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. See the images below.
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Obvious swelling of the right cheek.
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Side view. Fluctuant mass extending toward the buccal side of the gum end to the gingival-buccal reflection.
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.
Bahl et al conducted a retrospective study to evaluate the involvement of fascial spaces, their bacteriology, sensitivity to antibiotics and management of odontogenic infection in 100 patients of age less than 60 years. The authors concluded that odontogenic infections were mixed aerobic-anaerobic infections. Anaerobic as well as aerobic cultures were necessary to isolate all pathogens. Successful management of these infections depends on changing the environment through decompression, removal of the etiologic factor and by choosing the proper antibiotic.[1]
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.[2] Although lactobacilli are not primary causes, they are progressive agents of caries because of their great acid-producing capacity.
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.[3]
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 accounted for 49.1% of the deep neck abscesses in one study.[4]
Patients with neutropenia undergoing chemotherapy are at risk for certain pathogenic oral microorganisms that cause bloodstream infections, which increases 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.[5]
Patients with superficial dental 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.
Coloquially referred to as cavities, caries are caused by bacteria that erode the enamel outside shell of the tooth and the dentin underneath. Bacteria builds up on the surface of teeth as plaque which consists of both bacteria as well as food and saliva. As the starches in the mouth turn into acid, it dissolves the enamel and forms a pit that gradually grows in size.
Patients may not have symptoms when tooth decay is small, yet as the decay grows the tooth may become sensitive.
Caries can be prevented by brushing and flossing daily as well as using antibacterial mouthwash in order to reduce the amount of bacteria in the mouth.
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 is not usually 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.[6, 7] The condition is odontogenic in 90% of cases and arises from the second and third mandibular molars in 75% of cases.[6] If infection spreads through the buccopharyngeal gap (space created by styloglossus muscle between the middle and superior constrictor muscle of the pharynx), adjacent retropharyngeal and mediastinal infection is possible.
A retrospective study that included 270 patients with deep neck infections reported symptoms at presentation included throbbing pain (81%), neck swelling (77%), difficulty in swallowing (39%), ear ache (31%) and restricted mouth opening (30%).[8]
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.
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
In dental infections, a CBC count with differential is not mandatory, but a large outpouring of immature granulocytes may indicate the severity of the infection.
Blood cultures in patients who are toxic may help guide management if the course is prolonged.
Panorex and periapical dental films are used to identify involvement of tooth and surrounding bone in the infectious process. A limited facial series may also be performed to help visualize the offending area if these studies are not available; cooperation and communication with the radiology technician and radiologist is necessary.
A soft-tissue radiograph of the neck can be used to identify gas-producing infections and determines any mass effect that may potentially compromise the airway.
CT scan may be used for severe fascial plane infections to determine the extent, size, and location of the infectious process. Soft tissue planes may be seen; with increasing infection, inflammation, and fat streaking, the planes may be difficult to differentiate from adjacent muscle. CT scan helps elucidate abscesses, venous thrombosis, and lymph node involvement.
MRI is not yet favored because of cost and limited availability. CT scan is preferred for rapid visualization of odontogenic infections.
The source of the dental infection must ultimately be removed or controlled. Pain medication and antibiotics may be given if the patient is not systemically ill and appears to have a simple localized odontogenic infection or abscess.[9, 10]
Igoumenakis et al reported that in odontogenic maxillofacial infections, extraction of the causative tooth is associated with a faster clinical and biological resolution of the infection compared to treatment that did not include extraction.[11]
Localized infections
I&D may be performed if a periapical or periodontal abscess is identified, depending on the physician’s comfort level.
After anesthesia of the tooth, locally or with a dental block, make an incision in the mucosa large enough to accommodate a quarter-inch Penrose drain.
Bluntly dissect the abscess cavity with the tips of a hemostat. Suture in the Penrose drain with a silk suture and leave until suppurative drainage is no longer present (about 2-3 d).
Deep fascial infections
Infections of the neck's deeper fascial layers and masseteric layers have a higher chance of causing impingement on the airway directly or indirectly through extreme trismus.
Tracheostomy was the prior method of choice for establishing the airway; as of recently, management through fiberoptic nasoendotracheal intubation while the patient is awake is preferred.
Various drains and incisions are used for drainage of the affected fascial space.
Other
If the patient appears systemically ill with abnormal vital signs and/or is unable to take oral medication, consider admission with further diagnostic studies and intravenous antibiotics. Infections in the various fascial spaces require incision and drainage (I&D) by the consulting physician.
If airway issues are of concern (eg, Ludwig angina, retropharyngeal abscesses), call an anesthesiologist and otolaryngologist as soon as possible to establish an airway. Ensure that equipment for an emergent cricothyroidotomy is located at the bedside until a secure airway can be established.
Silver diamine fluoride is the first drug to receive Breakthrough Therapy Designation for the arrest of tooth decay by the FDA It has been used previously in other countries such as Japan for over 80 years with much success.
The silver in SDF acts as an antimicrobial killing bacteria allowing for the slowing down and stopage of tooth decay. The fluoride is used to prevent further demineralization. SDF plugs the lesion forming a protective layer decreasing dentinal sensitivity. As the lesion becomes more shallow, the lesion gradually remineralizes while simultaneously inhibiting proteins that break down the dentin matrix.
After drying the tooth, apply SDF to the lesion for sixty seconds. SDF hardens the tooth structure and common side effects consist only of staining gum tissues. When applied to caries, SDF plugs the lesion forming a protective layer decreasing dentinal sensitivity. As the lesion becomes more shallow, the lesion gradually remineralizes while simultaneously inhibiting proteins that break down the dentin matrix.
The goals of therapy are to treat the dental infection and prevent further complications. Amoxicillin is still the first-line drug of choice but with 34% of Prevotella species resistant to amoxicillin, the alternatives of amoxicillin/clavulanate, clindamycin, and metronidazole need to be considered.
Rastenienė et al analyzed treatment modalities and results in 1,077 patients with severe odontogenic maxillofacial infections during a 10-year period. The microbial analysis showed the highest susceptibility of predominant micro-organisms to penicillin was 76.9% and the highest resistance was to metronidazole (27.9%).[12]
Clinical Context:
This is a topical medication in which the silver acts as an antimicrobial and the fluoride promotes the remineralization of the tooth. Recommended maximum dose is one drop/25 μL per 10 kg per weekly treatment.
The main side effect has been darkening of the carious lesions.
Clinical Context:
Inhibits biosynthesis of cell wall mucopeptide and is effective during active replication. Inadequate concentrations may produce only bacteriostatic effects.
Clinical Context:
Drug combination that extends the antibiotic spectrum of this penicillin to include bacteria normally resistant to beta-lactam antibiotics. Indicated for skin and skin structure infections caused by beta-lactamase–producing strains of Staphylococcus aureus. Administer for a minimum of 10 d.
Clinical Context:
DOC in patients who are allergic to penicillin. Inhibits RNA-dependent protein synthesis, possibly by stimulating dissociation of peptidyl tRNA from ribosomes, inhibiting bacterial growth.
Clinical Context:
Lincosamide useful to treat serious skin and soft tissue infections caused by most staphylococci strains. Effective against aerobic and anaerobic streptococci, except enterococci.
Inhibits bacterial protein synthesis by inhibiting peptide chain initiation at the bacterial ribosome, where it preferentially binds to the 50S ribosomal subunit, causing bacterial growth inhibition.
Clinical Context:
An imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Usually used in combination with other antimicrobial agents except when used for Clostridium difficile enterocolitis in which monotherapy is appropriate. An addition for treating Ludwig angina.
A study that investigated the determinants of the length of hospitalization due to acute odontogenic maxillofacial infections (AOMIs) from 2009 to 2013 found that the most important determinants regarding longer hospitalization were indicators of infection severity such as an extension of the odontogenic infection and the need for an extraoral incision to drain the infection.[13]
Prophylaxis controversy continues regarding who should have antibiotic prophylaxis for dental procedures and which antibiotics to use.
Current recommendations by the American Heart Association 2007 for dental, oral, respiratory tract, or esophageal procedures, if the patient has one of the following conditions:[5]
Prosthetic cardiac valve
Previous infective endocarditis
Congenital heart disease (CHD)
Unrepaired cyanotic CHD, including palliative shunts and conduits
Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
Cardiac transplantation recipients who develop cardiac valvulopathy
Recommendations for dental, oral, respiratory tract, and esophageal procedures for patients with one of the conditions listed above include the following:
For adults, administer amoxicillin 2 g PO 1 hour before procedure. Administer amoxicillin 50 mg/kg PO for pediatric patients. If by IV, administer ampicillin 2 g for adults and 50 mg/kg for children within 30 minutes before the procedure.
For patients allergic to penicillin, give clindamycin 600 mg PO/IV 1 hour before the procedure. For pediatric patients, administer clindamycin 20 mg/kg PO/IV. Alternatively, azithromycin or clarithromycin 500 mg PO 1 hour before the procedure may be administered for adults and 15 mg/kg PO may be administered for pediatric patients.
Prophylactic regimens are for patients with prosthetic heart valves, previous bacterial endocarditis, congenital cyanotic heart disease, pulmonary shunt placement, cardiac myopathies, acquired valvular disease, and mitral prolapse with regurgitation.[5]
Only 25% of patients who should receive prophylactic antibiotics actually receive them.
With 100% compliance, estimates suggest that the incidence of bacterial endocarditis would be reduced 3-6%.
What are dental infections?What is the pathophysiology of dental infections?What is the US prevalence of dental infections?What is the global prevalence of dental infections?What is the morbidity associated with dental infections?Which patient groups are at highest risk for dental infections?Which age groups have the highest prevalence of dental infections?Which clinical history findings are characteristic of dental infections?Which physical findings are characteristic of caries in the evaluation of dental infections?Which physical findings are characteristic of local dental infections?Which physical findings are characteristic of mandibular dental infections?Which physical findings are characteristic of middle and lateral facial edema?Which physical findings are characteristic of gingivitis?What causes dental infections?What is the role of lab tests in the workup of dental infections?What is the role of imaging studies in the workup of dental infections?How are localized dental infections treated?How are dental infections treated?How are deep fascial dental infections treated?When is inpatient care indicated for the treatment of dental infections?How are airway issues managed in the treatment of dental infections?Which specialist consultations are beneficial to patients with dental infections?What is the role of surgery in the treatment of dental infections?What is the role of medications in the treatment of dental infections?Which medications in the drug class Antibiotics are used in the treatment of Dental Infections in Emergency Medicine?Which medications in the drug class Topical are used in the treatment of Dental Infections in Emergency Medicine?Which factors increase the length of inpatient care for dental infections?What are the guidelines on antibiotic prophylaxis for dental procedures?What are the possible complications of dental infections?
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
Disclosure: Nothing to disclose.
Coauthor(s)
Amin Antoine Kazzi, MD, Professor of Clinical Emergency Medicine, Department of Emergency Medicine, American University of Beirut, Lebanon
Disclosure: Nothing to disclose.
Enoch Peng, Rice University
Disclosure: Nothing to disclose.
Willard Peng, DDS, MS, Keck School of Medicine of the University of Southern California
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Jeff Burgess, DDS, MSD, (Retired) Clinical Assistant Professor, Department of Oral Medicine, University of Washington School of Dental Medicine; (Retired) Attending in Pain Center, University of Washington Medical Center; (Retired) Private Practice in Hawaii and Washington; Director, Oral Care Research Associates
Disclosure: Nothing to disclose.
Additional Contributors
Michael Glick, DMD, Dean, University of Buffalo School of Dental Medicine
Disclosure: Nothing to disclose.
Rebecca Cheng, Loma Linda University School of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Mark W Fourre, MD Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine; Program Director, Department of Emergency Medicine, Maine Medical Center
Harwood-Nuss A, Linden C, Luten R, eds. Dental, oral and salivary gland infections. The Clinical Practice of Emergency Medicine. 2nd ed. Philadelphia: Lippincott Williams & Wilkins Publishers; 1996. 73-77.
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