal and neck examination. Nasal endosco- al rhinosinusitis (ABRS). Recurrent ARS is when py and imaging are usually not required for an a patient has four or more acute episodes of initial diagnosis of any form of rhinosinusitis. ABRS per year without persistent symptoms However, these modalities may be very helpful between episodes.53 in obtaining a definitive diagnosis of rhinosinus- A common presenting symptom of ARS is itis. Patients with recurrent or complicated sinus facial pain or headache. The pain is usually disease may require imaging. CT is superior to accompanied by other symptoms, such as na- radiography because plain radiographs are im- sal congestion, anterior and posterior purulent precise at determining the extent of the disease nasal drainage, and hyposmia or anosmia. The and the patency of the sinus ostium.53,56,58,59 CT pain is a subjective complaint; however, tender- scanning of the sinonasal region has two major ness on percussion is a function of spinal cord roles in rhinosinusitis: pain processing (hyperalgesia). People with ARS had a significantly lower pain and sensory 1. To define the anatomy of the sinuses before detection threshold in their sinus regions com- surgery pared with a healthy control group.54,55 Sinus 2. To aid in the diagnosis and management of pain caused by inflammation induced by infec- chronic rhinosinusitis (CRS), complicated tion (bacterial or viral) or allergic rhinosinusitis ARS, or recurrent rhinosinusitis occurs when exudate blocks the sinus ostium and exerts pressure stimulating local trigemi- Acute rhinosinusitis. ARS is an acute in- nal nerve fibers. The local release of proinflam- flammatory condition involving the paranasal matory and proalgesic mediators is an early sinuses and the lining of the nasal passages. mechanism (this is probably as important as The most recent US classification defines ARS the pressure). when there is up to 4 weeks of purulent nasal The development of rhinosinusitis depends drainage (anterior, posterior, or both) accompa- on a variety of environmental and host factors, nied by nasal obstruction, facial pain/pressure/ and rhinosinusitis is considered to be a disease fullness, or both. with multifactorial causes. Host factors include ABRS is distinguished from ARS caused by genetic or congenital conditions (eg., cystic fi- viral URIs and noninfectious conditions. ABRS brosis, immotile cilia syndrome), allergic rhinitis, is diagnosed when (1) symptoms or signs of sinonasal anatomical abnormalities, and sys- ARS are present 10 days or more beyond the temic diseases. Environmental factors include onset of upper respiratory symptoms or (2) infectious agents, trauma, noxious chemicals, symptoms or signs of ARS worsen within 10 and iatrogenic causes. days after an initial improvement (double wors- Three major systems are used for classi- ening).53 The EPOS classification defines ARS fication of and for establishing diagnostic cri- in adults as sudden onset of two or more symp- teria relating to headaches and sinus disease: toms, one of which should be nasal blockage/ the working definitions recommended by the obstruction/congestion or nasal discharge (an- American Academy of Otolaryngology-Head terior/posterior nasal drip) with or without facial and Neck Surgery (AAO-HNS), the ICHD-3 cri- pain/pressure and with or without reduction teria, and the European Position Paper on Rhi- or loss of smell for less than 12 weeks, with nosinusitis and Nasal Polyps (EPOS).4,53,55–58 As symptom-free intervals if the problem is recur-

173 7 Otolaryngologic Aspects of Orofacial Pain

Box 7-2 Clinical criteria for the diagnosis of acute rhinosinusitis (ARS)

Major factors Minor factors • Purulent anterior nasal discharge • Headache • Purulent, discolored posterior nasal drainage • Ear pain/pressure/fullness • Nasal obstruction or blockage • Halitosis • Facial pain/pressure/congestion/fullness • Dental pain • Hyposmia or anosmia • Cough • Fever • Fever (all nonacute) •

rent, and with validation by telephone or by in- tubes, mechanical ventilation, failure of defense terview. ABRS is suggested by the presence of mechanisms, and pronged supine posture. Iso- at least three of the following symptoms/signs: lates from hospitalized patients usually contain discolored discharge (with unilateral predomi- gram-negative enterics such as P aerugino- nance) and purulent nasal secretions, severe sa, Klebsiella pneumoniae, Enterobacter sp, local pain (with unilateral predominance), fever Proteus mirabilis, Serratia marcescens, and (> 38oC), elevated erythrocyte sedimentation coagulase-negative S aureus.55 rate/C-reactive protein, or “double worsening” The diagnosis of ARS focuses on clini- (ie, deterioration after an initial milder phase of cal history and physical examination findings. illness).58 Imaging, hematologic and microbiologic in- The most common cause of ARS is a vestigations, and endoscopy are not routinely community-acquired viral infection leading to a required in the diagnosis of ARS or ABRS but self-limiting period of upper respiratory symp- may be needed in particular settings, such as toms.55 Viral ARS is characterized by cough, in research studies or in high-risk patients.53,58 sneezing, , sore throat, and nasal The clinical diagnostic criteria for ARS, as congestion. Antibiotics are not recommended defined previously by the Task Force on Rhi- for treating ARS because they are ineffective nosinusitis of the AAO-HNS, included major for viral illness and do not relieve symptoms and minor symptoms or signs and disease du- directly.53 Human is the most com- ration of less than 4 weeks (Box 7-2). According mon cause of viral ARS. Other viruses include to this classification, facial pain or pressure is , influenza A and B virus, parainflu- regarded as a major symptom, whereas head- enza virus, respiratory syncytial virus, and ad- ache is considered to be a minor symptom.55,56 enovirus. Occasionally, a secondary bacterial This classification was designed to be used infection of the paranasal sinuses occurs and by primary care physicians and specialists. A requires specific antimicrobial therapy.53,58 Aller- diagnosis of rhinosinusitis is possible if two or gic rhinitis, nasal polyposis, a foreign body in more major symptoms or one major symptom the nasal cavity, trauma, dental infection, and and two or more minor symptoms are present. other factors leading to inflammation of the However, nasal purulence is a strong indicator nose and paranasal sinuses can also predis- of an accurate diagnosis. Facial pain or pres- pose people to develop ARS. sure alone does not constitute a suggestive Commonly isolated bacteria in patients with history in the absence of another major nasal ABRS include S pneumoniae, nontype­able H symptom or sign. Fever in itself does not con- influenzae, S pyogenes, M catarrhalis, S au- stitute a strongly suggestive history in the ab- reus, and occasionally anaerobes.53,58 Noso- sence of another major nasal symptom or sign. comial rhinosinusitis often occurs in patients Rosenfeld et al53 define the clinical criteria who require extended periods of intensive care for ARS as up to 4 weeks of purulent nasal and involves such risk factors as nasogastric drainage (anterior, posterior, or both) accompa-

174 Facial Pain

Table 7-5 Diagnostic criteria for headache attributed to acute rhinosinusitis* Diagnostic criteria A. Any headache fulfilling criterion C B. Clinical, nasal endoscopic, and/or imaging evidence of acute rhinosinusitis C. Evidence of causation demonstrated by at least two of the following: 1. Headache has developed in temporal relation to the onset of the rhinosinusitis 2. Either or both of the following: a. Headache has significantly worsened in parallel with worsening of the rhinosinusitis b. Headache has significantly improved or resolved in parallel with improvement in or resolution of the rhinosinusitis 3. Headache is exacerbated by pressure applied over the paranasal sinuses 4. In the case of a unilateral rhinosinusitis, headache is localized ipsilateral to it D. Not better accounted for by another ICHD-3 diagnosis *Reproduced with permission from the International Headache Society.

nied by nasal obstruction, facial pain/pressure/ obstruction/congestion or nasal discharge (an- fullness, or both, in which (1) purulent nasal terior/posterior nasal drip) with or without facial discharge is cloudy or colored, in contrast to pain/pressure, with or without reduction or loss the clear secretions that typically accompany of smell, and the other of which should be ei- viral URI, and may be reported by the patient ther endoscopic signs of nasal polyps and/ or observed on physical examination; (2) na- or mucopurulent discharge, primarily from the sal obstruction may be reported by the patient middle meatus, and/or edema/mucosal ob- as nasal obstruction, congestion, blockage, struction primarily in the middle meatus, and/ or stuffiness, or may be diagnosed by physi- or CT changes, including mucosal changes cal examination; and (3) facial pain/pressure/ within the ostiomeatal complex and/or sinuses. fullness may involve the anterior face or peri- The EPOS further defines /ARS orbital region or may manifest with headache as duration of symptoms for less than 10 days; that is localized or diffuse. As discussed pre- acute postviral rhinosinusitis as increase of viously, they then divide ARS into viral ARS, in symptoms after 5 days or persistent symptoms which symptoms or signs of ARS are present after 10 days with less than 12 weeks duration; less than 10 days and the symptoms are not and ABRS in the presence of at least three of worsening, and ABRS, in which (1) symptoms the following symptoms/signs: (1) discolored or signs of ARS are present 10 days or more discharge (with unilateral predominance) and beyond the onset of upper respiratory symp- purulent secretion in the cavum nasi, (2) severe toms or (2) symptoms or signs of ARS wors- local pain (with unilateral predominance), (3) fe- en within 10 days after an initial improvement ver (> 38°C), (4) elevated erythrocyte sedimen- (double worsening). Note that Rosenfeld et al53 tation rate/C-reactive protein, and (5) “double recommend against radiographic imaging for worsening.”58 patients who clinically meet the diagnostic cri- The ICHD-3 diagnostic criteria for headache teria for ARS. attributed to ARS are presented in Table 7-5.4 The EPOS58 combines these two clinical In an immunocompetent person living in the classification schemes and includes the pos- general community, ARS is typically believed sibility of both endoscopy and imaging when to be induced by viruses. Only about 0.5% to the treating physician is an otolaryngologist. 2.0% of ARS episodes are complicated by a The EPOS defines the clinical criteria of ARS as bacterial infection.53 Therefore, antibiotics are inflammation of the nose and the paranasal si- not recommended when the treating physician nuses characterized by two or more symptoms, did not specifically diagnose ABRS. Initial treat- one of which should be either nasal blockage/ ment depends on the severity of the disease58:

175 7 Otolaryngologic Aspects of Orofacial Pain

disease causing facial pain (Fig 7-1). The pain is usually related to the affected maxillary an- trum but is often referred to the maxillary teeth (in which the roots are embedded in the max- illa and are intimately related to the floor of the maxillary sinus) or to the forehead. Purulent na- sal discharge in the middle nasal meatus and sensitivity to percussion over the cheek or teeth confirm the diagnosis.

Sinonasal toothache. Diseases in the maxil- lary sinus mucosa may refer pain to the maxil- lary teeth. The pain is usually felt in several teeth as dull, aching, or throbbing. Occasionally, the Fig 7-1 Radiographic image demonstrating left acute pain is associated with pressure below the maxillary rhinosinusitis with air-fluid level in the left max- eyes, which increases when bending the head, illary sinus (arrow). applying pressure over the sinuses, coughing, or sneezing. Tests performed on the teeth, such as applying ice, chewing, and percussion, may • Mild symptoms (viral, common cold): Start increase pain from a sinonasal origin. History of with symptomatic relief, such as analgesics URI, , or other sinus problem (eg, oral acetaminophen), saline irrigation, is suspicious for a sinus toothache. A thorough decongestants (eg, xylometazoline), herbal dental examination (clinical and radiographic) compounds excludes a primary dental cause. • Moderate symptoms: Add topical steroids • Severe symptoms (including ABRS): Add Acute ethmoiditis. Acute ethmoiditis causes topical steroids and consider antibiotics pain at the root of the nose or behind the eye. Seldom does ethmoiditis occur as an isolat- If the physician decides to treat ABRS with ed infection. More often it is part of an acute an antibiotic agent, a short-course treatment, pansinusitis involving the maxillary and frontal particularly for patients without severe disease sinuses as well, because all of these sinuses and complicating factors, might lead to few- drain into the osteomeatal complex in the mid- er adverse events, better patient compliance, dle nasal meatus. Purulent anterior and poste- a lower rate of resistance development, and rior nasal discharge and tenderness over the fewer costs.58 No significant differences have inner canthus of the eye are characteristic. The been found in clinical outcomes for ABRS pain may spread laterally into the orbit or ra- treated with different antibiotic agents. Clini- diate to the temporal region. Occasionally, an cians should therefore prescribe amoxicillin as orbital complication (eg, periorbital cellulitis or first-line therapy for most adults. Amoxicillin abscess) may occur when the infection spreads increases rates of clinical cure or improvement into the orbit through the thin lamina papyracea compared with placebo. The justification for or the venous system. amoxicillin as first-line therapy for most pa- tients with ABRS relates to its safety, efficacy, Acute frontal rhinosinusitis. Acute suppu- low cost, and narrow microbiologic spectrum. rative frontal rhinosinusitis is not very common, For penicillin-allergic patients, folate inhibitors apparently because of the vertical nature of the (trimethoprim-sulfamethoxazole) are a cost- frontal sinus and its natural advantage of de- effective alternative to amoxicillin. The macro- pendent drainage through the nasofrontal duct lide class of antibiotics may also be used for (Fig 7-2). Thus, the common forehead pain is patients with penicillin allergy.53 seldom due to an underlying frontal rhinosinus- itis. The characteristic pain is over the affect- Acute maxillary rhinosinusitis. Acute max- ed sinus and often along the upper orbital rim. illary rhinosinusitis is the most common sinus The pain may radiate to the vertex and behind

176 Facial Pain

Fig 7-2 Coronal CT scan demonstrating right acute Fig 7-3 Axial bone-window CT scan demonstrating frontal rhinosinusitis with opacification of the right frontal opacification of the right sphenoid sinus compatible sinus (arrow). with sinusitis. Note the dehiscence of the right internal carotid artery.

the eye. Tenderness is usually felt in the frontal preferred route of administration. When fre- sinus or along its floor. When frontal sinusitis quent dosing is required to maintain adequate is complicated by osteomyelitis of the frontal pain relief, administering analgesics at fixed in- bone, the pain is prominent, diffuse, and in- tervals may be more effective than a pro re nata tense, and it often worsens at night and keeps (as-needed) basis.53 the patient awake. Subacute rhinosinusitis. Subacute rhinosi- Acute sphenoiditis. Acute sphenoiditis is rare nusitis may represent a continuum of the nat- and is characterized by a wide variety of types ural progression of ARS that has not resolved and distributions of pain. These include severe completely. According to the US classification, occipital headache, retro-orbital dull and aching subacute rhinosinusitis is diagnosed after 4 pain, and a stabbing pain at the vertex. Defin- weeks’ duration of symptoms or signs of rhi- itive diagnosis is made by a CT scan (Fig 7-3). nosinusitis and lasts up to 12 weeks.53 Howev- er, the European group thought a separate term Pain assessment of ABRS. Pain relief is a to describe patients with prolonged ARS was major goal in managing ABRS, and it is often not necessary because the number of patients the main reason patients with ABRS seek med- who have such a prolonged course is small, ical assistance. Ongoing assessment of the and there are very few data on which to base severity of pain is essential for proper manage- evidence-based recommendations on how to ment. Severity may be assessed using a fac- manage these patients. They therefore define es pain scale or a simple visual analog scale ARS as an infection lasting up to 12 weeks and (VAS), or by asking the patient to qualitatively do not use the term subacute rhinosinusitis at rate the discomfort as “mild” versus “moder- all.58 ate/severe.”53 When using a VAS, the disease can be divided into mild, moderate, or severe Recurrent acute rhinosinusitis. Recurrent based on the total score on a scale of 0 to 1058: ARS is also classified only in the US litera- ture as a situation in which four or more ep- • Mild = VAS score of 0 to 3 isodes of ABRS occur per year, without signs • Moderate = VAS score > 3 to 7 or symptoms of rhinosinusitis between the • Severe = VAS score > 7 to 10 episodes. Although recognized as a distinct form of rhinosinusitis, only a few cohort stud- Frequent use of analgesics is often neces- ies have documented the characteristics and sary. Orally administered analgesics are the clinical impact of recurrent ARS. The proper

177 7 Otolaryngologic Aspects of Orofacial Pain

Box 7-3 Clinical criteria for the diagnosis of chronic rhinosinusitis (CRS)*

Major factors Minor factors • Nasal obstruction • Fatigue • Facial congestion • Headache • Facial pain/pressure/fullness • Ear pain/pressure • Nasal discharge (anterior/posterior purulent • Cough discharge) • Halitosis • Loss of smell • Dental pain • Fever

*Symptoms of CRS are milder than in the acute form, and CRS may present with only one symptom. However, according to the International Headache Society, CRS has not been validated as a cause of headache/facial pain.53

diagnosis of recurrent ARS requires that each discharge (anterior/posterior nasal drip); with episode meet the criteria for ABRS. Culture or without facial pain/pressure; with or without is most useful during an acute episode, and reduction or loss of smell; and lasting at least imaging is most useful between episodes to 12 weeks. This should be supported by demon- identify anatomical changes that may predis- strable disease by either endoscopic signs of pose a patient to recurrent disease. An allergy- nasal polyps; and/or mucopurulent discharge, immunology evaluation may be considered to primarily from the middle meatus; and/or ede- detect coexisting allergic rhinitis or an under- ma/mucosal obstruction, primarily in the middle lying immunologic deficiency. Surgical inter- meatus; and/or CT changes consisting of mu- vention, which is not appropriate for uncom- cosal changes within the ostiomeatal complex plicated ABRS, may have a role in managing and/or sinuses. recurrent ARS.53 CRS may be divided into two major catego- ries: CRS with nasal polyposis (CRSwNP) and CRS without nasal polyposis (CRSsNP). This Chronic rhinosinusitis subclassification is more pronounced in the The US classification defines CRS as 12 weeks European classification than in the US one.53,58 or longer of two or more of the following signs Recently, there has been discussion among rhi- and symptoms—mucopurulent drainage (ante- nologists regarding the possibility that CRSsNP rior, posterior, or both), nasal obstruction (con- and CRSwNP are two distinct entities and not gestion), facial pain/pressure/fullness, or de- a spectrum of the same disease process; how- creased sense of smell—accompanied by the ever, more research is required. In any case, presence of inflammation documented by one there is a paucity of accurate information on or more of the following findings: purulent (not the epidemiology and course of CRSsNP and clear) mucus or edema in the middle meatus CRSwNP. or ethmoid region, polyps in the nasal cavity or Symptoms of CRS vary in severity and prev- the middle meatus, and/or radiographic imag- alence. Nasal obstruction is most common ing showing inflammation of the paranasal si- (81% to 95%), followed by facial congestion/ nuses53 (Box 7-3 and Table 7-6). pressure/fullness (70% to 85%), discolored The Europeans classify CRS (with or without nasal discharge (51% to 83%), and hyposmia nasal polyps) in adults as58 presence of two or (61% to 69%).53 Facial pain or headache alone more symptoms, one of which should be na- is not suggestive of CRS in the absence of oth- sal blockage/obstruction/congestion or nasal er nasal symptoms or signs.53,58 Other causes of

178 Facial Pain

Table 7-6 Diagnostic criteria for headache attributed to chronic rhinosinusitis* Diagnostic criteria A. Any headache fulfilling criterion C B. Clinical, nasal endoscopic, and/or imaging evidence of current or past infection or other inflammatory process within the paranasal sinuses C. Evidence of causation demonstrated by at least two of the following: 1. Headache has developed in temporal relation to the onset of chronic rhinosinusitis 2. Headache waxes and wanes in parallel with the degree of sinus congestion, drainage, and other symptoms of chronic rhinosinusitis 3. Headache is exacerbated by pressure applied over the paranasal sinuses 4. In the case of a unilateral rhinosinusitis, headache is localized ipsilateral to it D. Not better accounted for by another ICHD-3 diagnosis *Reproduced with permission from the International Headache Society.

headache or facial pain should be considered approach to the skull base and orbit.60 In pa- in the differential diagnosis of such cases. Ac- tients with CRS or recurrent ARS, the purpose cording to the authors’ experience, headache of surgery is to restore the normal function of and facial pressure are much more prominent the sinuses; therefore, it is termed functional in CRSsNP and are rare in CRSwNP. endoscopic sinus surgery. The pathogenesis of CRS is described as multifactorial, and there is no clearly delin- Chronic frontal rhinosinusitis. Pain is sel- eated single molecular pathway. An emerging dom a symptom of CRS of the frontal sinus. consensus, however, posits that the persistent This condition is usually part of chronic pan- inflammation defining CRS results from a dys- sinusitis, which also involves the ethmoid and functional host-environment interaction involv- maxillary sinuses. The most common symptom ing various exogenous agents and changes is chronic purulent nasal discharge. in the sinonasal mucosa. In accordance with the definition of CRS as an inflammatory dis- Chronic maxillary rhinosinusitis. The order, there has been movement away from most characteristic symptom of this condition pathogen-driven hypotheses.58 is persistent purulent rhinorrhea with local- CRS has four basic clinical courses: resolu- ization of pus in the middle meatus (Fig 7-4). tion, persistence, development of adverse se- CRS in the maxillary sinus seldom gives rise quelae, and progression to generalized airway to facial pain or headache, except during an reactivity. CRS is predominately a medical con- episode of acute exacerbation or with pro- dition where surgery can relieve symptoms and gression toward maxillary pyocele or maxillary sometimes bring about a reversal in the course osteomyelitis. of the disease. Endoscopic sinus surgery has become the gold standard approach to sino­ nasal pathologies requiring surgical interven- Rhinosinusitis of dental origin: tion. Current indications for endoscopic sinus surgery include CRS, recurrent ARS, complica- Odontogenic rhinosinusitis tions of rhinosinusitis, nasal polyposis, muco- The close association of the maxillary teeth and cele, epistaxis, cerebrospinal fluid leakage, fun- gingiva to the maxillary sinus floor may explain gal balls, allergic fungal rhinosinusitis, invasive the common finding of acute or chronic maxil- fungal rhinosinusitis, removal of foreign bodies, lary sinusitis caused by a dental disease, which repair of choanal atresia, tumors, and, finally, is responsible for about 20% of maxillary sinus-

179 7 Otolaryngologic Aspects of Orofacial Pain

itis cases.61 The causes of odontogenic sinus- either side of the nose, the periorbital region, itis may include: the retro-orbital region, or the cheeks.49 The forehead is often affected as well. The pain is • Endodontic disease described as a dull ache, a feeling of pressure, • Periodontal disease (Fig 7-5) or tightness. Some patients may feel that their • Complication of tooth extraction nose is blocked, although they have no nasal • Dental material in the antrum (Fig 7-6) airway obstruction. The forehead and the oc- • Infected dental cysts/tumors (Fig 7-7) cipital region are affected simultaneously in • Oroantral communication/fistula (Fig 7-8) approximately 60% of patients.49 No consistent • Complications of dental implants/sinus ele- exacerbating or relieving factor is found. The vation (Fig 7-9) pain may be chronic or episodic, and the skin and soft tissues over the forehead or cheek may A prospective study on refractory acute be sensitive to palpation. Nasal endoscopy and maxillary sinusitis found that intrusion of teeth CT scan of the paranasal sinuses are typical- into the maxillary sinus antrum is a common ly clinically normal. MSP is the most common finding (in about 50% of patients) and is not cause of non-rhinologic facial pain seen in oto- necessarily associated with the formation of laryngologic practice. sinusitis. Yet, refractory cases should be ex- The etiology of MSP is uncertain, and it may amined by a dentist because a dental infection be myofascial or neurovascular in origin. How- may be the source of the resistant infection.62 ever, Olesen’s theory, which integrates the ef- fects of myofascial afferents, the activation of peripheral nociceptors, and their convergence Sinusitis caused by complications of on the caudal nucleus of the trigeminal nerve, sinus elevation and/or dental implants along with qualitative changes in the cen- Use of dental implants to replace missing teeth tral nervous system, provides one of the best is thought to date back to the time of the an- models.65,66 cient Egyptians. Since the first titanium implan- Leong et al67 characterized pretreatment tation in 1965, dental implants have become MSP patients using the Sino-Nasal Outcome extremely popular. Sinus elevation is a proce- Test (SNOT-22). Average SNOT-22 scores of dure for increasing bone height in the postero- patients with MSP were higher than those of superior alveolar region to allow oral rehabili- healthy volunteers. They concluded that MSP tation and to restore masticatory function by has an adverse effect on physical and psycho- means of insertion of a dental implant, even in logic well-being and proposed that the SNOT- an atrophic maxilla (Fig 7-10). This procedure 22 may be used in MSP to document disease has also gained popularity among dentists in severity and to measure response to treatment. recent years.63 Both procedures may cause The treatment of choice in this condition is ami­ acute or chronic maxillary sinusitis when per- triptyline for 6 months.49 formed improperly or in patients with a preop- erative maxillary sinus disease, even when they are asymptomatic.64 Persistent idiopathic facial pain Persistent idiopathic facial pain (PIFP) is most common in women over the age of 40 years. Midfacial segment pain The prevalence rates of PIFP are 0.03% to Midfacial segment pain (MSP) may have all the 1.0% in the general population and 3.0% to same pain characteristics as tension headache, 12% in patients who have undergone endodon- but it affects the face and may involve the na- tic procedures (nonsurgical and/or surgical root sion, the area under the bridge of the nose, canal treatments).68

180 Facial Pain

Fig 7-4 Coronal sinus CT scan demon- Fig 7-5 Coronal sinus CT scan showing strating right chronic maxillary and ethmoid opacification of the left maxillary and eth- rhinosinusitis with complete opacification of moid sinuses secondary to severe periodon- the right maxillary sinus and obstruction of tal disease (arrow). the sinus osteomeatal complex (arrow).

Fig 7-6 Coronal sinus CT scan demonstrat- Fig 7-7 Coronal sinus CT scan showing ing dental material in the left maxillary sinus an infected dental cyst in the right maxillary antrum. sinus antrum.

Fig 7-8 Oroantral fistula during surgical Fig 7-9 Complication of a right-sided den- closure. Note the dental implants. tal implantation with rupture of the mucosa during a sinus elevation procedure.

Fig 7-10 Coronal sinus CT scan after a suc- cessful right sinus elevation.

181 7 Otolaryngologic Aspects of Orofacial Pain

Table 7-7 Diagnostic criteria for persistent idiopathic facial pain* Diagnostic criteria A. Facial and/or oral pain fulfilling criteria B and C B. Recurring daily for > 2 hours per day for > 3 months C. Pain has both of the following characteristics: 1. Poorly localized and not following the distribution of a peripheral nerve 2. Dull, aching, or nagging quality D. Clinical neurological examination is normal E. A dental cause has been excluded by appropriate investigations F. Not better accounted for by another ICHD-3 diagnosis *Reproduced with permission from the International Headache Society.

PIFP is characterized by deep, achy, ill- ry to the face, maxillae, teeth, or gingiva (any defined, pulling or crushing pain involving dif- peripheral or proximal branch of the trigeminal fuse areas of the face in the territory of the tri- nerve) but typically persists after the initial nox- geminal nerve. The pain fluctuates in intensity ious event has healed and has no demonstrable and severity. Occasionally, patients use such local cause. However, psychophysical or neu- terms as sharp or knifelike to describe the pain. rophysiologic tests may demonstrate sensory The pain often worsens at night and can be ag- abnormalities.4 gravated by activity or stress. In most cases, Medical treatment of PIFP is often difficult only one side of the face is affected, but pain and less satisfactory than treatment of trigem- on both sides is possible. The pain may move inal neuralgia. The treatment of choice is ami­ from one part of the face to another and may triptyline for 6 months (see chapters 12 and be accompanied by such complaints as mucus 16). Conventional analgesic drugs, including moving in the sinuses.49 Interestingly, the pain opioids, can also be effective in some pa- often crosses the recognized neurologic der- tients, often accompanied by a comprehen- matomes. PIFP may be comorbid with other sive pain-management program. Behavioral pain conditions, such as chronic widespread medicine approaches are also recommended pain and irritable bowel syndrome.4 Many pa- to complement cognitive-behavioral therapy, tients suffering from PIFP show a significant coping strategies, relaxation techniques, bio- psychosocial disability or psychiatric comor- feedback, or psychotherapy.68 bidity, such as depression, and are unable to function normally as a result of the pain.4,49 According to the ICHD-3, PIFP is a per- Scuba diving and facial pain sistent facial and/or oral pain that has varying Orofacial pain and headache occasionally oc- presentations but recurs daily for more than cur during or after scuba diving.69 Although it 2 hours per day over more than 3 months in is often benign, headache may signal a serious the absence of clinical neurologic deficit.4 The neurologic disorder in some circumstances. ICHD-3 criteria are described in Table 7-7. In Jagger et al70 evaluated the prevalence of oro- some patients with PIFP, the symptoms may facial complications associated with scuba div- initially appear to be similar to trigeminal neu- ing in 125 divers by questionnaires. The preva- ralgia, but then they progress toward a PIFP lence of reported orofacial pain was 44%; 21% pattern. Whereas trigeminal neuralgia is char- of the respondents reported toothache, 27% acterized by quick episodes of jabbing or lanci- sinus pain, 16% jaw pain, and 12% other types nating pain, PIFP attacks always last longer of pain. than a few seconds, usually minutes or hours Several causes have been associated with (see chapter 12). Moreover, no trigger points on pain and diving: the face are detected in PIFP. PIFP usually has no specific cause. PIFP • Sinus pain: Sinus barotrauma, also known as may originate from a minor operation or inju- sinus squeeze, is caused by failure to equalize

182 Facial Pain

pressure during descent. Pressurized air can- induced headaches do not respond well to not be forced into the sinuses. The air within pain relievers. the sinus contracts and causes the walls of • Decompression sickness headache: Head- the sinus to bleed. This is accompanied by aches can be a symptom of decompression intense, sharp pain. Common causes of sinus sickness, which is caused by the formation barotrauma include allergic rhinitis, vasomo- of bubbles when dissolved nitrogen is dis- tor rhinitis, nasal deformity, nasal polyposis, charged from the tissues on ascent. Associ- acute URI, and chronic irritation (eg, smok- ated symptoms include joint pain and swell- ing, diesel fumes, chemicals, and prolonged ing, skin rash, itching, dizziness, nausea, use of decongestant nasal drops). Symptoms vomiting, tinnitus (ringing inside the ears), include pain in the area of the affected sinus and extreme exhaustion. Scuba divers are or in the maxillary teeth (when the maxillary at a higher risk of decompression sickness sinus is involved), and nose bleeding. The when they do not decompress after a long or frontal sinuses are the most frequently affect- deep dive or before surfacing, or when they ed because the nasofrontal duct draining the ascend too quickly or make a panic ascent. frontal sinus is longer and more tortuous. A reverse squeeze occurs during ascent, when Other causes of pain are otic barotrauma, air in the sinus expands without any ability hyperbaric-triggered migraine, cervical and to escape. This is extremely painful. The sit- temporomandibular joint strain, supraorbital uation is self-limiting, however, because air neuralgia, carotid artery dissection, and exer- is gradually absorbed into the mucosa lining tional and cold-stimulus headache syndromes.71 the sinuses. When a sinus squeeze occurs, Focal neurologic symptoms should not be a slow ascent to the surface generally allevi- ignored but rather treated with 100% oxygen ates most of the pain. Because the sinus may acutely. The patient should be referred without be filled with blood, the patient is at high risk delay to a facility with a hyperbaric chamber. of developing consequent sinusitis. Antibiot- ic therapy is recommended, along with oral and nasal topical decongestants to promote Sphenopalatine neuralgia drainage. Persistence of severe pain with Sphenopalatine neuralgia, also known as Slud- no signs of ARS may be treated by a short er’s neuralgia, is characterized by a unilater- course of steroids. Diving is not recommend- al headache behind the eyes with pain in the ed for patients with URI. maxilla or soft .72–74 Pain in the back of • Tension-type headache: Symptoms of a the nose, teeth, temple, occiput, or neck may tension-type headache include headache also occur. The pain is associated with sino­ and pain in the nape (see chapter 8). Tension nasal congestion, swelling of the nasal mucous headaches may be caused by muscle strain membranes, tearing, and redness of the face.74 due to anxiety and muscular rigidity. To pre- Sphenopalatine neuralgia is more common in vent the development of muscle strain and, women (2:1 ratio). The condition should be dis- consequently, a tension headache, divers tinguished from a cluster headache, although must learn to adopt a proper posture and re- both are characterized by similar symptoms. lax in the water. However, sphenopalatine neuralgia pain lasts • Carbon dioxide toxicity: A dull throbbing longer and is associated with inflamed nasal headache after diving is usually caused by mucosa on the involved side.75 Sphenopalatine carbon dioxide toxicity. This type of pain is neuralgia is evidently caused by an irritation of common in divers and is caused by an ac- the sphenopalatine ganglion from intranasal in- cumulation of carbon dioxide in the body. fection, deformity, or scarring. Hypoventilation happens when a scuba div- A topical decongestant may occasionally er does not inhale long, deep breaths from alleviate the nasal symptoms. Ganglion blocks the air tank or does not do this often enough. (by intranasal application or direct injection) are The best therapy for this type of headache effective for controlling the pain.76,77 Sumatrip- is taking slow, deep breaths to reduce the tan, which is effective in the treatment of cluster carbon dioxide retention. Carbon dioxide– headache, has given satisfactory results in pa-

183 7 Otolaryngologic Aspects of Orofacial Pain

tients with Sluder’s neuralgia; the outcomes are migraine model identifies the starting point in equivalent to those obtained by applying Bo- the central nervous system followed by sensiti- nain’s liquid (eg, lidocaine, menthol, phenol) be- zation of the peripheral neurons of the trigemi- low and behind the tail of the middle turbinate.75 nal nerve, including those supplying sensation to the meninges. When the peripheral early phase is not treated, central sensitization at Migraine and sinus headache the level of the caudal nucleus of the trigeminal The ICHD-3 lists operational diagnostic crite- nerve occurs, with concomitant repetitive firing ria for migraine (see chapter 10). Migraine and of the involved neurons and pain in the distribu- tension-type headache are often confused tion of the ophthalmic (V1) and/or maxillary (V2) with true sinus headache because of their sim- branches of the trigeminal nerve. These nerves ilar locations.4,78 Publications have stated that also provide sensation to the mucosa of the patients with sinus headache, at least those sinonasal cavity and are involved in the neu- with no obvious signs of infection, have a 58% robiology of primary sinonasal pain. The early to 88% incidence of a migraine-type head- sensitization phase is accompanied by cutane- ache.79,80 Migraine can cause symptoms similar ous allodynia (pain induced by stimulation that to those of rhinosinusitis, such as facial pain, is normally nonpainful) in most patients (80%), nasal congestion, and rhinorrhea. This form of and it often occurs in the distribution of V1 and migraine has been termed facial migraine and is V2.83 This may include stimulation of the nose, discussed in chapter 10. such as while breathing cold air. A migraine at- A certain proportion of patients seeking tack may include secondary nasal symptoms, treatment at an ear, nose, and throat clin- which are probably mediated by stimulation of ic suffer from some facial pain resulting from the parasympathetic nervous system via the migraine. A prospective evaluation of 100 se- superior salivary nucleus of the facial nerve (VII). quential patients who complained of “sinus This reflex activation is extensively discussed in headaches” demonstrated that 86% had mi- chapters 10 and 11. A report on patients with graine or “probable migraine,” while only 3% sinus headaches fulfilling the migraine criteria had actual sinus-related headaches.81 Eross demonstrated that 84% reported sinus pres- et al82 evaluated 100 consecutive patients with sure, 82% sinus pain, 63% nasal congestion, a self-diagnosed sinus headache. The actual 40% rhinorrhea, 38% watery eyes, and 27% diagnoses were migraine (52%), probable mi- itchy nose.79 Occasionally, sinonasal disease graine (23%), chronic migraine (11%), other un- or nasal allergy can play a role in triggering mi- classifiable headaches (9%), cluster headache graine, which may respond to nasal steroids or (1%), and hemicrania continua (1%). Only 3% leukotriene antagonists.83 The appearance of of the patients were accurately diagnosed with neurogenic rhinitis along with a sinus headache headache attributable to rhinosinusitis. Nasal in patients with migraine is often misunder- congestion was present in 73% of patients and stood and contributes to misdiagnosis. postnasal drip in 56%. Most patients reported The duration of sinus headache and sinus pain triggered by changes in weather or sea- symptoms is important for differentiating rhi- son, and many noted changes with allergies or nosinusitis from a migraine attack. In contrast altitude, which are common migraine triggers. to rhinosinusitis, migraine headache typically re- The reason for the high rate of patients solves within 72 hours. ARS pain typically wors- misdiagnosed with sinus headache by their ens after 5 to 7 days and is usually associated physicians is related to the pathophysiology with hyposmia or anosmia, fever, cough, max- of migraine and the nature of nasal pain. The illary dental pain, and ear fullness or pressure. neurovascular theory of migraine implicates the The diagnostic features of facial migraine are nervous system as being the initiator of the pro- primarily based on the patient’s history and the cess, and the blood vessel involvement occurs features reminiscent of typical migraine head- as a consequence of the neuronal process. This aches as defined in the ICHD-3 (see chapter 10).

184 Throat Pain

Box 7-4 Causes of throat pain

• Acute pharyngitis • Lingual tonsillitis • Tonsillitis • Pharyngeal space infections ––Acute ––Parapharyngeal space ––Chronic ––Retropharyngeal space • Peritonsillar cellulitis and abscess • Ludwig’s angina

The most common viruses causing viral Throat Pain pharyngitis are rhinovirus and adenovirus. Oth- er less common viruses include Epstein-Barr Throat pain, or a sore throat, is a common virus, herpes simplex virus, influenza virus, symptom described as pain, discomfort, or parainfluenza virus, coronavirus, coxsackie- raw feeling of the throat, especially while swal- virus, echovirus, respiratory syncial virus, and lowing. The vast majority of sore throats are cytomegalovirus. caused by viral infections of the pharynx or ton- Rhinovirus, which is responsible for the sils. Many people experience a mild sore throat common cold, is one of the most common at the beginning of a common cold. The differ- causes of viral pharyngitis. The virus does not ential diagnosis of sore throat also includes var- invade the pharyngeal mucosa but causes ede- ious diseases of the oropharyx (Box 7-4). ma and hyperemia of the mucous membranes and increases the secretory activity of the mu- cous glands. Bradykinin and lysyl-bradykinin Acute pharyngitis are generated in the nasal mucous membranes Acute pharyngitis is an infection of the phar- and stimulate pain nerve endings. ynx, which may involve the tonsils. The con- Adenovirus pharyngitis is common among dition may be part of a generalized URI or young children and military recruits. The most may be a specific localized infection inside the common adenovirus types causing pharyngitis pharynx. The most common cause of acute are adenovirus types 1 through 3 and type 5, pharyngitis is a viral infection, but it can also be which directly invade the pharyngeal mucosa. caused by a bacterial infection, such as group Specific symptoms include fever, sore throat A streptococci, M pneumoniae, and Chlamydia (more intense than that of the common cold), pneumoniae. The viruses causing viral pharyn- and conjunctivitis. gitis are highly contagious and tend to spread Epstein-Barr virus pharyngitis is usually as- quickly, especially during the winter. Throat sociated with infectious mononucleosis. symptoms include soreness, scratchiness, or Edema and hyperemia of the pharyngeal mu- irritation. Associated symptoms include fe- cosa and uvula, with enlargement of the tonsils, ver and discomfort while swallowing, or ody- are characteristic signs. Approximately half of nophagia. Fever is more prominent in young patients with infectious mononucleosis have children than in adults. Most viral pharyngitis gray-white thick patches of exudates distribut- cases are accompanied by a flu or cold, along ed over the tonsils and pharyngeal walls, thus with a stuffy, runny nose; sneezing; and gen- mimicking streptococcal pharyngitis. Palatal pe- eralized aches, such as arthralgia and muscle techiae associated with infectious mononucle- pain. Nonproductive cough and hoarseness osis tend to be confined to the soft palate. An may also be present. Edema and erythema of inflammatory exudate and nasopharyngeal lym- the pharyngeal walls are the typical findings on phoid hyperplasia (adenoiditis) may also devel- physical examination. Pharyngeal exudation op. Body temperature is usually high and may occurs infrequently and is generally less effu- reach up to 104oF (40oC). Generalized lymph- sive than in patients suffering from bacterial adenopathy is common and is usually promi- pharyngitis. nent in the anterior and posterior cervical trian-

185 7 Otolaryngologic Aspects of Orofacial Pain

gles. Splenomegaly is present in approximately Differentiating viral from bacterial pharyngitis 50% of patients and hepatomegaly in 10% to solely on the basis of physical examination is not 15%. Patients treated with ampicillin may de- easy. In viral pharyngitis, the total white blood velop a diffuse, pruritic maculopapular eruption. cell count may initially be slightly high, followed Herpetic pharyngitis is caused by herpes by a decrease to fewer than 5,000 cells after 4 to simplex virus types 1 and 2. This infection is 7 days of illness in about half of patients. Atypi- commonly observed in children and young cal lymphocytosis is frequently associated with adults. Herpes simplex virus may cause gin- viral pharyngitis. In infectious mononucleosis givitis or stomatitis. A sore throat with associ- pharyngitis, the peripheral blood smear reveals ated gingivostomatitis is the typical presenting relative and absolute lymphocytosis, with more symptom. Other associated symptoms include than 10% atypical lymphocytes. Liver function fever, odynophagia, , and malaise. test results are abnormal in 90% of infectious Enteroviral pharyngitis is usually caused by mononucleosis cases. A mononucleosis spot coxsackievirus or echovirus. Enteroviral lesions test (monospot) is usually positive and allows in the oropharyngeal mucosa are usually a re- rapid screening for heterophile antibodies. Im- sult of a secondary infection of small mucosal munoglobulin M antibody to Epstein-Barr virus vessels’ endothelial cells and occur during vire- capsid antigen and antibody to early antigen are mia. Coxsackievirus infection is common in the useful for diagnosing an acute infection, partic- late summer and early fall and may cause the ularly in patients who are heterophile negative. following pathologies: Rapid streptococcal antigen test and bacterial culture of a throat swab are negative. Leuko- • is usually caused by group A cox- penia and proteinuria may be seen in influenza sackieviruses and tends to occur in epidem- virus pharyngitis. ics, most commonly in infants and children. Treatment of viral pharyngitis includes bed The condition is characterized by multiple, rest, saltwater gargling, and drinking. Analge- small (1 to 2 mm), grayish papulovesicular sics and antipyretics are used to relieve pain lesions on the tonsils, tonsillar pillars, uvula, and fever. or soft palate. The lesions may occasion- ally grow up to 4 mm or have an erythem- atous ring as large as 10 mm. The vesicles Tonsillitis become shallow ulcers in about 3 days and Acute tonsillitis is inflammation of the palatine heal after a few days. The pharynx is usually tonsils, usually due to GABHS or, less common- not involved. Associated symptoms include ly, to a viral infection. Acute tonsillitis caused a sudden onset of fever with a sore throat, by Streptococcus sp usually occurs in children headache, , and frequently pain in ages 5 to 15 years. Approximately 10% to 20% the neck, abdomen, and extremities. of sore throats in adults are caused by strepto- • Acute lymphonodular pharyngitis is caused coccal infection. Fever, chills, sore throat, foul by coxsackievirus A10 and is characterized breath, dysphagia, odynophagia, and tender- by a distribution of oral and pharyngeal le- ness in the angle of the jaw characterize acute sions similar to those seen in herpangina. tonsillitis. The pain is frequently referred to the However, the lesions are protruding, whitish ears. Physical examination reveals hyperemic to yellowish nodules that do not evolve into and swollen palatine tonsils, uvula, tongue vesicles or ulcers. They remain papular and base, and pharyngeal walls, with irregular, thin, become grayish-white and nodular, second- nonconfluent patches of white exudates on the ary to infiltration by lymphocytes. tonsils forming the typical appearance of fol- • Hand-foot-and-mouth disease is usually licular tonsillitis. Submandibular lymph nodes caused by coxsackievirus A16 and is charac- are often enlarged and tender. Leukocytosis terized by 4- to 8-mm ulcers on the tongue, with an increased neutrophil count (shift to the buccal mucosa, and occasionally tonsillar left) is commonly present in bacterial infections. pillars. Vesicular exanthems develop on the Mere reliance on clinical criteria, such as the hands and feet, and, in infants, occasionally presence of follicular exudate, erythema, fe- in the diaper area. ver, and lymphadenopathy, is not an accurate

186 Throat Pain means for distinguishing streptococcal from children showed that corticosteroids provide viral tonsillitis. Throat culture is the gold stan- symptomatic relief of pain in sore throat, in dard for detecting GABHS tonsillitis with a sen- addition to antibiotic therapy, mainly in partic- sitivity of 80% to 95%. Rapid antigen detection ipants with severe or exudative sore throat.86 test confirms the presence of GABHS cell-wall carbohydrate from swabbed material and is considered less sensitive than throat cultures. Peritonsillar cellulitis and abscess However, the rapid antigen detection test has a Peritonsillar infection, also known as Quincy’s high specificity and produces results in signifi- angina, is an infection located between the cantly less time than a throat culture. tonsil and the superior pharyngeal constrictor Chronic tonsillitis is characterized by chron- muscle. The most common pathogen causing ic sore throat, halitosis, recurrent tonsillitis, peritonsillar cellulites/abscess is GABHS. An- and persistent tender cervical lymph nodes. A aerobic Bacteroides can also cause this type of polymicrobial bacterial population is observed infection. Occasionally, culture results are pos- in most cases, with alpha- and beta-hemolytic itive for multiple common throat bacteria. Pre- streptococcal species, S aureus, H influenzae, senting symptoms include severe throat pain, and Bacteroides sp identified. especially on swallowing, fever, , foul Complications of GABHS tonsillitis are clas- breath, trismus, “hot potato voice,” and uni- sified into suppurative and nonsuppurative. lateral referred otalgia. Limited mouth opening Nonsuppurative complications include scarlet (trismus) is always present in varying severity. fever, acute rheumatic fever, and poststrepto- The tonsil and uvula are displaced medially coccal glomerulonephritis. Suppurative com- by the peritonsillar infection. The soft palate plications include peritonsillar, parapharyngeal, and anterior pillar are swollen and hyperemic. and retropharyngeal cellulitis and/or abscess. Unilateral enlarged and tender submandibular Treatment of acute streptococcal tonsillitis lymph nodes are present. includes adequate hydration and caloric intake. Drainage, along with intravenous penicillin, Analgesics and antipyretics are used to relieve is required in peritonsillar abscess. Peritonsil- pain and fever. GABHS infection obligates an- lar cellulitis without pus formation usually re- tibiotic therapy, which is directed toward (1) sponds to intravenous penicillin therapy. Peri- preventing acute rheumatic fever, (2) preventing tonsillar abscess tends to recur when there is suppurative complications, (3) abating clinical history of recurrent tonsillitis, and tonsillectomy symptoms and signs, and (4) reducing trans- is then indicated. A dental source should be mission of GABHS to close contacts. Penicil- ruled out in de novo cases. lin is the treatment of choice in streptococcal tonsillitis. Cochrane analysis on the benefits of antibiotics for sore throat for patients in prima- Lingual tonsillitis ry care settings showed that antibiotic therapy Lingual tonsillitis is an infection of the lymphatic confers relative benefits in treating sore throat.84 tissue located in the base of the tongue. Most However, the absolute benefits are modest, and patients with lingual tonsillitis have undergone the therapy shortens the duration of symptoms palatine tonsillectomy in the past. Lingual ton- by about 16 hours overall.84 sillitis presents with fever, sore throat, glossal Analysis of different recommendations from pain, dysphagia, muffled voice, and pain at international guidelines for the management of the level of the hyoid bone during swallowing. acute pharyngitis in adults and children showed Lingual tonsillitis is visible only by means of a substantial discrepancies.85 However, all guide- laryngeal mirror or fiber-optic examination. The lines agree that narrow-spectrum penicillin is base of the tongue is enlarged, edematous, and the first choice of antibiotic for treating strep- covered by exudates. The pharynx may appear tococcal pharyngitis and that treatment should normal or mildly hyperemic. The anterior por- last for 10 days to eradicate the microorganism. tion of the neck may be tender at the level of A systematic review and meta-analysis that the hyoid bone, and cervical and submandib- evaluated whether systemic corticosteroids ular adenopathy may be observed. Treatment improve symptoms of sore throat in adults and includes intravenous penicillin.

187 7 Otolaryngologic Aspects of Orofacial Pain

Parapharyngeal space infection 1. Parapharyngeal lymphadenitis: Infection is located in the posterior part of the PPS The parapharyngeal space (PPS) (ie, lateral with no invasion into the parapharyngeal fat pharyngeal space, pharyngomaxillary space, and with no extensions into other cervical pterygomaxillary space, pterygopharyngeal spaces except the adjacent retropharynge- space) occupies an inverted pyramidal area al space. This condition is relatively benign, lateral to the superior constrictor muscles and intravenous antibiotics and nonsurgical and bounded by multiple components of the treatment are recommended. fascial system. The styloid process divides 2. Parapharyngeal abscess: With this condition, the PPS into an anterior or prestyloid com- also known as deep neck abscess, infection partment and a neurovascular or poststyloid is located in the anterior part of the PPS and compartment. involves the parapharyngeal fat. Diffusion PPS infections may follow an infection in the into the mediastinum and other severe com- pharynx, tonsils, adenoids, teeth, parotid gland, plications are frequent. Early diagnosis, ag- peritonsillar area, submandibular space, retro- gressive intravenous antibiotics, and urgent pharyngeal space, Bezold abscess (mastoid surgical drainage are recommended. abscess on the inner aspect of the mastoid tip along the digastric ridge), and adjacent lymph nodes. Despite the multitude of well-defined Retropharyngeal space infection potential sources, in nearly half of the cas- The retropharyngeal space (RPS) lies between es, the etiology cannot be defined. Signs and the visceral division of the middle layer of the symptoms of PPS infection differ depending deep cervical fascia behind the pharyngeal on whether the prestyloid or poststyloid com- constrictors and the alar division of the deep partment is involved. Anterior PPS infection is layer of the deep cervical fascia posteriorly. characterized by pain in the angle of the jaw, RPS infection may follow infection in the na- preauricular area, ear, and adjacent upper neck. sopharynx, oropharynx, sinonasal region, and Rotating the head and neck to the contralateral rarely mastoiditis. RPS infection may also oc- side intensifies the pain. Other symptoms in- cur directly after a traumatic perforation of the clude dysphagia, odynophagia, drooling, tris- posterior pharyngeal wall or esophagus, or in- mus (due to medial pterygoid muscle irritation), directly from the parapharyngeal space. Most fever, chills, and malaise. Edema and medial RPS infections in children are secondary to displacement or bulging of the lateral pharyn- URI, whereas trauma or foreign bodies cause geal wall and tonsil is a hallmark of PPS infec- most RPS infections in adults. Retropharyngeal tion. Swelling, induration, and tenderness at the lymph nodes tend to regress by the age of 5 angle of the mandible are also commonly ob- years, so infection in this area is much more served. Dyspnea and other symptoms of airway common in children than in adults. RPS infec- obstruction may occur in severe cases. Posteri- tion may drain into the prevertebral space and or PPS infection is not associated with trismus through this space into the chest, thus causing or tonsillar displacement and may have no lo- mediastinitis. Symptoms of RPS infection in- calizing signs on examination. Despite this, the clude sore throat, dysphagia, stiff neck, fever, patients appear to be toxic with parotid space and, rarely, posterior neck and shoulder pain swelling. Involvement of the neurovascular aggravated by swallowing. structures may lead to complications such as Examination reveals anterior displacement cranial neuropathies, Horner syndrome, septic or bulging of one or both sides of the posterior internal jugular thrombosis, and carotid artery pharyngeal wall due to involvement of lymph rupture. nodes, which are distributed lateral to the CT scan of the neck (with contrast medium) midline fascial raphe. Lateral neck radiograph facilitates the diagnosis and assessment of the (demonstrating widening of the retropharyngeal extent of PPS infection. Sichel et al87 redefined space) and neck CT scan with contrast facili- PPS infection into two different disorders that tate diagnosis and assessment of the extent of are clinically and therapeutically relevant: RPS infection.

188 Vestibular Syndromes Related to Orofacial Pain or Structures

Early diagnosis and aggressive intravenous a shift to the left. Airway management is the pri- antibiotics are mandatory. Transoral incision mary therapeutic concern. and drainage are recommended in cases with Airway control by endotracheal intubation abscess formation. is mandatory. Therapy includes intravenous broad-spectrum antibiotics and occasional- ly drainage of the swelling through a cervical Ludwig’s angina incision with placement of drains. Dental treat- Ludwig’s angina is a potentially life-threatening, ment may be needed to treat the initiating tooth rapidly expanding and spreading, gangrenous infection. Complications such as sepsis and cellulitis of the submandibular space. Swelling descending necrotizing mediastinitis may occur of this region can compromise the airway. Most through the retropharyngeal space and carotid Ludwig’s angina infections are odontogenic, sheath. usually from the second or third mandibular molar. Other causes include peritonsillar or parapharyngeal abscesses, mandibular frac- ture, oral lacerations or piercing, and, rare- Vestibular Syndromes ly, submandibular sialadentitis. Predisposing factors include dental caries, recent dental Related to Orofacial Pain treatment, systemic illnesses (eg, diabetes or Structures mellitus), malnutrition, alcoholism, compro- mised immune system (eg, AIDS), and organ transplantation. The term Ludwig’s angina is Vestibular migraine reserved for infections meeting the following Vertigo is an illusion that the environment is five criteria: moving or that the patient is moving in relation to the environment. Migraine associated with 1. Cellulitis (not an abscess) of the submandib- attacks of vertigo has been repeatedly docu- ular space mented in the medical literature. Various terms 2. Involvement of only the submandibular have been used to designate vertigo caused space, although this might be bilateral and by a migraine mechanism, including migraine- spread into secondary spaces associated vertigo, migraine-associated diz- 3. The finding of gangrene with foul sero- ziness, migraine-related vestibulopathy, mi- sanguineous fluid on incision but no frank grainous vertigo, benign recurrent vertigo, purulence and basilar migraine.88,89 The term vestibular 4. Involvement of the fascia, muscle, and con- migraine has been convincingly advocated as nective tissue, with sparing of the glandular a condition that stresses the particular vestib- tissue ular manifestation of migraine and thus best 5. Direct spread of infection rather than spread avoids confounding it with nonvestibular diz- by lymphatics ziness associated with migraine.90 Therefore, the Bárány Society, which represents the in- The most common microbes involved are ternational community of vestibular research, Streptococcus sp and oral anaerobic bacteria. and the Migraine Classification Subcommittee Symptoms include painful neck swelling, tooth of the International Headache Society have pain, dysphagia, odynophagia, dyspnea, fever, opted for vestibular migraine in their joint arti- and malaise. Ludwig’s angina is characterized cle on the classification of the disorder.91 The by a brawny induration of the mouth floor and term migraine with brainstem aura (formerly, suprahyoid region (bilaterally) with elevation basilar-type migraine) should be restricted to or protrusion of the tongue, thus potentially patients who fulfill the respective diagnostic obstructing the airway. Other signs include a criteria of the ICHD-3. tender, firm swelling in the submental and an- In 2013, the ICHD-3 listed new operational terior neck without fluctuance, tachypnea, stri- diagnostic criteria for vestibular migraine (sec- dor, trismus, muffled or “hot potato” voice, and tion A1.6.5), as shown in Table 7-8. Transient drooling. The white blood cell count is high with auditory symptoms, nausea, vomiting, prostra-

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