Dental Abscess 

  • Author: Jane M Gould, MD, FAAP; Chief Editor: Russell W Steele, MD   more...
 
Updated: Feb 5, 2010
 

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, 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  Assistant 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, and Society for Healthcare Epidemiology of America

Disclosure: AstraZeneca Salary Employment

Coauthor(s)

Jeffrey J Cies, PharmD, BCPS  Pharmacy Clinical Coordinator, Critical Care Clinical Pharmacist, St Christopher's Hospital for Children

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

Disclosure: Nothing to disclose.

Specialty Editor Board

Halim Hennes, MD  MS, Pediatric Emergency Medicine Research Director, Professor, Departments of Pediatrics and Emergency Medicine, Medical College of Wisconsin

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

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Wayne Wolfram, MD, MPH  Associate Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center

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

Disclosure: Nothing to disclose.

Daniel Rauch, MD, FAAP  Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine

Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine

Disclosure: Baxter Honoraria Consulting

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

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, and Southern Medical Association

Disclosure: None None None

References
  1. [Guideline] Krebs KA, Clem DS 3rd. Guidelines for the management of patients with periodontal diseases. J Periodontol. Sep 2006;77(9):1607-11. [Medline].

  2. Seow WK. Diagnosis and management of unusual dental abscesses in children. Aust Dent J. Sep 2003;48(3):156-68. [Medline].

  3. Stefanopoulos PK, Kolokotronis AE. The clinical significance of anaerobic bacteria in acute orofacial odontogenic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Oct 2004;98(4):398-408. [Medline].

  4. [Best Evidence] Brook I. Microbiology and management of endodontic infections in children. J Clin Pediatr Dent. 2003;28(1):13-7. [Medline].

  5. [Best Evidence] Robertson D, Smith AJ. The microbiology of the acute dental abscess. J Med Microbiol. Feb 2009;58(Pt 2):155-62. [Medline].

  6. Delaney JE, Keels MA. Pediatric oral pathology. Soft tissue and periodontal conditions. Pediatr Clin North Am. Oct 2000;47(5):1125-47. [Medline].

  7. Jain S, Nagpure PS, Singh R, Garg D. Minor trauma triggering cervicofacial necrotizing fasciitis from odontogenic abscess. J Emerg Trauma Shock. Jul 2008;1(2):114-8. [Medline].

  8. Kellogg N,. Oral and dental aspects of child abuse and neglect. Pediatrics. Dec 2005;116(6):1565-8. [Medline].

  9. Brauer HU. Unusual complications associated with third molar surgery: A systematic review. Quintessence Int. Jul-Aug 2009;40(7):565-72. [Medline].

  10. [Guideline] American Academy of Pediatrics Committee on Nutrition. Fluoride supplementation for children:interim policy recommendations. Pediatrics. 1995;95:777.

  11. Ferrera PC, Busino LJ, Snyder HS. Uncommon complications of odontogenic infections. Am J Emerg Med. May 1996;14(3):317-22. [Medline].

  12. Flynn TR, Shanti RM, Levi MH, et al. Severe odontogenic infections, part 1: prospective report. J Oral Maxillofac Surg. Jul 2006;64(7):1093-103. [Medline].

  13. Gill Y, Scully C. The microbiology and management of acute dentoalveolar abscess: views of British oral and maxillofacial surgeons. Br J Oral Maxillofac Surg. Dec 1988;26(6):452-7. [Medline].

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

  15. LeJeune HB, Amedee RG. A review of odontogenic infections. J La State Med Soc. Jun 1994;146(6):239-41. [Medline].

  16. Lewis MA, MacFarlane TW, McGowan DA. A microbiological and clinical review of the acute dentoalveolar abscess. Br J Oral Maxillofac Surg. Dec 1990;28(6):359-66. [Medline].

  17. Lewis MA, MacFarlane TW, McGowan DA. Antibiotic susceptibilities of bacteria isolated from acute dentoalveolar abscesses. J Antimicrob Chemother. Jan 1989;23(1):69-77. [Medline].

  18. Pynn BR, Sands T, Pharoah MJ. Odontogenic infections: Part one. Anatomy and radiology. Oral Health. May 1995;85(5):7-10, 13-4, 17-8 passim. [Medline].

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

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Obvious swelling of the right cheek.
Side view. Fluctuant mass extending toward the buccal side of the gum end to the gingival-buccal reflection.
Gingiva with swelling and erythema.
 
 
 
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