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Dental Abscess

  • Author: Jane M Gould, MD, FAAP; Chief Editor: Russell W Steele, MD  more...
 
Updated: Apr 21, 2015
 

Background

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.

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Pathophysiology

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 or impacted third molar.

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]

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Epidemiology

Mortality/Morbidity

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.

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Contributor Information and Disclosures
Author

Jane M Gould, MD, FAAP Associate Professor of Pediatrics, Drexel University College of Medicine; Hospital Epidemiologist, Attending Physician, Section of Infectious Diseases, St Christopher's Hospital for Children

Jane M Gould, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Society for Healthcare Epidemiology of America

Disclosure: Partner received salary from Teva Pharmaceuticals for employment.

Coauthor(s)

Jeffrey J Cies, MPH, PharmD, BCPS Pharmacy Clinical Coordinator, Critical Care Clinical Pharmacist, Infectious Diseases Clinical Pharmacist, St Christopher’s Hospital for Children

Jeffrey J Cies, MPH, PharmD, BCPS is a member of the following medical societies: American College of Clinical Pharmacy, American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

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

Halim Hennes, MD, MS is a member of the following medical societies: American Academy of Pediatrics

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.

References
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  15. Hall V, Collins MD, Hutson RA, et al. Actinomyces oricola sp. nov., from a human dental abscess. Int J Syst Evol Microbiol. 2003 Sep. 53(Pt 5):1515-8. [Medline]. [Full Text].

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  20. Sands T, Pynn BR, Katsikeris N. Odontogenic infections: Part two. Microbiology, antibiotics and management. Oral Health. 1995 Jun. 85(6):11-4, 17-21, 23 passim. [Medline].

 
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Obvious swelling of the right cheek due to dental abscess.
Side view. Fluctuant mass extending toward the buccal side of the gum end to the gingival-buccal reflection.
 
 
 
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