Oral Medicine

Foundations

Anatomy, Physiology, and Pathophysiology

Humans have 20 deciduous (primary) teeth and 32 permanent (secondary) teeth, which are supported and maintained in the maxilla (upper teeth) and mandible (lower teeth) by the periodontium. The portion of the tooth that is normally visible in the mouth above the gingival margin is called the crown, whereas the lower portion is the root ( Fig. 56.1 ).

The crown of the tooth has three layers; from outside to inside they are the enamel, dentin, and pulp. The enamel is the only part of the tooth that is visible in the absence of pathology (e.g., fracture s, caries) and is a hard coating that protects the tooth. The outermost layer of the root of the tooth is the cementum, which allows for attachment of the periodontal ligament to the adjacent alveolar bone. The next layer deep to the enamel (for the crown) or the cementum (for the root) is the dentin, which is an intermediate layer that is yellow in appearance. The dentin is comprised of porous microtubules that support the enamel and act as a cushion during mastication. If the dentin is exposed by caries or trauma, the patient will have sensitive teeth or pain. The deepest layer is the pulp cavity, which houses the tooth’s neurovascular supply.

The deciduous dentition (“baby teeth”) consists of 10 mandibular and 10 maxillary teeth ( Fig. 56.2 ). The lower central incisor is the first tooth to erupt at approximately 6 months of age; all primary teeth should be present by age 3. The permanent dentition begins to erupt at approximately 6 years of age with the appearance of the first molar followed by the second molars by age 13 and ending with the third molars (“wisdom teeth”) by age 17 to 21.

The permanent dentition consists of 32 teeth; there are 8 teeth per quadrant (e.g., right upper, right lower, left upper, left lower). From the midline outward, the names of the teeth in each quadrant are the central incisor, lateral incisor, canine, two premolars (also called bicuspids ), and three molars (also called tricuspids ). The permanent dentition is numbered from 1 to 32, starting with the upper right third molar (1) and moving to the upper left third molar (16), to the lower left third molar (17), and to the lower right third molar (32). The starting point for this numbering system can be recalled by the mnemonic “upright.” It is often easier to name the tooth or teeth involved; for instance, if tooth 8 is injured, the clinician could describe the tooth as the “right maxillary central incisor” or the “right upper central incisor.” If multiple teeth are involved, numbering is more concise.

Specific terminologies are also used to describe the various tooth surfaces in the mouth. The facial (also referred to as labial or buccal) surface faces outside the oral cavity; the oral (also referred to as palatal for upper teeth, or lingual for lower teeth) surface faces the tongue; the mesial surface is toward the midline; and the distal surface is toward the ramus of the mandible. The interproximal surface refers to the contacting area of adjacent teeth, and the occlusal surface refers to the biting area. Finally, apical is in the direction of the root, whereas coronal is toward the crown of the tooth.

Tooth decay, or dental caries or cavities, is caused by the breakdown of the teeth secondary to bacteria. Bacteria generate acid as a byproduct from cellular metabolism of food left on the tooth surface, subsequently demineralizing the enamel. Once the enamel is breached, the microporous dentin can transmit saliva, byproducts of the bacteria, and the bacteria to the pulp. The pulp initially reacts with a hyperemic response, which proceeds to an inflammatory state termed pulpitis, which can be reversed. Untreated, pulpitis can further progress to total degeneration and necrosis (irreversible pulpitis).

Clinical Features

Dental caries are the most common cause of odontogenic pain. The patient may give a variable history of a sudden or gradual onset of a sharp to dull, throbbing pain. In most cases, the patient can indicate the specific tooth involved, but pain may be generalized. Early (reversible) pulpitis is sensitive to changes in temperature and pressure; irreversible pulpitis can show pain without any stimulus.

The physical examination described here is applicable to all sections of this chapter. Ideally the patient should be placed in a dental or ear, nose, and throat chair or on a bed at a 45-degree angle with adequate lighting. Pediatric patients often are examined while sitting on the parent’s lap.

Pediatric patients may require distraction, familial assistance, anxiolysis, or sedation to permit adequate oral assessment and treatment of pain. Pediatric procedural sedation is described in Chapter 157 .

A complete intraoral examination includes inspection of the oral cavity, gingiva, teeth, and surrounding structures (e.g., throat, neck, sinuses). Assess teeth for caries or fractures. Localization of the involved tooth may be accomplished by percussing the teeth or by having the patient bite on a tongue blade. Exquisite pain to percussion suggests an underlying periapical abscess (discussed in the section Odontogenic and Deep Neck Infections).

An extraoral examination includes evaluation of the nares and sinuses for discharge and pain, respectively, to evaluate for sinusitis. Facial asymmetry in the appropriate clinical context may indicate a deep neck infection. Palpate the temporomandibular joint (TMJ) with opening and closing of the jaw to assess for “clicks” or “pops,” which may indicate the etiology of pain as TMJ disorder. In older individuals, palpate the temporal artery for tenderness and prominence.

Differential Diagnoses

Most dental pain is odontogenic, the most common cause being pulpitis due to caries. However, tooth pain is not always odontogenic. Unilateral upper tooth pain (usually the posterior teeth) can be related to maxillary sinusitis, dysbarism, or inflammation. Trigeminal neuralgia can present as tooth pain, but it is usually lancinating and may not be related to temperature changes or mastication. Atypical odontalgia is a centralized trigeminal neuropathy localized in a tooth or teeth. Frequently misdiagnosed, patients will often undergo multiple dental procedures with worsening of their pain. Atypical odontalgia causes persistent throbbing or burning pain that does not fulfill diagnostic criteria for another disorder and therefore is a diagnosis of exclusion. Elders with temporal (giant cell) arteritis may have pain with mastication because of jaw claudication.

Diagnostic Testing

Laboratory or radiographic testing are not routinely required. Panorex films, if available, can be obtained to assess for apical abscess if the diagnosis is not clinically apparent.

Management and Disposition

Management of dental caries with pulpitis consists in pain management and referral to a dentist for definitive care. Data are limited, but evidence suggests that antibiotics are not beneficial for the management of pulpitis, whether irreversible or not.

Severe pain can be treated with supraperiosteal infiltration of local anesthetic to provide temporary relief ( Fig. 56.3 ). To perform this, dry the area with gauze, apply a topical anesthetic to the gingiva (e.g., 20% benzocaine or 5% lidocaine) and allow it to sit for 5 minutes. Inject 1 to 2 mL of local anesthetic (e.g., 2% lidocaine) through the mucobuccal fold of the affected tooth with the bevel facing the tooth. Alternatively, an inferior alveolar nerve block may be used when multiple lower teeth are affected on one side. In adults, the supraperiosteal block is less effective for mandibular teeth due to the comparatively thicker bone surrounding the tooth compared to maxillary teeth.

The patient can be discharged with ibuprofen (400 to 600 mg every 6 to 8 hours). Nonsteroidal antiinflammatory drugs (NSAIDs) given at scheduled times (rather than as needed) are more effective than opioid analgesics. However, for severe odontalgia, a short course of opioid analgesics in addition to scheduled NSAID administration is reasonable. Opioid analgesics should not be prescribed for long-standing dental problems, such as chronic caries. The patient with odontalgia from dental caries should follow-up with a dentist within one week.

Foundations

Anatomy, Physiology, and Pathophysiology

The periodontium serves to hold the teeth in place and protect the root from bacteria. Collectively, the periodontal ligament, alveolar bone, and cementum comprise the attachment apparatus. The attachment apparatus plus the gingiva (“gums”) is referred to as the periodontium. The gingiva consists of the mucosal tissue that overlies the mandible and maxilla inside the mouth and, in the normal state, acts as a barrier to infection and injury.

Gingivitis and Periodontitis

Periodontitis is inflammation of the supporting structures of the teeth (gingiva, alveolar bone, cementum, and periodontal ligament). Degradation of this support structure leads to loss of the alveolar bone and subsequent loosening or loss of teeth.

In necrotizing periodontal diseases, polymicrobial bacteria (with a predominance of Fusobacterium and spirochetes) invade the tissue and cause pain, bleeding, and destruction. These diseases include necrotizing gingivitis (acute necrotizing ulcerative gingivitis [ANUG], or “trench mouth”) if the gingiva alone is involved, necrotizing periodontitis if the attachment apparatus in addition to the gingiva is involved, and necrotizing stomatitis if the disease extends to the surrounding oral mucosa ( Fig. 56.4 ). Infection that further involves the tonsils and pharynx is termed Vincent angina. The most diffuse necrotizing disease is termed noma (cancrum oris, fusospirochetal gangrene) where the entire mouth is involved and is often fatal; this disease is most commonly encountered in young children in developing countries ( Fig. 56.5 ).

Pericoronitis

The gingiva and surrounding tissue can also become inflamed leading to a condition known as pericoronitis. As teeth start to erupt, debris and bacteria can accumulate between the tooth and the surrounding soft tissue. The flap of gum overlying these teeth is called the operculum and is the source of pain and swelling during inflammation ( Fig 56.6 ). This condition is exacerbated by trauma from mastication. The third molar (“wisdom tooth”) is most commonly implicated, and symptoms typically occur in the second or third decade of life. This condition is more common with teeth that are malerupted or impacted.

Gingival Hyperplasia

Gingival hyperplasia is an overgrowth of the gum tissue surrounding the teeth. It can occur secondary to poor oral hygiene, dental plaque build-up or as an adverse reaction to medications. The most commonly associated drug classes are anticonvulsants, calcium channel blockers, and immunosuppressants ( Table 56.1 ).

TABLE 56.1

Medication Classes and Their Risk of Drug-Induced Gingival Overgrowth

From Song HJ. Periodontal considerations for children. Dent Clin North Am . 2013; 57(1):17–37, Table 1.

Category	Pharmacologic Agent	Prevalence
Anticonvulsants	Phenytoin	50%
	Sodium valproate (valproic acid)	Rare
	Carbamazepine	None
Immunosuppressants	Cyclosporine	25%–30% (adults) 70% (children)
Calcium channel blockers	Nifedipine	6%–15%
	Felodipine	Rare
	Amlodipine	Rare
	Verapamil	<5%
	Diltiazem	5%–20%

Clinical Features

The presentation of periodontitis is variable, depending on the severity of the disease. Simple gingivitis presents with swollen or tender gingiva, gingival bleeding after manipulation (e.g., brushing teeth, flossing), and halitosis from bacterial overgrowth. Periodontitis involves the attachment apparatus as well and in more advanced cases, gingival recession from loss of alveolar bone and concomitant teeth loosening can be seen. Individuals with more severe periodontitis may also report fevers and malaise. Obtain a medication history to assess for drug-induced gingival overgrowth (see Table 56.1 ).

Inspect the gingiva for erythema, edema, and hyperplasia. The interdental papillae are normally pointed but, in necrotizing disease, the interdental papillae become blunted, “punched out,” ulcerated, and covered with a whitish-yellow pseudomembrane of necrotic tissue and bacteria. The triad for necrotizing periodontal diseases includes papillary necrosis, gingival bleeding, and pain. More severe infection (e.g., necrotizing stomatitis) may also have an associated submandibular lymphadenopathy.

Mobile teeth suggest alveolar bone loss, where the disease has progressed deeper than the gingiva. Partially erupted teeth should be examined for evidence of pericoronitis. The overlying tissue (operculum) should be assessed for bleeding and inflammation.

Differential Diagnoses

Ulceration of the mucosa can be caused by necrotizing stomatitis and also by aphthous ulcers and other oral lesions. Aphthous ulcers are small (2 to 3 cm), superficial, and tender mucosal lesions that typically have a whitish center. They usually do not become infected. The neighboring gingiva should not be affected and appear healthy. Recurrent aphthous lesions can occur with Behçet disease and human immunodeficiency virus (HIV). Treatment is symptomatic with hydrogen peroxide rinses and topical anesthetics. Another consideration is acute herpetic gingivostomatitis, which is the most common manifestation of primary herpes simplex virus infection in children. In patients with gingival hyperplasia, an infiltrative process (such as leukemia) should be considered, especially if the patient has adequate oral hygiene or is not on medications associated with hyperplasia.

Diagnostic Testing

Management