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.
View Image | Obvious swelling of the right cheek. |
View Image | 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.
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.[3]
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.
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.
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.
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]
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.
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.
See the list below:
See the list below:
See the list below:
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).
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.
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: Combination antimicrobial agent that utilizes a beta-lactamase inhibitor with ampicillin. Gives better anaerobic coverage.
Clinical Context: Used for deep space infections. Inhibits biosynthesis of cell wall mucopeptide and is effective during stages of active growth.
Antipseudomonal penicillin plus a beta-lactamase inhibitor that provides coverage against gram-positive, gram-negative, and anaerobic organisms.
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.
Therapy must cover all likely pathogens in the context of the clinical setting.
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]
Recommendations for dental, oral, respiratory tract, and esophageal procedures for patients with one of the conditions listed above include the following:
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]