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Orofacial Pain

Orofacial Pain

QUINTESSENCE INTERNATIONAL OROFACIAL

Noboru mimicking trigeminal autonomic cephalalgia: A report of four cases

Noboru Noma DDS, PhD1/Kohei Shimizu DDS, PhD2/Kosuke Watanabe DDS3/Andrew Young DDS, MSD4/ Yoshiki Imamura DDS, PhD5/Junad Khan BDS, MSD, MPH, PhD6

Background: This report describes four cases of cracked All cases mimicked trigeminal autonomic cephalalgias, a group tooth syndrome secondary to traumatic occlusion that mim- of primary headache disorders characterized by unilateral icked trigeminal autonomic cephalalgias. All patients were facial pain and ipsilateral cranial autonomic symptoms. referred by general practitioners to the Orofacial Pain Clinic at Trigeminal autonomic cephalalgias include , Nihon University Dental School for assessment of atypical facial paroxysmal hemicrania, hemicrania continua, and short-lasting pain. Clinical Presentation: Case 1: A 51-year-old woman unilateral neuralgiform headache attacks with conjunctival presented with severe pain in the maxillary and mandibular injection and tearing/short-lasting neuralgiform headache left molars. Case 2: A 47-year-old woman presented with sharp, attacks with cranial autonomic features. Pulpal , when shooting pain in the maxillary left molars, which radiated to caused by cracked tooth syndrome, can manifest with pain the temple and periorbital region. Case 3: A 49-year-old man frequencies and durations that are unusual for , as was presented with sharp, shooting, and stabbing pain in the max- seen in these cases. Conclusion: Although challenging, dif- illary left molars. Case 4: A 38-year-old man presented with ferentiation of cracked tooth syndrome from trigeminal intense facial pain in the left supraorbital and infraorbital areas, autonomic cephalalgias is a necessary skill for dentists. which radiated to the temporoparietal and maxillary regions. (Quintessence Int 2017;48: 329–337; doi: 10.3290/j.qi.a37688)

Key words: cracked tooth syndrome, orofacial pain, trigeminal autonomic cephalalgias

Cracked tooth syndrome (CTS) was described by Cam- 1 Associate Professor, Department of Oral Diagnostic Sciences, Nihon University School of ; and Division of Clinical Research, Dental Research Center, eron1 as “incomplete fracture of a vital posterior tooth Nihon University School of Dentistry, Tokyo, Japan. involving and possibly pulpal tissue.” Patients 2 Assistant Professor, Department of , Nihon University School of Dentistry, Tokyo, Japan. complain of pain when consuming cold or hot foods or 3 Research Student, Department of Oral Diagnostic Sciences, Nihon University beverages, or while chewing, particularly hard foods.2,3 School of Dentistry; and Division of Clinical Research, Dental Research Center, Nihon University School of Dentistry, Tokyo, Japan. Dentinal tubular fluid flow may explain the presence of 4 Assistant Professor, Department of Dental Practice, Arthur Dugoni School of Dentistry, University of the Pacific, San Francisco, California, USA. pain when the cusp is loaded during movement 4 5 Chief and Professor, Department of Oral Diagnostic Sciences, Nihon University between fracture sites. The pulpal tissue of affected School of Dentistry; and Division of Clinical Research, Dental Research Center, Nihon University School of Dentistry, Tokyo, Japan. teeth may become inflamed because of irritation 6 Assistant Professor, Department of Diagnostic Sciences, Rutgers School of Den- caused by microleakage, which can induce thermal tal Medicine, 110 Bergen Street, Newark, New Jersey, USA. sensitivity. Eventually, crack propagation leads to Correspondence: Dr Noboru Noma, Department of Oral Diagnostic Sciences, Nihon University School of Dentistry, and Division of Clinical necrotic or irreversible pulpitis. Other potential Research, Dental Research Center, Nihon University School of Dentistry, causes are parafunctional habits such as clenching and 1-8-13, Kandasurugadai, Chiyoda-ku, Tokyo 101-8310, Japan. Email: [email protected] damage caused by dental preparations.5 Previous stud-

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ies showed that presence of an extensive preparation CASE PRESENTATION or amalgam restoration and parafunctional habits increased the risk of crack line development. However, Case 1 other studies reported that 60% of teeth with cracks A 51-year-old woman presented to the Orofacial Pain had no restoration.6,7 Clinic at Nihon University with severe pain in the maxil- Diagnosis of CTS is not always straightforward. lary and mandibular left molars. The maxillary left molar Incomplete tooth fracture is sometimes easy to identify pain had begun 10 years previously but was sporadic. with conventional testing, such as selective bite tests, Approximately 2 weeks before seeking treatment at the staining solutions, and transillumination. In other cases, clinic, the patient had seen a neurologist, who pre- however, such fractures can be difficult to localize and scribed neurotrophin, which did not result in significant diagnose when pain symptoms mimic conditions such relief. One week later, she saw a general dentist for as , disorders, head- what had become severe dental pain, in the mandibu- ache, ear pain, or atypical orofacial pain.8,9 Dentists lar left region. The dentist diagnosed possible trigemi- must therefore be familiar with various odontogenic nal and prescribed loxoprofen. The severe and nonodontogenic causes of orofacial pain, so that pain gradually spread superiorly. When severe, the pain they can differentiate CTS from other conditions. occasionally radiated to the periorbital region. While The trigeminal autonomic cephalalgias (TACs) are a eating noodles, the patient felt what she described as a group of primary headache disorders characterized by “hot, burning poker in the eyes.” During exacerbations, unilateral symptoms, namely, prominent headache and the pain would reach an intensity of 9 to 10 out of 10. ipsilateral cranial autonomic features such as conjunc- Exacerbations occurred three times per day. They tival injection, lacrimation, and rhinorrhea. In the Inter- lasted from a few minutes to a few hours but were national Headache Society Classification (ICHD-3-beta) superimposed on constant pain. The periorbital loca- the TAC category includes cluster headache (CH), par- tion and “hot” quality in the eye suggested CH. oxysmal hemicrania (PH), short-lasting unilateral neu- ralgiform headache attacks with conjunctival injection Clinical examination and tearing (SUNCT)/short-lasting neuralgiform head- Intraoral examination revealed extensive . ache attacks with cranial autonomic features (SUNA), The maxillary left second molar was sensitive to percus- and hemicrania continua (HC).10 These conditions can sion and bite testing. Electrical pulp testing (EPT) be differentiated by their attack duration and fre- showed hyposensitivity in the maxillary left second quency, and by response to treatment. HC is continu- molar (Fig 1a). No fracture or decay was seen in intra- ous and responsive to indomethacin. CH is character- oral radiographs of the maxillary and mandibular left ized by excruciatingly painful attacks that occur in molars (Figs 1b and 1c). At this point, CTS and CH were discrete episodes lasting 15 to 180 minutes, at least considered in the differential diagnosis. CH was once every 2 days. PH is more frequent and of shorter included because of the periorbital location, the “hot” duration than CH and, like HC, is responsive to indo- quality in the eye, the frequency and duration of pain, methacin. SUNCT/SUNA has the shortest duration and and the absence of obvious dental . highest frequency; attacks can occur more than 100 A diagnostic anesthetic block eliminated the pain. times a day. Patients often present to dentists for symp- The patient was therefore referred to the endodontic toms associated with these types of headaches.10 department, for (RCT). An incom- This report describes four cases of CTS that mim- plete fracture was observed in the maxillary left second icked TACs. molar (Fig 1d). The patient has been followed for more than 2½ years and is currently pain-free.

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Fig 1a Percussion stimulation and bite tests showed high sen- b sitivity in the maxillary left second molar (circle), but no cracks or decay were observed (mirror view).

c Fig 1d An incomplete fracture was seen in the distal wall of the Figs 1b and 1c Dental radiographs show no cracks or decay in left maxillary second molar (arrow). the maxillary and mandibular left second molars.

Case 2 Clinical examination A 47-year-old woman presented with a chief complaint The patient appeared healthy and responsive, and her of sharp, shooting pain in the maxillary left molar area, medical history was noncontributory. She was not which radiated to the temple and periorbital region. using any medications. A musculoskeletal examination The intensity was rated as 9 to 10 out of 10, and the revealed no abnormalities except in the left masseter frequency and duration were 10 times per day for muscle, which produced slight discomfort on palpa- approximately 5 to 10 minutes each episode. The tion. However, this was localized and did not reproduce patient reported that the pain occasionally woke her the chief complaint. Intraoral examination revealed while sleeping. Approximately 2 weeks before present- extensive tooth wear (Figs 2a to 2c). The maxillary left ing to the clinic, she had seen a general dentist who fi rst and second molars were not sensitive to percus- diagnosed infl ammation of the temporomandibular sion or thermal stimulation. EPT showed hyposensitiv- joint. He treated her with an occlusal appliance, to ity in the maxillary left premolar and second molar. A reduce mechanical overloading of the temporoman- dental radiograph showed a root canal fi lling in the dibular joint, followed by occlusal adjustments. How- maxillary left fi rst molar (Fig 2d) but no causative fac- ever, this did not relieve the pain. tors.

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b Fig 2a A photograph showing extensive tooth wear.

c Fig 2d A dental radiograph showing root canal filling in the Figs 2b and 2c Photographs showing composite resin (circle) maxillary first molar and restorative material in the maxillary in the maxillary second molar but no cracks or decay (mirror second molar. views).

Treatment Case 3 The absence of radiographic and clinical evidence of A 49-year-old man presented with sharp, shooting, and dental pathology and the patient’s history (pain quality, stabbing pain in the maxillary right molars. The pain intensity, duration, frequency, and location) were con- occasionally radiated to the orbital and periorbital sistent with PH. Indomethacin was started at 25 mg/ regions. The patient reported being unable to eat day, and the dose was titrated up to 75 mg/day for 3 during an attack. The pain intensity was rated as 9 out days. This was followed by a very slight decrease in the of 10 on a visual analog scale, and the frequency was frequency, intensity, and duration of pain. A diagnostic described as five to six attacks per day, lasting for anesthetic block eliminated the pain. The patient was approximately 2 to 5 minutes. The patient reported referred to the endodontic department, and RCT was that the pain woke him from sleep. performed. Microscopic observation during RCT revealed partial and incomplete fracture Clinical examination in the maxillary left second molar. The patient has been The patient was healthy overall and had a noncontrib- followed for 5 years and is currently pain-free. utory medical history. He denied use of medications, except for occasional over-the-counter acetaminophen, which did not provide pain relief. A musculoskeletal examination showed no abnormalities. Intraoral exam-

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seen a dentist for mild dental pain in the maxillary left region. Bite adjustments had been performed by the general dentist to “stabilize the occlusion.” After treat- ment, pain in the left anterior region gradually wors- ened, and a throbbing sensation developed in associa- tion with the pain, which sometimes woke him from sleep, usually in the early morning. When severe, the pain manifested as throbbing in the left eye. It was most intense in the supraorbital and infraorbital areas and radiated to the ipsilateral temporoparietal and maxillary regions. Pain exacerbation occurred 1 to 5 times per week, lasting from minutes to a few hours. Fig 3 A dental radiograph showing no cracks or decay in the maxillary first premolar and second molar (arrows). Clinical examination The patient was healthy overall but seemed anxious ination revealed extensive tooth wear. A hairline frac- because of the pain. His medical history was noncon- ture was present in the maxillary right second molar. tributory, and he reported no use of medications. A The maxillary right first premolar and second molars musculoskeletal examination revealed no abnormali- were slightly sensitive to bite testing but not to percus- ties. During the intraoral examination, the maxillary left sion or thermal stimulation. EPT showed hyposensitiv- lateral incisor was sensitive to palpation but was with- ity in the maxillary right premolar and no response in out cracks or decay. After finger palpation was per- the second molar. A dental radiograph showed a root formed, the patient reported sensitization of the entire canal filling in the maxillary right first molar, but no facial region. He thus declined all intraoral tests, includ- cracks or decay were found from the maxillary first pre- ing thermal testing and an EPT. A dental radiograph molar through the second molar (Fig 3). CTS and possi- revealed no abnormal findings (Fig 4a). ble short-lasting, unilateral, neuralgiform headache with conjunctival tearing (SUNCT) were considered in Treatment the differential diagnosis, because of the pain duration, A differential diagnosis of pulpitis was made, secondary intensity, frequency, and location. A diagnostic anes- to traumatic occlusion, and possible CH. Initial treat- thetic block eliminated the pain. The patient was there- ment was conservative: an oral appliance to prevent fore referred back to the general practitioner for treat- and diclofenac, 75 mg/day, for 3 days. ment of odontogenic pain, which prevented direct The tooth pain was relieved by these treatments. How- monitoring of his symptoms. However, the records of ever, the patient returned with a crack and abscess in the general practitioner indicate that CTS with partial the maxillary left central incisor 1 week later (Fig 4b). pulp necrosis was observed during subsequent RCT for Dental radiographs showed a radiolucency involving the maxillary right first premolar and second molar. He that tooth (Fig 4c), and the patient was referred to the has been followed for 5 years since the RCT and is pain- endodontic department, where RCT was performed. He free. has been followed for 3 years and is pain-free.

Case 4 DISCUSSION A 38-year-old man presented with a chief complaint of left facial pain. Approximately 1 month before being CTS usually affects adults aged 30 to 50 years, although evaluated at the orofacial pain clinic, the patient had some studies report that CTS is more prevalent among

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Fig 4a A dental radiograph Fig 4b A photograph showing incomplete fracture of the max- Fig 4c A dental radiograph showing no cracks or decay in illary left central incisor (arrows). showing a radiolucency involv- the maxillary left central incisor. ing the maxillary left central incisor (arrows).

middle-aged and older adults.1 CTS may be associated mal tests.17 However, in cases of pulp necrosis in trau- with reduced elasticity of dentin and supporting tis- matized teeth, thermal pulp vitality testing with heat sues, which usually worsens with aging.11,12 Addition- and cold, electrical tests, and bite tests are not com- ally, some evidence suggests that more and larger res- pletely reliable.18,19 The diagnostic criteria for pulpal torations and occlusal parafunction are associated with necrosis in traumatized teeth have not been standard- CTS development.13 Other habits, particularly ice chew- ized. Therefore, diagnostic anesthetic blocking can be ing, eating hard candy, and even gum chewing might extremely valuable in determining the source of tooth also be contributory. pain. The second and third cases presented here did Parafunctional occlusal habits increase the likeli- not exhibit typical features for vitality tests or abnormal hood of . CTS or pulp canal oblit- radiolucencies, even though the patients had CTS. eration from occlusal trauma may lead to pulp necrosis Diagnostic anesthetic blocking indicated odontogenic due to rupture of the nerve and blood supply to the pain, which was confi rmed by subsequent endodontic pulp, thereby allowing a route for bacteria to gain access to the teeth. access to the pulp. All the present patients originally TACs are classifi ed based on well-defi ned criteria for had oral habits such as grinding or clenching of the location, attack frequency, duration, and accompany- teeth, and these pathologic occlusal habits may have ing signs and symptoms.10 Standard diagnostic features caused CTS, resulting in pulp necrosis or irreversible of TACs include episodic pain that is unilateral, pulsa- pulpitis.14 tile, or sharp, severe in intensity, and awakening, and is Marked infl ammation and pulp necrosis are fre- accompanied by autonomic phenomena such as tear- quent fi ndings in patients with moderate to severe ing and rhinorrhea.20-22 CH and PH are usually located in dental pain. The severity and duration of pain appear to the periorbital region or in the center of the face. CH be related to the status of pulp. A previous study sug- may cause strong intraoral pain that mimics pulpitis.21 gested that severe pain is most frequent when the his- Previous studies reported that pain symptoms with tologic diagnosis is chronic partial pulpitis.15,16 Pain is CTS mimic other conditions, including sinusitis, less intense when the histologic diagnosis is total pulp temporomandibular joint disorders, headache, ear necrosis. pain, , and atypical orofacial pain.9 In general, CTS can be readily identifi ed by conven- CTS symptoms vary in relation to pulp stage.23 Pulpitis tional test procedures such as EPT, bite tests, and ther- with CTS may result in pain of atypical intensity, fre-

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Table 1 Differentiating features of trigeminal autonomic cephalalgias and cracked tooth syndrome in vital teeth

Features Cluster headache Paroxysmal hemicrania SUNCT/SUNA Hemicrania continua Cracked tooth syndrome Sex 3M, 1F 1M, 2F 1.5M, 1F 1M, 1.6F 1M, 2F Age (years) 20–40 30 40–70 50 30–50 Sharp/stabbing/ Sharp/stabbing/ Electrical/ Sharp/stabbing/ Quality Throbbing/constant throbbing throbbing stabbing throbbing Severity Very severe Very severe Severe Moderate to severe Moderate to severe Pain Distribution V1>C2>V2>V3 V1>C2>V2>V3 V1>C2>V2>V3 V1>C2>V2>V3 V2>V3>V1 Duration 15–180 min 2–30 min 1–600 sec NA Seconds to all day Continuous with Frequency 1–8/day 5–10/day 3–100/day Inconsistent exacerbations Autonomic Yes Yes Yes Yes No Awakening pain Yes Yes No Yes Yes

C, cervical; SUNA, short-lasting neuralgiform headache attacks with cranial autonomic features; SUNCT, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing; V, trigeminal.

quency, or duration, and continuous pain may be peri- or severe unilateral head pain, with orbital, supraor- odically exacerbated for short (minutes) or long (hours) bital, temporal, and/or other trigeminal distribution, periods.24 lasting for 1 to 600 seconds and manifesting as one or TACs are distinguished by their attack duration and a series of stabs or a saw-tooth pattern. The findings for frequency and by response to treatment.10 CH is char- Case 3 were very similar to these criteria: pain persist- acterized by severe or very severe unilateral orbital, ing for 120 to 300 seconds and a stabbing quality in the supraorbital, and/or temporal pain persisting for 15 to maxillary right molars that occasionally radiated to the 180 minutes. CH attacks have a frequency of 1 to 8 orbital and periorbital regions. In addition, the pain was times per day for most of the time the disorder is active. awakening, as in Cases 2 and 3. A fractured or cracked The findings for Cases 1 and 4 were consistent with CH; tooth caused from biting down on something hard or a namely, short attack duration, frequent recurrence, blow to the tooth that moves the nerve within the excruciating intensity, and pulsatile pain quality. As socket can also result in pulpitis. Pulpitis pain can also compared with CH, PH is characterized by shorter but be exacerbated by bending over or lying down. Some- more frequent attacks; specifically, severe unilateral times, the pain is so severe that it awakens the person orbital, supraorbital, and/or temporal pain lasting 2 to at night and prevents further sleep. The short duration 30 minutes, with a frequency greater than five per day of attacks and the frequency, excruciating intensity, most of the time. PH also has an absolute response to and pulsatile pain quality contribute to misdiagnosis indomethacin, which is diagnostic and characteristi- (Table 1). cally long-lasting. PH may be mistaken for dental pulpi- A flowchart was developed to differentiate CTS tis. It sometimes manifests in the maxillary region, from TACs (Fig 5). If a patient presents to a dental prac- increasing the likelihood of being misdiagnosed as titioner with a chief complaint of short-lasting unilat- tooth pain.20 The symptoms of Case 2 resembled the eral orofacial pain and headache, other possible dental pain quality, duration, and location of PH, but indo- conditions, such as pulpal pathology and dental hyper- methacin did not provide significant relief. sensitivity, should be ruled out with the appropriate SUNCT is the shortest of the TACs mentioned here testing. Dental pathology should be investigated first (Table 1). It is described in the ICHD-3-beta as moderate because dental structures are the most common

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Short-lasting unilateral orofacial pain and/or headache

Exclude other dental pathology (pulpal pathology, dental hypersensitivity, etc)

Exclude other pain conditions (neuropathic, sinus-related, intercranial pathology, psychogenic, etc)

Likely CTS Possible CTS Possible TAC Likely TAC

Electrical quality? Involves C2? Ipsilateral autonomic features?

No Yes

Dental restoration on aff ected side?

Yes No

Diagnostic anesthetic injection Complete Partial relief Partial relief No relief relief Indomethacin regimen trial No Partial relief Partial relief Complete relief relief (HC, PH)

Final diagnosis based on above fi ndings

Fig 5 Flowchart for diagnosis of a chief complaint of short-lasting unilateral orofacial pain and headache.

causes of orofacial pain,25 and because dental condi- After all dental pathology and other pain conditions tions can usually be quickly and defi nitively identifi ed have been excluded, CTS and TACs can be more carefully by visual fi ndings or standardized tests. If no dental considered. The presence of an electrical pain quality pathology (excepting possible CTS) is seen, other pain and/or involvement of the C2 dermatome are not essen- conditions that cause short-lasting unilateral orofacial tial for a TAC diagnosis, but their presence is highly indic- pain and headache should then be ruled out. Such ative of TACs (assuming neuropathic pain has been ruled conditions include trigeminal neuralgia, herpetic neur- out in the previous step) and unusual for CTS. Ipsilateral algia, sinusitis, intracranial bleeds and tumors, and autonomic features are a requirement for a TAC diagno- multiple sclerosis. Psychogenic pain is also a possibility, sis. Any autonomic features in CTS would be coinciden- but is very rare.26 It can usually be excluded relatively tal. Dental restorations increase the likelihood of CTS. early in the diagnostic process, if the pain appears to However, the vast majority of restored teeth do not crack, be reasonably consistent with one or more known and CTS can occur in virgin teeth,6,7 so their presence or physical pain conditions. If it is not ruled out early, it absence is not conclusive evidence of CTS or TACs. should only be diagnosed (by a qualifi ed specialist) A diagnostic anesthetic injection should then be after the remaining diagnostic process in Fig 5 is com- performed. Again, assuming that all conditions but CTS pleted. and TACs have already been ruled out in the previous

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steps, CTS should be completely eliminated by anes- REFERENCES thesia, and a TAC should be completely unaffected by 1. Cameron CE. The cracked tooth syndrome: additional findings. J Am Dent it. However, a partial response might be observed. The Assoc 1976;93:971–975. 2. Homewood CI. Cracked tooth syndrome: incidence, clinical findings and placebo effect can result in a report of partial anesthe- treatment. Aust Dent J 1998;43:217–222. sia in a TAC patient. In contrast, central sensitization 3. Christensen GJ. Tooth sensitivity related to Class I and II resin restorations. J Am Dent Assoc 1996;127:497–498. from chronic CTS can prevent complete anesthesia. 4. Brannstrom M. The hydrodynamic theory of dentinal pain: sensation in prep- While very useful when a patient presents with pain at arations, caries, and the dentinal crack syndrome. J Endod 1986;12:453–457. 5. Opdam NJ, Roeters JM. 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