A dentoalveolar abscess is an acute lesion characterized by localization of pus in the structures that surround the teeth. Most patients are treated easily with analgesia, antibiotics, drainage, and/or referral to a dentist or oral-maxillofacial surgeon. However, the physician should be aware of potential complications of simple dentoalveolar abscess.
The term dentoalveolar abscess comprises 3 distinct processes, as follows:
A periapical abscess that originates in the dental pulp and is usually secondary to dental caries is the most common dental abscess in children. Dental caries erode the protective layers of the tooth (ie, enamel, dentin) and allow bacteria to invade the pulp, producing a pulpitis. Pulpitis can progress to necrosis, with bacterial invasion of the alveolar bone, causing an abscess.
A periodontal abscess involves the supporting structures of the teeth (periodontal ligaments, alveolar bone).[1] This is the most common dental abscess in adults, but may occur in children with impaction of a foreign body in the gingiva.
Pericoronitis describes the infection of the gum flap (operculum) that overlies a partially erupted tooth.
Developmental and acquired conditions are associated with dental abscesses in childhood. Developmental conditions include abnormal morphology of the crown (eg, dens invaginatus, dens evaginatus) and abnormal structure of the dentine (eg, dentine dysplasia, dentinogenesis imperfecta, osteogenesis imperfecta, familial hypophosphatemia). Acquired conditions include pre-eruptive intracoronal resorption and mandibular infected buccal cyst.[2]
Odontogenic infections are polymicrobial, with an average of 4-6 different causative bacteria. The dominant isolates are strictly anaerobic gram-negative rods and gram-positive cocci, in addition to facultative and microaerophilic streptococci. Anaerobic bacteria outnumber aerobes 2-3:1.[3] In general, strictly anaerobic gram-negative rods are more pathogenic than facultative or strictly anaerobic gram-positive cocci.
Generally, a nonpathologic resident bacterium gains entry when the host's defenses are breached, rather than when a nontypical microorganism is introduced. The predominant species associated with dental abscess include Bacteroides, Fusobacterium, Actinomyces, Peptococcus,Peptostreptococcus, and Porphyromonas as well as Prevotella oralis, Prevotella melaninogenica, and Streptococcus viridans. Beta-lactamase producing organisms occur in approximately one third of dental abscesses.[4]
The use of molecular techniques such as 16S rRNA gene sequencing and polymerase chain reaction (PCR) have identified difficult-to-culture organisms and expanded knowledge of the microflora associated with dental abscess. Examples include Treponema, Atopobium, Bulleidia extructa, and Mogibacterium species, as well as Cryptobacterium curtum.[5] A recent Brazilian study using 16S rRNA PCR and sequencing performed on cultivable bacteria from acute apical abscesses revealed the most common identified bacteria were Prevotella sp, Pseudoramibacter alactolyticus, Parvimonas micra, Dialister invisus, Filifactor alocis and Peptostreptococcus stomatis. Recently, a study using 16S rRNA sequencing in 15 patients with primary endodontic infections with and without a sinus tract to the oral cavity revealed Propionibacterium acnes as the most prevalent isolate recovered from lesions with an intraoral communication. Additionally, the authors found no difference in the number of species identified from lesions with or without intraoral communication.[6]
Mortality is rare and is usually due to airway compromise. Morbidity relates to pain, probable tooth loss, and dehydration. See Complications.
Race
No race predilection is observed.
Sex
No sex predilection is noted.
Age
Dental abscess is rare in infants because abscesses do not form until teeth erupt. In children, periapical abscess is the most common type of dental abscess. This is because of the combination of poor hygiene, thinner enamel, and the primary dentition having more abundant blood supply, which allows for an increased inflammatory response. In adults, periodontal abscess is more common than periapical abscess.
Fluctuant mass that usually extends toward the buccal side of the gum and to the gingival-buccal reflection
Parulis or "gum boil" (a soft, solitary, reddish papule located facial and apical to a chronically abscessed tooth that occurs at the endpoint of a draining dental sinus tract)[7]
Teeth: The tooth that is most frequently involved is the lower third molar, followed by other lower posterior teeth; upper posterior teeth are involved much less frequently, and anterior teeth are rarely involved.
Increased mobility (mostly periapical abscess)
Pressure or percussion tenderness (mostly periapical abscess)
Extrusion
Regional lymph node involvement
More severe infection
Trismus, indicating involvement of the masticator space
"Infant-bottle" tooth decay or "nursing" caries: The term "early childhood" caries is replacing these terms because the description also includes dental caries in breastfed babies. The American Academy of Pediatrics (AAP) along with the American Academy of Pediatric Dentistry issued a clinical report entitled "Oral and Dental Aspects of Child Abuse and Neglect," which states that the caregivers of children who present for dental care with severe early childhood caries must be carefully interviewed to differentiate caregivers with adequate knowledge and willful failure to seek dental care from caregivers without knowledge or awareness of a child's dental needs. Failure to seek dental care may result from many socioeconomic factors, and clinicians should determine if dental care is readily available and accessible when considering the possibility of negligence. Physicians and dentists are required by law to report suspected cases of child negligence and abuse.[9]
Plaque: This is a noncalcified precipitate of microorganisms and their byproducts that adheres to the enamel of teeth.
In immunocompromised patients, bacteria may hematogenously spread to invade the pulp of the tooth.
Gingivitis is an inflammation of the gingiva without attachment loss or with nonprogressing attachment loss.
Posttraumatic infection or postsurgical infection may also cause dental abscess.
Depending on severity of abscess based on clinical presentation the following is recommended:
Periapical radiography is the first level of investigation. It provides a localized view of the tooth and its supporting structures. Widening of the periodontal ligament space or a poorly defined radiolucency may be noted.
Panoramic radiography (pantomography) is most helpful in emergency situations because it provides the most information for all teeth and supporting structures.
If cellulitis swelling extends beyond local area then the following is indicated:
Lateral and anteroposterior neck views to rule out a soft tissue neck mass that impinges on the airway.
CT scanning with intravenous contrast is the most accurate method to determine the location, size, extent, and relationship of the inflammatory process to the surrounding vital structures.
Confirm presence of the abscess via needle aspiration.
If pus is obtained, do not aspirate more than 1-2 drops. Leave the abscess as large as possible to make the area easier to find for further management.
If pus cannot be aspirated, manage medically until a more localized infection develops.
Incision and drainage may be performed only if pus can be aspirated.
Packing a periapical abscess is generally not necessary.
The flora at different oral sites varies. The surface of the carious tooth usually contains acid producing aerobic and anaerobic bacteria including Streptococcus mutans, Lactobacillus acidophilus, and Actinomyces viscosus. S mutans is the only organism recovered from decaying dental fissures. Obligate anaerobes such as Propionibacterium, Eubacteria, Arachnia, Lactobacillus, Bifidobacterium, and Actinomyces constitute most organisms isolated from carious dentin. The bacteria isolated from inflamed pulp and root canals are aerobic, facultative anaerobic and strict anaerobic organisms, in addition to yeast.
Anaerobes usually outnumber aerobes and facultative anaerobes.
Most odontogenic infections involve plaque organisms.
Supragingival plaque mainly consists of gram-positive facultative anaerobes or microaerophilic cocci and rods.
Subgingival plaque consists of anaerobic gram-negative rods with motile form, including spirochetes.
In patients with dental abscess, assess the airway upon respiratory distress, oropharyngeal tissue swelling, or inability to handle secretions; then, secure the airway via endotracheal intubation or tracheostomy.
Properly collect specimen for Gram stain and aerobic and anaerobic cultures.
Administer empiric antibiotic therapy if necessary.
The primary therapeutic modality is surgical drainage of any pus collection. A pulpectomy or incision and drainage is the recommended management of a localized acute apical abscess in the permanent dentition. Incision and drainage or spontaneous rupture of the abscess quickly accelerates resolution of the infection. The addition of antibiotics is not recommended for a localized dental abscess.
Emergent surgery is indicated in the operating room if the airway is threatened or if the patient's condition is rapidly deteriorating.
Third molar removal is a common surgical procedure.[10]
A retrospective analysis of all patients affected by an odontogenic infection that received surgical therapy from 2004 to 2011 under stationary conditions reported that two patients per week affected by an odontogenic infection required stationary surgical treatment and about two patients per year were likely to require additional intensive medical care. The study also reported that if well-known risk factors are present in patients affected by odontogenic infection, appropriate interdisciplinary management should be considered as early as possible.[11]
When drainage cannot be achieved or the patient shows signs of systemic involvement, antibiotic therapy is indicated; in addition, an increasing number of immunocompromised patients require antibiotic therapy.
A national survey study demonstrated a significant shift from prescribing penicillin V to amoxicillin as the first choice by U.S. endodontists as well as a significant increase in the use of clindamycin for penicillin-allergic patients. Overuse of antibiotics in clinical situations where they were typically not indicated occurred most often because of patient expectations. The southeastern region of the U.S. was a significant predictor of increased antibiotic prescribing.[12]
A study by Roberts et al reported that an antibiotic (penicillin or clindamycin) was prescribed in 65% of ED visits for any dental diagnosis even though dental procedures were usually the recommended treatment.[27]
Clinical Context:
Traditionally been considered the DOC for the treatment of a dental abscess. Antibiotic therapy alone, without surgical drainage, may not be effective because of poor antibiotic penetration into the abscess cavity, ineffectiveness at low pH levels, and the inoculum effect. Bactericidal against sensitive organisms when adequate concentrations are reached and is most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects. Binds to one or more penicillin binding proteins, which interferes with bacterial cell wall synthesis during active multiplication. Final transpeptidation step of peptidoglycan synthesis is inhibited leading to death.
Emergence of beta-lactamase producing bacteria may decreased efficacy, although it remains the antibiotic of choice for mild-to-moderate infections.
Clinical Context:
May be an option for the treatment of a dental abscess in patients who are allergic to penicillin or beta-lactam. Binds to the 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, inhibiting bacterial RNA-dependent protein synthesis. Concentrates in phagocytes and fibroblasts, as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues. Indicated for mild-to-moderate microbial infections.
Clinical Context:
Effective against obligate anaerobic organisms. It can be combined with penicillin if anaerobic organisms that produce beta-lactamase enzymes are a concern. Compliance must be considered with a 2-drug regimen. It inhibits DNA synthesis by affecting the helical DNA structure leading to DNA strand breakage causing cell death.
Clinical Context:
Can be used in patients who are penicillin or beta-lactam allergic. Inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit preventing peptide bond formation. Excellent activity against PO aerobes and anaerobes; penetrates bone and abscess cavities.
Clinical Context:
Amoxicillin works by binding to one or more of the penicillin-binding proteins, which interferes with bacterial cell wall synthesis during active bacterial replication. The final transpeptidation step of peptidoglycan synthesis is inhibited leading to cell death. Clavulanic acid binds and inhibits beta-lactamase enzymes that inactivate amoxicillin resulting in an expanded spectrum of activity for Augmentin. For children, the dosing should be based on the amoxicillin component.
Clinical Context:
Binds to one or more of the penicillin binding proteins, which interferes with bacterial cell wall synthesis during active replication. The final transpeptidation step of peptidoglycan synthesis is inhibited leading to cell death. It is a second-generation cephalosporin with activity against some gram-positive cocci, gram-negative rods, and anaerobic bacteria. Infections caused by cephalosporin-resistant or penicillin-resistant gram-negative bacteria may respond to cefoxitin.
Empiric antimicrobial therapy must be broad spectrum to cover anaerobes, Staphylococcus aureus, non-typeable Haemophilus influenzae, and others, depending on the context of the clinical setting. The most commonly prescribed antibiotic is amoxicillin/clavulanate.
Follow-up care should be obtained as recommended by a physician. Most dentists would see the patient after 1-2 days of antibiotics if it is a primary tooth involved for dental extraction and then continue antibiotics for 2-3 more days for a total antibiotic course of 5 days. For a dental abscess in a secondary tooth the patient is typically seen back after 5 days of antibiotics for a root canal procedure followed by an additional 5-10 days of antibiotics. Pain control is typically achieved with acetaminophen or non-steroidal anti-inflammatory medications for outpatients. For inpatients whose pain is not adequately controlled with these medications morphine sulfate can be utilized.
A cross-sectional study found that periodontal abscess can be considered as possible oral clinical diagnostic criteria for the diagnosis of diabetes mellitus in the elderly.[13]
The most effective preventive measure against dental caries and, thus, dentoalveolar abscess in addition to homecare with brushing and flossing is fluoridation of communal drinking water.[26]
In fluoride-deficient areas, prevention can be obtained with dietary fluoride supplements. The AAP and the American Dental Association recommend administration of fluoride if the concentration of fluoride in the drinking water is less than 0.30 parts per million (ppm) or 0.30-0.60 ppm for individuals aged 3-16 years. Administer fluoride according to the following age-appropriate schedule (all doses are per day):[14]
Age 0-6 months - None
Age 6 months to 3 years - 0.25 mg if fluoride in drinking water is less than 0.30 ppm, none if fluoride in drinking water is more than 0.3 ppm
Age 3-6 years - 0.50 mg if fluoride in drinking water is less than 0.30 ppm, 0.25 mg if fluoride in drinking water is 0.30-0.60 ppm
Age 6-16 years - 1 mg if fluoride in drinking water is less than 0.30 ppm, 0.50 mg if fluoride in drinking water is 0.3-0.6 ppm
The other effective preventive measure against dental caries and dentoalveolar abscess is proper dental hygiene. This includes brushing teeth after meals and regular dental check-ups.
Dentocutaneous fistulae arise from chronic dental infections. The fistulous pathway develops as the chronic inflammation erodes through the alveolar bone, perforates the periosteum, and spreads into the surrounding soft tissues. The diagnosis is often missed because a chronic asymptomatic dental infection is usually present and the skin lesion is mistakenly thought to arise locally.
Acute suppurative osteomyelitis was common before the era of antibiotic therapy. Osteomyelitis is an inflammation of the medullary cavity and adjacent cortex of bone. The mandible is more commonly involved than the maxilla because the maxilla has a better blood supply. Garr é osteomyelitis is a chronic nonsuppurative sclerosing osteomyelitis that is characterized by a localized, hard, nontender swelling of the mandible and is usually associated with dental caries of the lower first molar. Radiography may reveal a focal area of bone proliferation with a periosteal reaction that has an onion-peel or laminated appearance.
Cavernous sinus thrombosis (CST) may be a complication. Approximately 10% of patients with CST have an odontogenic focus. Spread of infection from dental abscesses to the cavernous sinus is believed to occur via the valveless pterygoid venous plexus by way of the retromandibular vein. Patients often present with headache, unilateral retro-orbital pain, periorbital edema, fever, proptosis, chemosis, and ptosis. Treatment consists of antibiotics, anticoagulants, and, occasionally, surgery.[15]
Ludwig angina is rapidly spreading cellulitis of the bilateral sublingual, submandibular, and submental spaces. Abscesses of the second and third mandibular molars account for 75% of cases. Ludwig angina manifests as swelling of the floor of the mouth with elevation and posterior displacement of the tongue. A rapidly spreading gangrenous cellulitis produces a brawny edema of the suprahyoid region of the neck. The infection begins unilaterally but quickly spreads to include the entire neck. The most common presenting symptoms include oral, neck, and dental pain; neck swelling; odynophagia; drooling; dysphagia; dysphonia; trismus; and tongue swelling. The patient may lean forward in order to maintain airway patency. The infection can extend into the retropharyngeal space and the mediastinum. This is a life-threatening infection. Ludwig angina is unusual in children.
Maxillary sinusitis may occur from direct extension of an odontogenic infection or from perforation of the floor of the sinus during extraction. Case reports exist of odontogenic orbital abscess secondary to spread of infection to the maxillary sinus. These patients can present with facial edema, ocular pain, ophthalmoplegia and proptosis.[16]
Facial-space swelling secondary to spread of the infection most often involves the following areas:
Submandibular swelling is caused by dental abscesses from the second or third molars whose roots lie below the attachment of the mylohyoid bone. This space contains the submandibular gland, Wharton duct (the opening of the submandibular salivary gland), lingual and hypoglossal nerves, facial artery, and vein. A firm, ill-defined, and often significant-sized swelling is present below the mandible. The inferior border and angle of the mandible are difficult to palpate. The patient may have mild trismus.
Sublingual swelling is caused by any lower tooth whose apex is above the mylohyoid muscle attachment (ie, incisors, canines, premolars, mesial roots of the first molar). Infections produce a unilateral elevation of the floor of the mouth near the offending tooth but can spread across the midline, causing pain, dysphagia, and an elevation of the base of the tongue, leading to potential airway compromise.
Buccal swelling originates from infected maxillary or mandibular molars. Clinically, infection produces a large tender swelling of the cheek without trismus. Boundaries for this type of infection may extend from the philtrum of the lip, to the border of the parotid, and up to the eye.
Less frequently involved facial-space swellings include submental, masticator, canine, lateral pharyngeal, and retropharyngeal. Retropharyngeal space infections are serious infections with the potential to cause airway obstruction and infection of the organs in the mediastinum.
Necrotizing fasciitis of the face or neck that results from an odontogenic abscess is very rare.
Inquire if drinking water is fluorinated. If not, counsel parents about fluoride supplementation (see Deterrence/Prevention).
Instruct patients about proper dental hygiene, including brushing teeth after meals, flossing, and regular dental check-ups.
For excellent patient education resources, visit eMedicineHealth's Teeth and Mouth Center and Infections Center. Also, see eMedicineHealth's patient education articles Dental Abscess, Toothache, When to Visit the Dentist, and Antibiotics.
What is a dentoalveolar abscess?What is the pathophysiology of dentoalveolar abscess?What are the developmental and acquired conditions associated with dental abscess?What is the role of odontogenic infections in the pathophysiology of dental abscess?How does bacterium gain entry in dental abscess?Which microflora are associated with dental abscess?What is the mortality and morbidity of dental abscess?What are the racial predilections of dental abscess?How does the prevalence of dental abscess vary by sex?In which age groups is dental abscess most common?What are the signs and symptoms of dental abscess?Which physical findings are characteristic of dental abscess in gingiva?Which physical findings are characteristic of dental abscess in teeth?Which physical findings suggest severe infections in dental abscess?What causes dental caries in dental abscess?Besides dental caries, what causes dental abscess?What are the differential diagnoses for Dental Abscess?What is the role of lab studies in the evaluation of dental abscess?What is the role of imaging studies in the evaluation of dental abscess?What is indicated by cellulitis swelling extending beyond local area in dental abscess?How is the presence of a dental abscess confirmed?Which historical finding are characteristic of dental abscess?What is the initial medical care for dental abscess?What is the role of surgery in the treatment of dental abscess?Which specialist consultations are needed for the management of dental abscess?What are dietary restrictions during treatment of dental abscess?What are activity restrictions during treatment of dental abscess?What is the role of antibiotic therapy in the treatment of dental abscess?Which medications in the drug class Antibiotics are used in the treatment of Dental Abscess?When should follow-up care be obtained for dental abscess?When is inpatient care needed for dental abscess?How are dental abscesses prevented?How are dental abscesses prevented in fluoride-deficient areas?What is the role of dental hygiene in the prevention of dental abscess?What are the complications of dental abscess?What causes facial space swelling in dental abscess?What causes necrotizing fasciitis in dental abscess?What is the prognosis of dental abscess?What information about dental abscess should patients receive?
Jane M Gould, MD, FAAP, Medical Epidemiologist, Public Health Physician
Disclosure: Spouse receives salary support from GlaxoSmithKline pharmaceutical company.
Coauthor(s)
,
Disclosure: Nothing to disclose.
Jeffrey J Cies, PharmD, MPH, BCPS (AQ-ID), Pharmacy Clinical Coordinator, Critical Care Clinical Pharmacist, Infectious Diseases Clinical Pharmacist, St Christopher’s Hospital for Children
Disclosure: Nothing to disclose.
Specialty Editors
Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Wayne Wolfram, MD, MPH, Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center; Chairman, Pediatric Institutional Review Board, Mercy St Vincent Medical Center, Toledo, Ohio
Disclosure: Nothing to disclose.
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
Halim Hennes, MD, MS, Division Director, Pediatric Emergency Medicine, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Director of Emergency Services, Children's Medical Center
Disclosure: Nothing to disclose.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Karen Schneider, MD, to the original writing and development of this article.
[Guideline] American Academy of Pediatrics Committee on Nutrition. Fluoride supplementation for children:interim policy recommendations. Pediatrics. 1995. 95:777.
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