Updated: Aug 11, 2009
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.
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.
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.1 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.
In the United Kingdom, a 39% decline in caries occurred from 1970-1980. In Denmark, a 39% decline occurred from 1972-1982.2
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.3
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.4
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.
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.
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.
Therapy must cover all likely pathogens in the context of the clinical setting.
Inhibits biosynthesis of cell wall mucopeptide and is effective during active replication. Inadequate concentrations may produce only bacteriostatic effects.
250-500 mg PO q6h
50 mg/kg/d PO divided qid
Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing a decrease in the effectiveness of penicillins when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal impairment
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.
500/125 mg PO tid
40 mg/kg/d PO divided tid
Coadministration with warfarin or heparin increases risk of bleeding
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Give for a minimum of 10 d to eliminate organism and prevent sequelae (endocarditis and rheumatic fever); following treatment, perform cultures to confirm eradication of streptococci
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.
250-500 mg PO q6h
30-50 mg/kg/d PO divided qid
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
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.
600-900 mg IV q8h
20-40 mg/kg/d IV divided q6-8h
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis
Combination antimicrobial agent that utilizes a beta-lactamase inhibitor with ampicillin. Gives better anaerobic coverage.
1.5-3 g IV q6h
<3 months: Not established
3 months to 12 years: 100-200 mg ampicillin/kg/d (150-300 mg Unasyn) IV divided q6h
>12 years: Administer as in adults; not to exceed 4 g/d sulbactam or 8 g/d ampicillin
Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of PO contraceptives
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction
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.
3.1 g IV q6h
75 mg/kg IV q6h
Tetracyclines may decrease effects of ticarcillin; high concentrations of ticarcillin may physically inactivate aminoglycosides if administered in same IV line; effects when administered concurrently with aminoglycosides are synergistic; probenecid may increase penicillin levels
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with oral penicillin during acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBCs prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; exercise caution in patients with hepatic insufficiencies; perform urinalysis and BUN and creatinine determinations during therapy, and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
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.
1 g loading dose IV; then 500 mg IV q6h
15 mg/kg loading dose IV; then 7.5 mg/kg q6h
May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity of metronidazole; disulfiram reaction may occur with orally ingested ethanol
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy
Complications of dental infections include the following:
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:4
Recommendations for dental, oral, respiratory tract, and esophageal procedures for patients with one of the conditions listed above include the following:
Current recommendations by the American Heart Association for genitourinary/GI procedures are for patients with GI or GU tract infection, if they have any of the conditions listed above (same as for dental), then the patient should undergo prophylaxis and have the antibiotic regimen include an agent active against enterococci, such as penicillin, ampicillin, piperacillin, or vancomycin.4
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.4
Maruyama F, Kobata M, Kurokawa K, et al. Comparative genomic analyses of Streptococcus mutans provide insights into chromosomal shuffling and species-specific content. BMC Genomics. Aug 5 2009;10(1):358. [Medline].
Holmstrup P, Poulsen AH, Andersen L, Skuldbol T, Fiehn NE. Oral infections and systemic diseases. Dent Clin North Am. Jul 2003;47(3):575-98. [Medline].
Daramola OO, Flanagan CE, Maisel RH, Odland RM. Diagnosis and treatment of deep neck space abscesses. Otolaryngol Head Neck Surg. Jul 2009;141(1):123-30. [Medline].
[Guideline] Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of Infective Endocarditis. Guidelines From the American Heart Association. A Guideline From the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. Apr 19 2007;[Medline].
Harwood-Nuss A, Linden C, Luten R, eds. Dental, oral and salivary gland infections. In: The Clinical Practice of Emergency Medicine. 2nd ed. Philadelphia: Lippincott Williams & Wilkins Publishers; 1996:73-77.
Kuriyama T, Williams DW, Yanagisawa M, Iwahara K, Shimizu C, Nakagawa K, et al. Antimicrobial susceptibility of 800 anaerobic isolates from patients with dentoalveolar infection to 13 oral antibiotics. Oral Microbiol Immunol. Aug 2007;22(4):285-8. [Medline].
Marioni G, Rinaldi R, Staffieri C, Marchese-Ragona R, Saia G, Stramare R, et al. Deep neck infection with dental origin: analysis of 85 consecutive cases (2000-2006). Acta Otolaryngol. Aug 22 2007;1-6. [Medline].
Pogrel MA. Antibiotics in general practice. Dent Update. Sep 1994;21(7):274-80. [Medline].
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].
Reznick J. Infections of odontogenic origin. Oral Health. 1993;1-6.
Roberts J, Hedges JR. Emergency dental procedures. In: Clinical Procedures in Emergency Medicine. 2nd ed. Philadelphia: W B Saunders Co; 1991:1045-1069.
Rosen P, Barkins R. Dental emergencies. In: Emergency Medicine: Concepts and Clinical Practice. Vol 3. 3rd ed. St Louis: Mosby-Year Book; 1992:2381-2398.
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].
dental infection, tooth infection, retropharyngeal space infection, Ludwig angina, Ludwig's angina, gingivitis, odontogenic infection, infection of tooth, dental caries, pulpitis, necrotic dental pulp, Streptococcus mutans, deep neck infection, hot potato voice, Horner syndrome, upper respiratory infection, URI, cellulitis, airway obstruction, lymphadenopathy, erythematous gingiva, treatment, diagnosis
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
Lynnus F Peng, MD is a member of the following medical societies: Alpha Omega Alpha and American Society of Anesthesiologists
Disclosure: Nothing to disclose.
A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
Willard Peng, MS, Doctor of Dental Surgery Candidate, Department of Oral Medicine, University of Southern California
Disclosure: Nothing to disclose.
Rebecca Cheng, University of California at San Diego
Disclosure: Nothing to disclose.
Michael Glick, DMD, Professor and Acting Chair, Department of Diagnostic Sciences, New Jersey Dental School, University of Medicine and Dentistry of New Jersey
Michael Glick, DMD is a member of the following medical societies: American Academy of Oral Medicine and American Dental Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Mark W Fourre, MD, Program Director, Department of Emergency Medicine, Maine Medical Center; Associate Clinical Professor, Department of Surgery, University of Vermont School of Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
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