| Key Points |
 Pain in the oral cavity and adjacent craniofacial structures (both acute and chronic) is a common complaint in both healthy and medically complex patients. |
 Diagnosis of oral pain can be complicated by referred or radiating pain and by the proximity of multiple afferent nerve fibers. |
 Even though painful conditions of various etiologies may overlap, typically there are distinguishing features that will direct the clinician to the correct diagnosis. |
 Dental and periodontal pains generally have an infectious/inflammatory etiology but in rare instances may be due to systemic or extraoral causes. |
 Mucosal (soft tissue) oral pain has a more varied etiology, with viral, fungal, autoimmune, and iatrogenic causes predominating. |
Toothaches may occasionally confound the clinician during the diagnostic process, as tooth pain can be caused by dental disease or can arise in other tissues and be referred from other sources. Dental pathology may also refer pain to other teeth or distant locations in the head, neck, and jaws, which can mimic other types of facial pain. In addition, regional pain from adjacent structures, other orofacial pain disorders, and distant disease, such as central nervous system (CNS) lesions (eg, tumors), may refer pain to teeth and mimic the symptoms of toothache. Whereas most dental pain can be easily located, the clinician must be aware of these other possibilities, which become more likely with intractable symptoms.
As a first step, the clinician must determine if the pain is truly odontogenic in origin. If it can be attributed to dental disease, it is then necessary to determine if the pain is of pulpal or periodontal origin. (Nonodontogenic sources of pain that may mimic toothache are reviewed at the end of this chapter, and the codes from The International Classification of Diseases, Tenth (ICD-10) and Ninth (ICD-9) Editions are presented for each disorder throughout the chapter.) Pulpal and periodontal pains have characteristics that are similar but often unique enough to distinguish them from each other.
Pulpal pain (ICD-10 K04.0; ICD-9 522.0)
The dental pulp is a visceral tissue, and pain that originates there has characteristics similar to other types of visceral pain: deep, dull, or aching pain that is of a threshold nature and may sometimes be difficult to localize.1
Pulpal pain can arise only from vital teeth with functioning nerves. In these teeth, pain may arise from reversible or irreversible inflammation of the tissue (pulpitis).
Reversible pulpitis
Reversible pulpitis is characterized by a quick, sharp, hypersensitive response that subsides seconds after the stimulus is removed. The pain must be provoked and does not occur spontaneously. Irritants such as sugary foods or drinks or caries may cause focal stimulation that produces a brief pain.2 It is worth noting that pain from reversible pulpitis is a condition, not a disease process.
Irreversible pulpitis
Irreversible pulpitis is characterized by prolonged pain, either spontaneous or provoked by a stimulus. This type of pain tends to be variable and may be intermittent or continuous, moderate or severe, sharp or dull, localized or diffuse, and affected by the time of day or body position. The intensity of the pain may also vary over time, and the tooth may go through asymptomatic periods. Pulpal inflammation is typically more severe and more widespread than in reversible pulpitis; it may progress to pulpal necrosis.2
Nonvital tooth pain
Pulpal necrosis (ICD-10 K04.1; ICD-9 522.1)
results from untreated irreversible pulpitis, traumatic injury, or other events that cause long-term interruption of the blood supply to the tissue. Pulpal necrosis may be partial or total. Partial necrosis may present some of the symptoms associated with irreversible pulpitis, which is common in multirooted teeth. Total necrosis is asymptomatic as long as no other disease process (ie, infection) affects the adjacent innervated tissues.2 If pulpal disease extends beyond the apex of the tooth, pain becomes both spontaneous and continuous and can be exacerbated by percussion but not by temperature changes.
Etiology of pulpal pain
Tooth sensitivity may occur when dentinal tubules are exposed to the oral environment.3 Attrition (ICD-10 K03.0; ICD-9 521.1), abrasion (ICD-10 K03.1; ICD-9 521.2), abfraction, erosion (ICD-10 K03.2; ICD-9 521.3), dental caries (ICD-10 K02.9; ICD-9 521.0), gingival recession (ICD-10 K06.0; ICD-9 523.2), toothbrush trauma, periodontal diseases (ICD-10 K05.30; ICD-9 523.4), or periodontal surgery may expose coronal and/or radicular dentin. The factors leading to acute pulpal pain can be grouped into three general categories: bacterial, traumatic, and iatrogenic.
Bacterial. Bacteria or their metabolic byproducts are introduced into the pulp as a result of dental caries,4 fractures,5–7 anomalous tracts8 from the periodontium,9 or from the systemic blood supply (retrograde infection).10
Traumatic (ICD-10 K03.81; ICD-9 521.81). Direct trauma to a tooth can cause pulpitis, acute pulpalgia, incomplete fracture,6 or complete fracture with exposure of dentin or the pulp.5,6 Trauma may subluxate or completely avulse a tooth, with consequent disruption of the apical blood supply and subsequent pulpitis or necrosis.11 Repeated microtrauma, such as chronic awake or sleep bruxism, may also cause pulpal inflammation or impact the blood flow to the pulp, which may lead to necrosis.
Iatrogenic. The process of restoring teeth may cause pulpitis and acute pulpalgia. Heat and vibration from dental procedures, depth of preparation, dehydration of dentin, insertion of pin-retained restorations, and accidental pulp exposure have been well documented. Pulpal changes have also been reported following impressions in which bacteria were forced through the dentinal tubules. Furthermore, many materials and chemicals used in dentistry have the potential to irritate or injure the pulp.
Pathophysiology of pulpal pain
Myelinated (Aδ) and unmyelinated (C) afferent nerve fibers innervate the dental pulp. The Aδ fibers arborize in the coronal part of the tooth, just below the odontoblasts, where they lose their myelin sheath and form the plexus of Raschkow.12 This plexus sends free nerve endings onto and through the odontoblastic cell layer, where they contact the odontoblastic processes at the pulpal end of the dentinal tubules.13 The intimate association of Aδ fibers with the odontoblast is referred to as the pulpodentinal complex.14 If the cellular or fluid contents of the dentinal tubules are sufficiently disturbed to involve the odontoblastic cell layer, the Aδ fibers become excited.15–17 These nociceptive signals are perceived as sharp (bright), momentary pain that resolves when the stimulus is removed.14 If an external irritant is of significant magnitude to cause pulpal inflammation, a vascular response (hyperemia) can lead to an increase in tissue pressure (perceived as pain), which increases as inflammation increases.18
A tooth with localized inflammation can also produce Aδ fiber pain with other types of excitation. Inflammatory mediators, such as bradykinin, 5-hydroxytryptamine (5-HT, also known as serotonin), and prostaglandin E2, can sensitize the Aδ fibers, heightening their response to stimulants. As exaggerated Aδ fiber pain subsides, a dull, throbbing ache remains, associated with inflammatory involvement of nociceptive C fibers.14 This type of pain occurs with more severe tissue injury and is modulated by chronic inflammatory mediators, vascular changes in blood volume and blood flow, and increases in tissue pressure. When C-fiber pain dominates over Aδ fiber pain, the symptom is more diffuse and poorly localized and may be referred to other sites. C-fiber pain typically signifies irreversible tissue damage as the inflammation increases.14 Pain may begin as a short, lingering discomfort, which can escalate to intense, prolonged episodes or constant, throbbing pain. When a caries lesion contacts the pulp, the cellular inflammatory response changes from mostly mononuclear to polymorphonuclear leukocytes, resulting in microabscesses within the inflammatory lesion,19,20 and pulpitis becomes irreversible.21 Complete necrosis of the pulp may occur rapidly, or it may take years to develop; this process may be associated with significant pain, or it may occur painlessly.
Clinical characteristics of pulpal pain
Pulpal pain usually presents as a visceral, deep, dull, aching sensation.22 This pain may be superimposed with pulsing and throbbing, or it may be sharp, burning, and lancinating, due to local nerve sensitization rather than to vascular or neuropathic mechanisms.
Clinical symptoms correlate poorly with the histologic status of the pulp.23–25 Pain that is severe may be associated with early histopathologic changes. Conversely, a tooth that is asymptomatic may be necrotic. Pulpal pain can be modified by many factors including heat and cold, pressure from occlusal contact, head position, and the intensity of the offending stimulus. In addition, pain perception is complex, affected by pain signaling, the patient’s emotional state, and the patient’s sociocultural background.1,22
When the pain is referred, it tends to follow a laminated segmental pattern within the trigeminal system. Maxillary teeth commonly refer pain to maxillary and mandibular teeth on the same side and to cutaneous locations on the face superior to the maxillary teeth; mandibular teeth tend to refer pain to maxillary and mandibular teeth on the same side. Anterior teeth may refer pain to both sides of the face.26–28 Cutaneous referral patterns start at the level of the ear and project to locations on the face inferior to the ear.
Differential diagnosis of pulpal pain
The first step in the diagnostic process is to determine whether the patient with a toothache is experiencing pain from an odontogenic or a nonodontogenic source. The tooth causing the odontogenic pain is usually identified by the presence of pathology to explain the pain (eg, caries or large restoration combined with historical, clinical, and radiographic findings).22 When a suspicious tooth is located, diagnosis may be confirmed by increased pain on application of noxious stimulation (chemical, thermal, mechanical, or electrical sources). If pain can be influenced by local irritation, the tooth should be anesthetized to determine if pain is blocked. If local anesthesia has no effect, pain from a nonodontogenic source should be considered. If administration of anesthesia decreases but does not eliminate the pain, there may be an additional nonanesthetized contributor to the pain. Once a conclusion regarding the source has been reached, the next step is to determine if the pain is pulpal or periodontal in origin.
Pain of pulpal origin tends to respond to a stimulus at a given threshold and may be difficult to localize. Teeth that have only pulpal involvement are generally not sensitive to percussion. Teeth that have periodontal and/ or periapical involvement typically respond to percussion/pressure on a graduated basis, and the pain is easier to localize.22
Reversible pulpitis is characterized by stimulated pain of brief duration that ceases seconds after removal of the stimulus. Cold and electrical stimulation provoke a brief response, and sensitivity to percussion is uncommon.29
Irreversible pulpitis is characterized by stimulated pain of prolonged duration and/or by spontaneous pain. There may be no sensitivity to percussion until the inflammatory process extends to the periapex.29
A necrotic pulp is asymptomatic until it becomes infected and inflammation extends to periapical tissues. The tooth is not responsive to either cold or electrical pulp testing; however, there may be extreme sensitivity to percussion if the periapex is inflamed.29
Management considerations for pulpal pain
Treatment for dentin sensitivity is directed at reducing fluid movement in the dentinal tubules. Treatment modalities include30–32: (1) formation of a smear layer on the sensitive dentin by burnishing the exposed surface; (2) application of agents such as oxalate compounds that form insoluble precipitates within the tubules; (3) impregnation of the tubules with plastic resins; and (4) application of dentin bonding agents to seal the tubules.
Treatment for reversible pulpitis targets removal of the pain-causing stimulus, such as caries, and restoration of lost tooth structures. Treatment of irreversible pulpitis or a necrotic pulp requires root canal treatment or extraction of the tooth. Systemic antibiotics are contraindicated when disease is localized to the pulp. A necrotic pulp is devoid of blood circulation; hence, no systemic medication will penetrate the space.
Acute periodontal pain
The periodontium (periodontal ligament and alveolar bone) is of mesenchymal origin. Hence, periodontal pain tends to be more localized in comparison with visceral pain of pulpal origin. Localization of the source of pain is attributed to the proprioceptive and mechanoreceptive sensation of the periodontium.33 Periodontal pain is generally dull and aching. Inflammatory fluid may cause displacement of the tooth in the socket, with a resulting acute malocclusion and typical localization of the pain with biting or chewing. The diseased site readily responds to provocation proportionate to the stimulus.1 At minimal levels of stimulation, the patient may describe an innocuous sensation such as itching or moderate dull aching; at severe levels, the patient may describe unrelenting, aching, and throbbing pain.
Factors that may increase periodontal pain include occlusal contact, head position, the intensity of the stimulus, and CNS modulation.
Periodontal pain, like pulpal pain, may stimulate secondary central excitatory activity, resulting in regional pain referral around the head and neck, muscle overload with the potential to develop myofascial trigger points, and autonomic effects, such as sinus congestion, conjunctival injection, and puffy eyelids. Sites of prior pain are more likely to be sites of referred pain.
Periodontal pain localized to a single tooth is usually associated with a gingival/periodontal abscess or a combined periodontal-endodontic lesion.34
Gingival abscess (ICD-10 K05.00; ICD-9 523.0)
Clinical characteristics. The gingival abscess is a relatively rare entity. It usually arises as the result of trauma to previously healthy tissue and is confined to the marginal gingiva. It presents as a painful, possibly fluctuant swelling. The surface may be erythematous, smooth, and shiny. Spontaneous drainage is common.35
Etiology. The precipitating cause of a gingival abscess is usually trauma followed by infection.
Pathophysiology. The gingival abscess consists of a purulent focus in the connective tissue surrounded by an inflammatory infiltrate.
Management considerations. Treatment is by incision and drainage followed by oral rinses with warm saline and may require removal of the causative agent. On rare occasions, irrigation and debridement of the soft tissue lesion may be required.
Periodontal abscess (ICD-10 K05.20; ICD-9 523.3)
Clinical characteristics. Periodontal abscesses arise as acute or recurrent inflammatory swellings in periodontally diseased dental sites. The typical periodontal abscess is a localized swelling of the gingiva and/or the alveolar mucosa. These lesions often have an erythematous, violaceous, or cyanotic appearance and may be fluctuant.36,37 Pain is variable and can range from a deep ache of low intensity to severe discomfort. The pain is often exacerbated by chewing and percussion. The affected tooth may be mobile and may be slightly extruded. In more severe cases, cellulitis and systemic symptoms with lymphadenopathy, fever, and malaise may occur.38 Suppuration may be noted from the pocket orifice. The tooth is usually vital.38
Etiology. The infectious cause of the lesion is the periodontal microbial flora, which is usually composed of pathogens such as Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, Peptostreptococcus micros, and Bacteroides forsythus.39–41 It may arise from chronic periodontitis that cannot drain into the periodontal pocket42 or from trauma or extension of pulpal inflammation into the periapical tissues.29 A lateral pulp canal may also cause an abscess in the periodontal space, which technically is not a periodontal abscess and requires root canal treatment.
Pathophysiology. A periodontal abscess is usually an exacerbation of a preexisting chronic periodontal condition. More than 300 species of microorganisms have been isolated from periodontal pockets, but only a small number are considered pathogenic.43
Most of the tissue destruction found in established periodontal lesions is a result of the mobilization of the host immunity via activation of monocytes, lymphocytes, fibroblasts, and other host cells. Engagement of these cellular elements by bacterial factors, in particular bacterial lipopolysaccharide, is thought to stimulate production of both catabolic cytokines and inflammatory mediators, including arachidonic acid metabolites such as prostaglandin E2. Cytokines stimulate inflammatory responses that cause tissue destruction via activation of tissue metalloproteinases, a major pathway for connective tissue attachment loss and bone loss in most forms of periodontitis.44,45
Management considerations. Treatment consists of establishing drainage (usually through the pocket orifice) and debridement of the root surface and pocket wall under local anesthesia, accompanied by copious irrigation. Occlusal adjustment is sometimes indicated. Unless the tooth is beyond salvage, it is usually prudent to resolve the symptoms and then reassess the periodontal status. The endodontic status (vitality) of the tooth should also be determined.
Periradicular (periapical) abscess (ICD-10 K04.7; ICD-9 522.5)
Clinical characteristics. Pulpal infection may induce an inflammatory reaction that may lead to periradicular abscess formation. Clinical characteristics include rapid onset, spontaneous pain, acute response to percussion, purulence, and swelling.2 It must be distinguished from the periodontal abscess, although both processes may be operant in the case of a combined periodontal-endodontic lesion. One helpful element for differentiation is that the periodontal abscess occurs in a setting of periodontal attachment loss and pocket formation.
The initial pain associated with a radicular abscess is intense when confined to bone, and it subsides following formation of a fistulous tract (drainage) into the soft tissues. The infection may spread along fascial planes and can result in cellulitis. In addition, bacteremia may occur, resulting in systemic infection. If the infection localizes, it may progress to a fluctuant swelling that eventually drains.
Etiology. A periradicular abscess usually develops from a necrotic pulp that becomes infected, with spread of the infection into the periradicular tissues.14 Occasionally, it may develop from exacerbation of chronic periodontitis located near the tooth apex (phoenix abscess).
Pathophysiology. The periradicular abscess is initiated by infiltration of bacteria into the apical periodontal ligament from an infection in the pulp, causing an acute inflammatory reaction.
Management considerations. Management involves treating the cause of the abscess, endodontics, or extraction of the offending tooth. Spread of the infection may require drainage of exudates and/or systemic antibiotics.
Pericoronitis (ICD-10 K05.20; ICD-9 523.3)
Clinical characteristics. Pericoronitis is a localized infection within the soft tissue that surrounds the crown of an impacted or partially erupted tooth, most commonly a third molar. Clinical features may include an erythematous, swollen, suppurating gingival lesion that is tender and may cause radiating pain to the ear, throat, and floor of the mouth. The patient may experience a bad taste and an inability to open or fully close the jaws. Swelling of the cheek in the region of the angle of the jaw and lymphadenopathy are common. The patient may also experience signs and symptoms of systemic complications, such as fever, leukocytosis, and malaise.36,38
Etiology. The typical process involves bacterial colonization of the pericoronal space, which triggers inflammation. Food debris or foreign objects may also become lodged under the gingival tissue covering the crown, thereby contributing to the inflammatory process.
Pathophysiology. Streptococci are common in the oral cavity and can produce hyaluronidase, which makes these organisms the typical cause of pericoronitis. Cellulitis may follow the spread of the infection posteriorly into the oropharyngeal area and medially to the base of the tongue, making it difficult for the patient to swallow. Depending on the severity of the infection, lymph node involvement of the submandibular, posterior cervical, deep cervical, and retropharyngeal regions may occur.46,47
Management considerations. An irrigating syringe should be used to perform lavage under the gingiva with sterile saline or chlorhexidine solution. Removal of the tooth is generally indicated when the acute episode has resolved. Removal of the operculum is sometimes advocated in lieu of extraction; however, the soft tissue frequently regrows, resulting in the same local conditions that lead to infection. Abscess formation is common and leads to the need for surgical drainage and appropriate antibiotic therapy. Patients presenting with trismus, fever greater than 101°F, and facial swelling are candidates for referral to an oral and maxillofacial surgeon.48 Cellulitis that extends along fascial planes to involve other anatomical spaces requires aggressive treatment due to the potential for morbidity and, rarely, mortality.
Combined periodontal-endodontic lesions
These lesions may be of primary pulpal origin or of periodontal origin.49 They may occur in a patient with preexisting periodontitis or in a setting of relative periodontal health. If the lesion is primarily endodontic in origin, root canal treatment alone may lead to resolution; however, this can only occur if the lesion is of recent onset.
Clinical characteristics. The clinical presentation includes pain on pressure and percussion, increased tooth mobility, probing depth/attachment loss, and swelling of the marginal gingiva, simulating a periodontal abscess. The suppurative process may cause the formation of a narrow, deep pocket that may be traced to the apex with a gutta-percha cone or a periodontal probe. Pulp testing is negative, or, in a multirooted tooth, it may show an abnormal response.50 All these signs, including radiographic findings, are somewhat variable.
Etiology and pathophysiology. The etiology and pathophysiologic processes are detailed in the previous sections on periodontal and periradicular abscesses.
Management considerations. The periodontal component of the combined lesion may resolve subsequent to endodontic therapy, and therefore it is preferable to perform the endodontic therapy first and allow for a suitable period of healing. If the periodontal lesion persists, further treatment will be required.51
Pulpal and periodontal pain secondary to fractured teeth
Tooth fractures occur in approximately 5% of adults annually.52 In most cases, the fracture of a cusp or split tooth is readily diagnosed. Surface cracks, or craze lines, are considered incomplete tooth fractures. These incomplete fractures are usually asymptomatic, but, when painful, they may be due to cracked tooth syndrome, which can be difficult to diagnose.2
Clinical characteristics. Patients with a cracked tooth may have complaints of sporadic, sharp, momentary pain upon biting or releasing, along with occasional pain from cold stimuli. Sometimes patients may indicate that the pain occurs minutes after chewing.2 In contrast with other tooth-related pains, the pain of a cracked tooth is usually easily located.53
Etiology. A fracture rarely occurs in teeth that have no or small restorations and are caries free.54,55 Predisposing factors include loss of support due to caries or large restorations, inadequate cusp protection by restorations,56–58 developmental weaknesses of the tooth,55 a history of local trauma, and clenching or bruxing habits.
Pathophysiology. The pain associated with a cracked tooth occurs when occlusal forces spread portions of the crown, exposing the underlying dentin. Momentary hydrostatic movement of fluid within the dentinal tubules causes pain.
Differential diagnosis. The diagnosis of a cracked tooth is usually made from history and clinical tests. Generally, percussion, palpation, mobility, and probing are within normal limits if the crack is confined to the crown. The most useful test is biting on successive cusps with a firm object, such as a wood stick or Tooth Slooth (Professional Results), until the pain is reproduced. Staining and transillumination may also disclose subtle fractures. Electrical pulp testing will produce normal responses unless the pulp is involved. Cold testing may be productive, whereas heat may not be helpful. Fracture lines are not visible on radiographs when they run mesiodistally and are not in the plane of the x-ray beam.2,53
If the fracture extends into the root, a periodontal defect may be observed adjacent to the fracture. At this point, the pulp may have become necrotic. Sharp pain and cold sensitivity are not common. Typically, a dull ache on biting might be present when the periodontal ligament is inflamed, resulting in tenderness with percussion.14
Management considerations. Early detection of cracked teeth is essential,55–58 and therapy depends on the severity of symptoms and location of the crack. Temporary stabilization can be achieved with an orthodontic stainless steel band or a temporary crown until an overlay or full crown can be fabricated.53 Endodontic treatment with or without stabilization has been advocated.54,57,59 In cases with extensive cracks, extraction may be necessary.2
Systemic factors associated with dental infection
Systemic conditions that may modify host response to infection include diabetes, anemia, diseases causing altered neutrophil count and function, immunosuppression (pathologic or medically induced), tobacco use, nutrient and caloric deficiencies, hormone abnormalities, and emotional stress.60–63
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