Evaluation of Acute Orofacial Pain and Swelling

Edward T. Lahey III

The primary care physician often encounters patients whose presenting complaints are orofacial pain and/or swelling. The differential diagnoses can be broad and include infections, neuropathy, neoplasms, autoimmunity, vascular malformations, trauma, and inflammation of structures such as the masticatory apparatus (teeth, gums, jaws, muscles) or salivary glands. Dental decay is the most prevalent infectious disease in the United States and a major cause of conditions leading to orofacial pain and swelling. Because dental symptoms may be referred to nondental structures and because an odontogenic infection may involve areas of the head and neck seemingly unrelated to the teeth, the patient may first seek the advice of a physician rather than of a dentist. Prompt recognition and effective initial treatment may well prevent the development of a serious complication such as abscess formation and avoid delays in patients being referred to the appropriate specialist.

PATHOPHYSIOLOGY AND CLINICAL PRESENTATION (1, 2, 3, 4 and 5)

Odontogenic Disease

Causes range from tooth decay to abscesses and their complications.

Tooth Decay and Inflammation of the Pulp

Caries or dental decay is a multifactorial disease. Risk factors include high intake of refined carbohydrates, lack of fluoride exposure during tooth development, poor oral hygiene, inadequate saliva production, and a cariogenic bacterial milieu. Metabolism of refined dietary carbohydrates by tooth-adherent bacteria results in acidic by-products that lower oral pH. Prolongation of a lowered pH, lack of salivary buffering activity and lavaging effect, and poor oral hygiene lead to decalcification of susceptible enamel, resulting in a “cavity” or carious lesion.

In its initial stages, tooth decay is asymptomatic as the enamel, the acellular outermost layer of the crown of the tooth, lacks innervation. However, once decay progresses into the dentin beneath the enamel, its cellular appendages can trigger aching pain when the affected tooth comes into contact with hot, cold, or sweet substances. Referred pain may make localization of the offending tooth difficult and is one reason a patient may first consult the physician rather than the dentist. Referred odontogenic pain may require differentiation from otalgia (see Chapter 218) or sinus symptoms (see Chapter 219). Caries can be cured at this point by debridement and placement of a dental restoration or filling. A similar pain can result from gingival recession that occurs either due to aggressive tooth brushing or periodontal disease. In this instance, the etiology is not decay but exposure of the dental root, which lacks a protective enamel covering.

Unchecked decay will progress through the dentin until it encroaches upon and enters the pulp, resulting in inflammation and infection {pulpitis). The symptoms will be unchanged until the dental pulp becomes necrotic, heralded by deep, throbbing pain on exposure to hot foods or drinks that is abruptly relieved by ice or cold water. This symptom complex is distinct from the paroxysmal lancinating pain of trigeminal neuralgia, which has no relationship to extremes of temperature but may be related to eating because of the presence of trigger zones in the oral cavity (see Chapter 176). Once the pulp is completely necrotic, patients will often experience resolution of pain until the infection spreads beyond the tooth.

Tooth Abscess

Simple dental decay, pulpitis, and pulpal necrosis are not associated with fever, swelling, or leukocytosis. However, when the
infection of the pulp spreads beyond the confines of the tooth to involve the periodontal ligament and the adjacent alveolar bone at the root apex, an acute alveolar abscess may develop. In this condition, the affected tooth is tender to percussion (tapping on the surface) or to masticatory forces and is often mobile. The abscess will spread along the path of least resistance beyond the alveolar bone to reach adjacent soft tissues, resulting in edema, erythema, heat, and tenderness. The location of the involved tooth will determine the location of the swelling. Abscessed anterior maxillary teeth will produce labial or infraorbital edema, while posterior maxillary teeth can lead to sinus inflammation; an infected mandibular tooth will produce submandibular edema. The apices of posterior mandibular teeth often sit below the floor of the mouth so pharyngeal tissues are more often involved with less obvious outward swelling. Lymphadenopathy of the cervical chain can be seen in either maxillary or mandibular infection.

Complications

Complications occur by either hematogenous spread or direct extension of infection along fascial planes, leading to facial or cervical cellulitis and abscess formation. Inflammation of the masticatory muscles or deep space abscess formation will lead to limitation in mandibular movement (trismus), and progressed infections may lead to odynophagia and dysphonia, heralding possible progression to airway compromise. Patients with progressed odontogenic infections will appear toxic and manifest systemic findings such as fever and leukocytosis. Although uncommon, infections can result in life-threatening complications, such as cavernous sinus thrombosis, meningitis, Ludwig angina, or mediastinitis.

Periodontal Infection

Acute bacterial infection of the periodontal tissues is most often localized to the gingiva or mucosa adjacent to the involved tooth. The typical patient will complain of a “gum boil,” and examination will reveal a discrete fluctuant swelling, which may drain easily on manual palpation.

In the late-adolescent years, infection of the soft tissue surrounding impacted third molars or wisdom teeth (pericoronitis) is common. Low-grade chronic infection may be accompanied by symptoms described as “teething”; acute infection will result in pain, swelling, and trismus as the adjacent masticator space becomes involved.

Salivary Gland Disease

Acute swelling of the major salivary glands (parotid, submandibular, and sublingual) results most commonly from obstruction to salivary flow or salivary gland inflammation (sialadenitis). Neoplastic causes of enlargement generally have a more insidious onset with discrete enlargement versus the diffuse enlargements detailed below.

Salivary Obstruction

Sialolithiasis is the usual cause of a low-flow state, but other causes include dehydration, anticholinergic medications, and previous radiation therapy. Major salivary ducts can also be obstructed by strictures from repeated infection, congenital atresia, and mucous plugging. Both mucous plugs and sialoliths are more common in the submandibular gland than the parotid. Unilateral, periprandial swelling of the neck or face is a common presenting complaint.

Infectious Sialadenitis

Acute infections of the major salivary glands are most often viral or bacterial. Viral parotitis (mumps) occurs most frequently in school-aged children and appears either unilaterally or bilaterally. (The efficacy of immunization programs has made this disease a relative rarity.) HIV-associated salivary gland disease is often due to lymphoepithelial cysts and can lead to pain and profound enlargement. Bacterial sialadenitis occurs in an ascending fashion as bacteria gain access to a gland predisposed by virtue of advanced age, recent surgery and anesthesia, malnutrition, immunosuppression, or decreased salivary flow. As noted, ductal obstruction may lead to decreased salivary flow and consequent infection.

The parotid gland is the usual target of sialadenitis; involvement is more often unilateral than bilateral. Purulent drainage can be obtained from the duct orifice. Acute suppurative parotitis is seen more frequently in elderly and sick patients with Staphylococcus aureus being the most common pathogen. This is contrasted by submandibular sialadenitis caused by streptococci, which more frequently involves the presence of a sialolith and occurs in a healthier cohort of patients.

Noninfectious Sialadenitis

Noninfectious salivary gland swelling may occur with diabetes mellitus, uremia, Laennec cirrhosis, chronic alcoholism, bulimia nervosa, and malnutrition. A toxic reaction to a variety of drugs, such as iodine, mercury, and guanethidine, causes a painless bilateral parotid gland swelling.

Autoimmune disease, especially Sjögren syndrome, may present as sialadenitis with xerophthalmia and xerostomia. When occurring on its own, it is sometimes referred to as primary Sjögren syndrome, and when in association with another chronic autoimmune/connective tissue disorder (e.g., rheumatoid arthritis, systemic lupus erythematosus, and polyarteritis nodosa), it may be designated as secondary Sjögren syndrome. Sjögren syndrome often presents without apparent systemic disease. Lymphoma may develop in a patient with long-standing Sjögren syndrome. Sarcoidosis and systemic lupus erythematosus may also present as salivary gland enlargement.

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