7.4 Preventing PTTN

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An Overview ofChronic Neuropathic Orofacial Pain

7.3 Risk Factors forPTTN

• Preoperative phase (specic to the patient): psychosocial factors, genetic/pain modulatory mechanisms, comorbidities like sleep disorders

• Intraoperative phase: surgical or procedural technique, associated nerve/tissue injury, and analgesic regimens

• Postoperative phase: patient’s coping ability, postoperative pain intensity

7.4 Preventing PTTN

Some strategies that can be employed to prevent PTTN include providing preemptive analgesia to reduce discomfort and heightened pain perception, selecting an alternative surgical approach that can minimize tissue damage and nerve injury, providing adequate local or regional anesthesia, and adequate postoperative analgesics to ensure minimal to no perioperative pain.

7.5 Management ofPTTN

Patient education is crucial to the successful management of PTTN.Informing the patient of the condition and the likely etiology and clear communication of the prognosis and various management strategies available help the patient understand that less than a 100% pain relief is an expected outcome.

Pharmacotherapy includes using tricyclic

antidepressants like amitriptyline, serotonin norepinephrine reuptake inhibitors like duloxetine, or anticonvulsants like gabapentin as rst-line therapy. Topical medications delivered using neurosensory stents for intraoral PTTN have been reported.

PTTN is a chronic, persistent neuropathic

pain condition requiring long-term management. There are reports of its association with an increased risk for development of depression. As such, employing multiple modalities for its management including cognitive behavioral

therapy (CBT), acupuncture, physical therapy, and psychosocial interventions has been recommended.

8 Continuous Neuropathic

Orofacial Pain

8.1 Persistent Idiopathic Dentoalveolar Pain

Previously used terms: atypical odontalgia, persistent idiopathic facial pain

Persistent idiopathic dentoalveolar pain is a continuous type of chronic orofacial pain localized to a dentoalveolar area that is frequently misdiagnosed, leading to incorrect and unnecessary dental treatments aimed at reliving the patient’s “dental” pain. This type of persistent, chronic pain is not attributable to any other disorder, and that is why the term “idiopathic” is used which refers to a condition or disorder that “arises spontaneously or from an obscure or unknown cause.” Diagnosis is made after history, exam, and radiographic assessment fail to identify a cause for the pain. The likely pathologic mechanism is thought to be short-circuiting or a dysfunction of nerves that carry pain sensations from the teeth and jaws.

The 2020 International Classication of Orofacial Pain (ICOP 6.3) denes persistent idiopathic dentoalveolar pain (PIDP) as a “persistent unilateral intraoral dentoalveolar pain, rarely occurring at multiple sites, with variable features but recurring daily for more than 2hours per day for more than 3 months, in the absence of any preceding causative agent.”

8.2 Diagnostic Criteria

A. Intraoral dentoalveolar pain fullling criteria

B and C (below).

B. Recurring daily for more than 2h/day and for

more than 3months.

C. Pain has both of the following

characteristics:

R. Shekar

1. Localized to a dentoalveolar site (tooth or alveolar bone)

2. Deep, dull, pressure-like quality

D. Clinical and radiographic examinations are

normal, and local causes have been excluded.

E. Not better accounted for by another ICOP or

International Classication of Headache Disorders- 3 (ICHD-3) diagnosis.

However, persistent idiopathic dentoalveolar pain is a diagnosis of exclusion based on an observational study that found that patients with persistent idiopathic dentoalveolar pain shared a few common features including the following:

• Most patients reported no nocturnal awaken-

ing due to the pain.

• The sulcus surrounding the affected tooth/

teeth being painful to light touch in a signi-

cant proportion of patients.

• Females being more commonly affected than

males.

• Pain being described as throbbing, burning,

and pulsating.

8.3 Management ofPersistent

Idiopathic Dentoalveolar Pain

The rst step in the management of PIDP is to reassure the patient that their pain is real. Often, the patient has already visited several providers who have either not offered them a diagnosis or been dismissive of their concerns. It is also important to educate the patient that the pain is not of dental origin and, therefore, they are not going to benet from any dental and/or surgical intervention.

The rst-line pharmacologic therapy is a tricyclic antidepressant such as amitriptyline. Serotonin-norepinephrine reuptake inhibitors such as duloxetine can also be employed. Alternative systemic medications include anticonvulsants/membrane stabilizers like gabapentin and pregabalin.

Psychosocial therapy techniques like cognitive behavioral therapy (CBT) are aimed at improving the patient’s management of their pain

and reducing the resultant impact on their quality of life. Clinicians should recognize that patients with persistent idiopathic dentoalveolar pain are long-term chronic pain patients and require continued support with a multidisciplinary team involving orofacial pain specialists and neurologists along with psychiatric and psychological evaluations to identify comorbidities like depression and anxiety.

8.4 Continuous Neuropathic Orofacial Pain

8.4.1 Burning Mouth Syndrome

Burning mouth syndrome is a chronic neuropathic pain condition affecting the oral mucosa in the absence of any clinically evident pathology. In most cases, symptoms are localized to the anterior two-thirds of the tongue, but other oral mucosa may be involved including the hard palate, labial and buccal mucosa, gingiva, and oor of the mouth. Patients often describe their symptoms as a painful burning sensation over these sites. Burning mouth syndrome can also present as tingling, itching, pricking, or numbness in these areas. The pain is often intractable, though often linked to a stressful or traumatic event like the loss of a family member, a divorce, or even a dental procedure. The International Headache Society denes burning mouth syndrome as “an intraoral burning or dysesthesia sensation, recurring daily for more than 2 hours per day over more than 3 months, without clinically evident causative lesions.”

The clinician is required to perform comprehensive diagnostic and laboratory tests, examining psychological, local, and systemic factors such as parafunctional habits, dysgeusia, salivary changes, nutritional deciencies, diabetes, and hormonal deciencies or imbalances. A complete blood count and panel workup, with tests for blood glucose, iron, ferritin, vitamin B12, vitamin D, and thyroid hormone/panel, should be performed and investigated. Burning mouth syndrome is a diagnosis of exclusion where a diagnosis is arrived at after all other possible causes for the burning symptoms have been eliminated

An Overview ofChronic Neuropathic Orofacial Pain

based on a comprehensive history, physical evaluation, imaging (when indicated), and specic laboratory tests.

8.5 Management

Burning mouth syndrome is a challenging condition for the clinician to manage as well as an ordeal for the patient. Having empathy for your patient and reassuring them that a diagnosis has been achieved and that it is not a malignancy or cancer, which is often what the patient is concerned about, are helpful.

A crucial step in the management of burning mouth syndrome is to have a frank conversation with the patient, setting expectations and realistic treatment goals. Inform them that treatments are symptomatic and not curative, and although complete remission is the goal, it may not always be achieved. Also, with any therapy or combination of therapies, it may take several weeks to months before maximum benets are achieved. There is no known cure for burning mouth syndrome, but some symptomatic relief may be achieved using a variety of medications.

Clonazepam (Klonopin) is a benzodiazepine agent with a long duration of action. Oral disintegrating clonazepam tablets are used at 0.5–3.0mg daily, starting with 0.5mg. One tablet is cut in half and dissolved in a glass of water. The solution is rinsed/swished in the mouth and then expectorated, starting initially once daily at night before bedtime. This regimen may be repeated three times daily depending on side effects and tolerance. Clonazepam has the potential to cause dependence and should not be prescribed to patients with a substance dependence problem. Alternative medications that can be used are amitriptyline (nortriptyline) and gabapentin. Drowsiness is a side effect of these medications, especially in the rst couple of weeks. Patients should be instructed to take the medication once daily at bedtime, initially, and not drink alcohol or drive.

Capsaicin is another medication that may be used to manage burning mouth syndrome. It is an alkaloid present in chili peppers and pepper

sauces and is the active ingredient in Zostrix. Capsaicin rinses can be formulated at home by dissolving 5–6 drops of Tabasco (R) sauce in 1 teaspoon of water and rinsing or swishing in the mouth, four times a day. The initial feeling is one of burning, but within a few minutes, some patients report that the overall burning is much reduced. However, capsaicin is not easily palatable for many patients due to the burning pain associated with its application leading to low adherence.

Alpha-lipoic acid, also known as lipoic acid, is a potent antioxidant with neuroprotective properties that has been used in the management of burning mouth syndrome. Although it is synthesized naturally, the quantities are insufcient for metabolic needs. Dietary supplements in doses of 200–600mg are available and are typically well tolerated with little or no adverse effects.

Non-pharmacologic approaches to management may be used alone or in combination with medications. Stress management/reduction, meditation, yoga, exercise, and psychotherapy are all helpful in the management of burning mouth syndrome. Patient reassurance and education are critical factors in the optimal management of burning mouth syndrome. Treatment should be multimodal and multidisciplinary to manage all aspects of this condition, with conservative options being attempted rst to minimize adverse drug reactions.

9 Summary

Although the focus of this text is the temporomandibular joint, its dysfunction, and its associated symptoms, it is critical for the treating dentist or physician to appreciate that craniofacial pain is a complex matter requiring a deep understanding of head and neck anatomy as well as an understanding of the complete differential diagnosis. Limits placed upon the potential elements of a differential diagnosis will result in a delay or failure to achieve the correct diagnosis and associated patient distress and suffering.

R. Shekar

1 Introduction

The temporomandibular joint (TMJ) stands out as a distinctive anatomical structure, being the sole diarthrodial synovial joint within the human body. It remains under constant load, even during periods of inactivity, necessitating robust biomechanical integrity to withstand the substantial mechanical stresses it encounters during its functioning.

The TMJ consists of extracapsular elements, including nerves, vessels, ligaments, and a capsule, which will not be discussed in this chapter because they are not easily visualized on TMJ imaging. The intracapsular components (Figs. 1 and 2) can be categorized into two groups: osseous elements and soft tissue

components. The osseous components encompass (1) the glenoid (mandibular) fossa and articular eminence and (2) the mandibular condyle. Cross-sectional hard tissue imaging techniques like cone beam CT (CBCT) or traditional CT are recommended to assess these osseous components effectively. CBCT is often preferred due to its lower radiation exposure. It offers the advantage of generating sub-millimetric custom cross sections from the same dataset which aids in the early detection of articular surface deterioration.

This chapter discusses the common conditions of TMJ and the radiographic methods employed to investigate potential deterioration in TMJ’s biomechanical stability. This chapter will not cover trauma, cysts, and neoplasm of TMJ.

H. Demirturk · A. Potluri (*) Department of Diagnostic Sciences, University of Pittsburgh School of Dental Medicine, Pittsburgh, PA, USA e-mail: hud25@pitt.edu

H. Demirturk and A. Potluri

Fig. 1 CBCT sagittal and coronal views demonstrate the TMJ normal anatomy. In sagittal (a) and coronal (b) planes, the bony elements appear rounded and create an irregular joint structure. In adult condyles, the outer cortex of the condylar articulation is notably thin. The marrow spaces exhibit uniformity and lack any signs of sclerosis.

In the sagittal view, the expected normal disc space should resemble the shape of a bow tie, representing the disc positioned between the joint surfaces. Meanwhile, in the coronal view, it should resemble the crescent shape of the posterior band of the disc

Imaging oftheCommon Conditions oftheTemporomandibular Joint

c d

Fig. 2 MRI axially corrected sagittal and coronal views demonstrate the TMJ normal anatomy in open and closed positions. In a closed sagittal MRI (a and c), the posterior band of the bow tie-shaped disc is positioned at the 12 o’clock position on the condyle (arrow). The intermediate zone is between the incongruent articulations, while the anterior band rests on the lateral pterygoid muscle bers. The posterior attachment (line arrow) is connected to the posterior band of the disc, and the marrow spaces exhibit low to intermediate signals on the PDWI (a and b) and

T2WI (d) and high signals on T1WI (c). The cortical outlines are continuous and uniform (a). In a coronal closed MRI (b), the posterior band of the disc takes on a crescent shape (arrow) and is positioned evenly superior to the condyle. It tapers toward the poles and attaches to the neck of the condyle with the medial and lateral collateral ligament. In an open sagittal MRI (d), the condyle translates to the crest of the articular eminence, and the disc is positioned between the crest of the eminence and the condyle. (Courtesy K.Orhan, DDS)

H. Demirturk and A. Potluri

2 Imaging Techniques

andProtocols

Various imaging techniques exist for examining the TMJ.Some traditional plain-lm techniques including transcranial, Towne, submentovertex, and lateral tomographic projections have been superseded by three-dimensional imaging methods that provide superior precision regarding tissue morphology and spatial relationships and will not be discussed in this chapter.

A. Panoramic radiography: A panoramic

radiograph can provide basic information about the osseous components of the TMJ. However, it falls short in accurately assessing the spatial relationships of the TMJ because the teeth are in a protrusive position during image capture to align both jaws within the focal trough.

B. Cone beam computed tomography

(CBCT): CBCT offers a comprehensive view encompassing not only the osseous components of the TMJ but also the impact of TMJ conditions on the entire craniofacial complex.

Evaluation of asymmetry (whether one side is enlarged or decreased in size and length), changes in growth, alterations in occlusion (bite), neck posture, and risk factors associated with sleep-disordered breathing are analyzed (Fig.3).

Imaging protocol: To assess all of the abovementioned aspects, a eld of view of at least 16cm or larger is necessary to visualize these structures and their interplay within a single volume. During imaging, the teeth should be in maximum intercuspation, and the head posture should closely mimic the natural head posture. Common standard reformations aid in the evaluation of TMJ and craniofacial complex:

• Custom cross-sectional images of the

TMJs

• Sagittal and coronal oblique sections of

the TMJs

• TMJ axial view

• Panoramic reformation

• 3D frontal and lateral reformations

• Analyses of airway morphology and

volume

Fig. 3 CBCT airway analysis, highlighting the anatomical structures and dimensions relevant to the assessment of the upper airway

Imaging oftheCommon Conditions oftheTemporomandibular Joint

C. Multidetector computed tomography

(MDCT): MDCT images can fulll the same

objective as CBCT; however, MDCT involves higher radiation exposure. Therefore, whenever CBCT is available, it should be the preferred choice as it provides the same information with lower radiation exposure for the patient. MDCT has similar imaging protocols to CBCT.

D. Magnetic resonance imaging (MRI): MRI

provides valuable information and is considered the gold standard about the state and positioning of the soft tissue components within the temporomandibular joint (see also chapter “The Neurological Aspects of the Trigeminal Cranial Complex and Its Role in the TMJ Dysfunction and Multiple Movement Disorders”).

Articular disc: The normal articular disc is clearly visible in fast spin echo sequences, appearing as a hypointense (low signal intensity) brocartilaginous biconcave structure positioned between the temporal bone and the mandibular condyle. When viewed in sagittal oblique images, the disc resembles a bow tie, where a thinner central intermediate zone connects the anterior and posterior triangular bands. Normally, in a closedmouth position, the posterior band of the disc is typically situated at approximately the 11–12 o’clock position in relation to the condyle (Fig.2). However, when the mouth opens, both the condyle and the disc translate forward beneath the articular eminence. This results in the central portion of the disc aligning over the apex of the condyle. The section of the disc positioned between the articular surfaces should constitute the junction between the anterior band and the intermediate zone. Simultaneously, the condyle should be situated inferior to the level of the articular eminence (Fig.2). In the coronal view, the posterior band of the disc should appear like a crescent positioned on top of the condyle, tapering gently toward the poles of the condyle (Fig.2).

Indications: Assessing the disc and its attachments, other soft tissues, joint effusion, soft tissue neoplasia, or neoplastic-like lesions. The

morphology of osseous components and bone marrow integrity can be evaluated. However, subtle osseous alterations indicative of early active degenerative change or joint disease are better seen with CBCT.

Common imaging protocols: T1 or proton density (PD) and T2 and/or short tau inversion recovery (STIR) in both closed-mouth (maximal intercuspal) and open-mouth positions. Crosssectional images should be acquired, including axially corrected sagittal oblique and coronal oblique sections along the long axes of the condyles and at right angles to them.

The closed-mouth position with the teeth in maximum intercuspation shows the condition and position of the disc and other soft tissues, aiding in determining disc displacement. The open-mouth position shows whether a displaced disc has been recaptured by the condyle during the opening of the jaw.

3 Imaging ofCommon TMJ

Pathological Conditions

3.1 Developmental Disturbances

ofTMJ

TMJs are not fully developed at birth, making them susceptible to developmental disturbances before and after birth. Kaneyama and colleagues have classied developmental disturbances as follows:

• Hypoplasia or aplasia of the condyle

– Congenital or primary hypoplasia or

aplasia

– Acquired or secondary hypoplasia or

aplasia

• Condylar hyperplasia

• Bid condyle

1. Condylar hypoplasia or aplasia

Condylar aplasia refers to the absence or nondevelopment of the mandibular condyle, while condylar hypoplasia indicates insufcient growth or underdevelopment of the condyle. Both aplasia and hypoplasia can

H. Demirturk and A. Potluri

manifest as congenital or acquired conditions and may affect one side or both sides (Fig.4).

Various congenital conditions associated with hypoplasia or aplasia include the Pierre Robin sequence, hemifacial macrosomia, Treacher Collins syndrome, oculo-auriculovertebral syndrome, and Hurler syndrome. In congenital cases, bilateral TMJs are often affected; however, the predominant clinical presentation may be seen as unilateral. On the other hand, acquired or secondary hypoplasia or aplasia can occur due to various factors, such as local factors that disrupt condyle development, including trauma, infections affecting the mandible or middle ear, and therapeutic radiation.

Imaging:

• Affects the condyle along with underdevel-

opment of the same-side ramus and man-

dibular body.

• Condyle is small but retains its normal

shape and morphology.

• Small mandibular fossa.

• The posterior border of the ramus and the

condylar neck may display a posterior

inclination.

• Unilateral cases are more common than

bilateral.

• Mandibular asymmetry and TMJ

dysfunction.

• Extent of resulting asymmetry varies based

on the age at which condylar growth is

affected.

• Chin frequently deviates toward the

affected side, and on opening, mandible

deviates toward the affected side.

2. Condylar hyperplasia Condylar hyperplasia is characterized by

the unilateral enlargement of the condyle (Fig. 5). While the exact cause remains unclear, some theories suggest that mild, chronic inammation may play a role, triggering a condition akin to proliferative osteomyelitis, and may stimulate condylar growth or surrounding structures. The unilateral nature strongly indicates a localized phenomenon. Obwegeser and Makek have classied condylar hyperplasia as follows:

• Type A: Hemimandibular hyperplasia, resulting in vertical plane asymmetry. This type is characterized by unilateral vertical growth with minimal chin deviation.

• Type B: Hemimandibular elongation, leading to transverse plane asymmetry. This type causes chin deviation toward the opposite side without vertical asymmetry.

• Type C: Combination of types A and B, showing hyperplastic characteristics either unilaterally or bilaterally.

• Imaging:

• Large condylar process with normal subchondral bone and cortical outline.

• Condylar process is notably larger in comparison to the dimensions of the corresponding fossa.

• Unilateral enlargement of condylar process, ascending ramus, and mandibular body on the same side.

• Osseous midline of the mandible may deviate toward the opposite side.

• Instead of being concave, ramus posterior border and mandible inferior border often exhibit a convex shape.

Fig. 4 3D volume renderings from anterior (a) and lat- eral (b) view, sagittal (c and d) and coronal (e and f) CBCT images show mandibular asymmetry associated with right condylar hypoplasia. 3D volume renderings illustrate mild mandibular asymmetry, where the right side is smaller than the left due to right condylar hypoplasia. Right condyle (c and e) is small compared to the left

(d and f) but has a normal morphology. When aligning the two sides of the skull base, orbits, and zygomas on the lateral view, the lower border of the right mandible appears higher relative to the left (b, arrow). Any alteration in the dimensions of a condyle, regardless of its underlying origin—whether developmental, degenerative, or inammatory—will lead to mandibular asymmetry

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7.4 Preventing PTTN

8.1 Persistent Idiopathic Dentoalveolar Pain

8.2 Diagnostic Criteria

8.4 Continuous Neuropathic Orofacial Pain

8.4.1 Burning Mouth Syndrome

8.5 Management

9 Summary

Suggested Readings

1 Introduction