eMedicine Specialties > Emergency Medicine > Ear, Nose, & Throat

Dental, Infections

Author: Lynnus F Peng, MD, Assistant Clinical Professor, Department of Anesthesia, University of California at Irvine; Chairman of Anesthesia, Department of Surgery, St Jude Medical Center at Fullerton
Coauthor(s): A Antoine Kazzi, MD, Chief of Service, Department of Emergency Medicine, Medical Director of the Emergency Unit, American University of Beirut; Willard Peng, BA, BS, MS, Doctor of Dental Surgery Candidate, Department of Oral Medicine, University of Southern California; Rebecca Cheng, University of California at San Diego
Contributor Information and Disclosures

Updated: Sep 26, 2007

Introduction

Background

Infections of the teeth have plagued humans constantly, despite a quest for better oral hygiene. As early as 200 BCE, a bronze wire root canal filling was found in the skull of a Nabataean warrior. Infections usually arise from pulpitis and associated necrotic dental pulp that initially begins on the tooth's surface as dental caries. The infection may remain localized or quickly spread through various fascial planes.

Pathophysiology

Odontogenic infection may be primary or secondary to periodontal, pericoronal, traumatic, or postsurgical infections. A typical odontogenic infection originates from caries, which decalcify the protective enamel. A balance of demineralization and remineralization of the tooth structure occurs in the development of carious lesions. Greater demineralization of the tooth occurs with high bacterial activity and low pH. Greater remineralization occurs with a pH higher than 5.5 and high concentrations of calcium and phosphate from the saliva.

Once enamel is dissolved, the infectious caries can travel through the dentinal tubules and gain access to the pulp. In the pulp, the infection may develop a track through the root apex and burrow through the medullar cavity of the mandible or maxilla. The infection then may perforate the cortical plates and drain into the superficial tissues of the oral cavity or track into deeper fascial planes. If the infection does not drain, it will remain localized and develop into a periapical or periodontal abscess.

Serotypes of Streptococcus mutans (cricetus, rattus, ferus, sobrinus) are primarily responsible for causing oral disease. Although lactobacilli are not primary causes, they are progressive agents of caries because of their great acid-producing capacity.

Frequency

United States

Dental caries is the most common chronic disease in the world. The late 1970s signaled a decline in caries in certain segments of the world due to the addition of fluoride to public drinking water. In the United States, a 36% decrease in caries occurred from 1972-1980.

International

In the United Kingdom, a 39% decline in caries occurred from 1970-1980. In Denmark, a 39% decline occurred from 1972-1982.¹

Mortality/Morbidity

Dental caries is not a life-threatening disease; however, if an odontogenic infection spreads through fascial planes, patients are at risk for sepsis, airway compromise (eg, Ludwig angina, retropharyngeal abscess), and odontogenic infection, which accounts for 40% of the deep neck infections.

• Neutropenic patients undergoing chemotherapy are at risk for certain pathogenic oral microorganisms causing bloodstream infections, which increase the chance of morbidity and mortality.
• Odontogenic infections carry significant morbidity of pain and cosmetic defect. The US bill for dental care was estimated at $27 billion in 1985.
• The oral cavity contains approximately 30-50% viridans group streptococci that are resistant to penicillins and macrolides.

Age

The National Preventive Dentistry Program found that 60% of caries occurred in 20% of children, who were generally minorities or of lower socioeconomic status.²

Clinical

History

Patients with superficial infections may complain of localized pain, edema, and sensitivity to temperature and air. Patients with deep infections or abscesses that spread along the fascial planes may complain of fever and difficulty swallowing, breathing, and opening the mouth.

Physical

• Local infections
  • Typically, the tooth is grossly decayed, although it may be normal with cavitated lesions that may have a surrounding chalky demineralized area and swollen erythematous gingiva. Affected teeth generally are tender to percussion and temperature.
  • Dentoalveolar ridge edema is evidenced by a periodontal, periapical, and subperiosteal abscess. Infection from the tooth spreads to the apex to form a periapical or periodontal abscess. With further invasion, the infection may elevate the periosteum and penetrate adjacent tissues.
  • Pericoronal infection occurs in an erupting or a partially impacted tooth when tissue covering the tooth's crown becomes inflamed and infected. An abscess may form and require incision and drainage (I&D). The tooth itself usually is not involved.
• Mandibular infections
  • Submental space infection is characterized by a firm midline swelling beneath the chin and is due to infection from the mandibular incisors.
  • Sublingual space infection is indicated by swelling of the mouth's floor with possible tongue elevation, pain, and dysphagia due to anterior mandibular tooth infection.
  • Submandibular space infection is identified by swelling of the submandibular triangle of the neck around the angle of the jaw. Tenderness to palpation and mild trismus is typical. Infection is caused by mandibular molar infections.
  • Retropharyngeal space infection is identified by stiff neck, sore throat, dysphagia, hot potato voice, and stridor with possible spread to the mediastinum. These infections are due to infections of the molars.
    • With spread to the deeper areas of the neck, signs and symptoms of vagal injury, Horner syndrome, and lower cranial nerve injury may be seen.
    • Infection in this space is more common in children younger than 4 years.
    • Etiology usually is due to an upper respiratory infection (URI) with spread to retropharyngeal lymph nodes.
    • Because of high potential for spread to the mediastinum, retropharyngeal space infection is a serious fascial infection.
  • Ludwig angina (name derived from sensations of choking and suffocation) is characterized by brawny boardlike swelling from a rapidly spreading cellulitis of the sublingual, submental, and submandibular spaces with elevation and edema of the tongue, drooling, and airway obstruction.³ The condition is odontogenic in 90% of cases and arises from the second and third mandibular molars in 75% of cases.³ If infection spreads through the buccopharyngeal gap (space created by styloglossus muscle between the middle and superior constrictor muscle of the pharynx), potential exists for adjacent retropharyngeal and mediastinal infection.

• Middle and lateral facial edema
  • Buccal space infection is typically indicated by cheek edema and is due to infection of posterior teeth, usually premolar or molar.
  • Masticator space infection always presents with trismus manifestation and is due to infection of the third molar of the mandible. Large abscesses may track toward the posterior parapharyngeal spaces. Patients may require fiberoptic nasoendotracheal intubation while awake.
  • Canine space infection is evidenced by anterior cheek swelling with loss of the nasolabial fold and possible extension to the infraorbital region. This is due to infection of the maxillary canine and potentially may spread to the cavernous sinus.
• Gingivitis
  • Acute necrotizing ulcerative gingivitis (Vincent angina, trench mouth) is a condition in which patients present with edematous erythematous gingiva with ulcerated, interdental papillae covered with a gray pseudomembrane.
  • Patients may have fever and lymphadenopathy and may complain of metallic taste. The condition is caused by invasive fusiform bacteria and spirochetes but is not contagious.

Causes

• Serotypes of S mutans are thought to cause initial caries infection. Infections through the fascial planes usually are polymicrobial (average 4-6 organisms). Dominant isolates are anaerobic bacteria.
• Anaerobes (75%) - Peptostreptococci, Bacteroides and  Prevotella organisms, and Fusobacterium nucleatum
• Aerobes (25%) - Alpha-hemolytic streptococci

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