Orofacial odontogenic infections: Review of microbiology and current treatment

Orofacial odontogenic infections: Review of microbiology and current treatment

Orofacial odontogenic infections: Review of microbiology and current treatment Y. Gill, DMD. AL!%” and C. Scully, BDS, MD, MD.!?, PhD, FDSRCPS, MRCPat...

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Orofacial odontogenic infections: Review of microbiology and current treatment Y. Gill, DMD. AL!%” and C. Scully, BDS, MD, MD.!?, PhD, FDSRCPS, MRCPath,b Bristol, England CENTRE SURGERY







Orofacial odontogenic infections are common. Current evidence indicates that anaerobes play a major role in these infections and that the most common microbial isolates are Bacferoides, fusobacteria, peptococci, and peptostreptococci as well as some viridans streptococci. Drainage must be established where possible. Penicillin is still the drug of first choice for therapy, with metronidazole a good alternative. Nevertheless, not all clinicians are aware of current views and, therefore, this article is a state-of-the-art review for the practicing clinician of the microbiology and antimicrobial therapy of orofacial odontogenic infections. (ORAL SURC ORAL MED ORAL PATHOL 1990;70:155-8)


ost odontogenic infections arise in otherwise healthy patients as a sequelto pulp necrosis causedby caries or trauma. Periodontal infections, pericoronitis, trauma, and surgery are other sources.Many odontogenic infections drain spontaneously, but drainage may need to be established. Antimicrobials may be indicated. Most odontogenic infections resolve with little consequencesalthough, occasionally, complications may lead to more severe infections of the head and neck, particularly in immunocompromised or debilitated patients.lp9 The role of anaerobes in orofacial odontogenic infections is now well established, as is the rationale for the selection of appropriate antimicrobial treatment,4*5*1o-27 but recent studies suggestthat oral and maxillofacial surgeons still hold traditional rather than current views as to both the microbiology and treatment of orofacial odontogenic infections.28-30 This article therefore briefly reviews the microbiology and antimicrobial treatment of odontogenic infections for the practicing clinician. MICROBIOLOGY

The flora at different oral sites varies qualitatively and quantitatively, but anaerobesequal or outnumber aerobesand facultative anaerobesat virtually all oral aResearch Fellow. Now Head of Hospital Dentistry, ernment Hospital, Tiberias, Israel. bProfessor. 7/12/12586

Poriya Gov-

sites5931,32 Most odontogenic infections involve plaque organisms. Supragingival plaque consists mainly of gram-positive facultative anaerobesor microaerophilic cocci and rods, whereas subgingival plaque consists mainly of anaerobic gram-negative rods and motile forms including spirochetes. Orofacial odontogenic infections are now known to be polymicrobial and the bacteriology, though complex, often reflects the commensal oral flora.i”* ’ 1Although organisms from supragingival plaque are initially associated with dental caries and consequent pulp infection, there is later infection by anaerobes. It is microorganisms from subgingival plaque, however, that are associatedwith pericoronitis and the various forms of periodontitis.lOT33 The reported microbiology of odontogenic infections was for a long time inconsistent, but a major role for anaerobeshas becomeapparent with the development of improved microbial isolation and culture techniques.22It is now evident that orofacial odontogenie infections are usually polymicrobial, consisting of both anaerobesand aerobes;indeed, more than 65% of the speciesisolated are obligate anaerobesi2y34and these are isolated from virtually all odontogenic infections, although aerobes are also isolated from about one third of infections.lO, 34Obligate anaerobic gram-negative rods (such as Bacteroides and fusobacteria), anaerobic gram-positive cocci (such as Peptococcus and Peptostreptococcus), and facultative anaerobic gram-positive streptococci such as


Gill and Scully


Table I. Antimicrobial agents useful in the treatment of orofacial odontogenic infections Agent

Comment Most bacteria implicated in orofacial odontogenic infections are susceptible. Active against all strictly anaerobic bacteria strains. Excellent activity against oral anaerobes but may induce pseudomembranous colitis. Same antimicrobial spectrum as penicillin but anaerobes are often resistant or develop resistance. Poorly absorbed when administered orally. Effective against many oral bacteria but some are resistant and both aerobes and anaerobes rapidly develop resistance.

Penicillin Metronidazole Clindamycin Erythromycin


milleri are the organisms most frequently isolated.4, 10,12-17,X 35-38Which microorganisms are causal and which are passengersor secondary infectious agents is unclear but some anaerobes, including somegram-positive nonsporing rods such as lactobacilli, are probably not pathogenic39 whereas others, such as Fusobacterium nucleatum, seemto be associated with severe orofacial infections4’





Acute odontogenic infections are often characterized by painful soft tissue swelling, pyrexia, regional lymph node enlargement, spasm of adjacent muscles and trismus, leukocytosis, and increased erythrocyte sedimentation rate (or increased plasma viscosity). Established pus may perforate the bone into soft tissue, tracking along planes of least resistance, usually to discharge into the mouth. The spread of odontogenic infections is dictated primarily by the thicknessof the overlying bone and the location of the apices of the infected tooth in relation to muscle attachments as well as the host defenses.41 Infection can occasionally spread along fascial spaces or by the lymphatics to lymph nodes and, rarely, via the bloodstream. The fascial spacesthat may be infected most often are the sublingual, submandibular, pterygomandibular, and buccal spaces,but others such as the temporal, masseteric, parotid, lateral pharyngeal, and retropharyngeal spacesare less frequently involved.41 Hematogenous spread may lead rarely to cavernous sinus thrombosis, septicemia, or pyemia. Other serious but rare complications of odontogenic infections may include: 0 Maxillary sinusitis,3, 5,7,42 which may result from direct extension of an odontogenic infection (or from perforation of the sinus floor during ex-

traction of those maxillary teeth whose roots lie close to the antrum). 0 Osteomyelitis is a rare complication of odontogenie infections and usually arises when host resistance is reduced, for example, by previous radiation to the area, or in diabetes mellitus, alcoholism, corticosteroid therapy, osteopetrosis, or Paget’s disease.The mandible is the most common site affected, and osteomyelitis is often associated with removal of impacted third molars or difficult extractions, particularly in the presence of poor oral hygiene.*, 9 l

Dysphagia, edema of the larynx, thrombosis of the internal jugular vein, and erosion of the internal carotid artery may follow lateral pharyn-

geal space infection. Infections of both the submandibular and sublingual spaces (Ludwig’s angina) may lead to respiratory obstruction6 0 Intracranial suppuration, especially cavernous sinus thrombosis, is a rare43 but serious complication usually caused by infection passing through emissary veins. l Other rare complications include septicemia and, rarely, mediastinitis, which may follow retropharyngeal fascial space infections.44 THERAPY

Removal of the source of the infection and surgical drainage are the most important aspects of early treatment, but antimicrobials may be indicated, particularly in fascial spaceinfections or when the patient is severely ill. Penicillin

Most of the microorganisms implicated in orofacial odontogenic infections, including the anaerobes, are susceptible to penicillin, and amoxicillin in particular is still the antimicrobial treatment of first choice.28,38 However, penicillin treatment may promote the emergence of resistant Bacteroides39, 45and is ineffective for the treatment of infections caused by Wactamase-producing organisms such as certain Bacteroides species (e.g., B. melaninogenicus, B. oralis. B. ruminicola, and B. fragilis) and fusobacteria such as F. nucleatum;antimicrobials with a broader spectrum against anaerobes are then required12,25,27,35i46-49 (see as follows), Oral streptococci of the viridans group are increasingly resistant to penicillin or develop resistance after penicillin therapy.50-53 Nitroimidazoles (metronidazole, ornidazole, and tinidazole) are active against all strict anaerobes and are the best alternatives to penicillin in the treatment of orofacial odontogenic infections when the infections are by @-lactamase-producing anaer-

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obes or when the patients are allergic to penicillin 23-25, 33, 54-55

Erythromycin has essentially the same antimicrobial spectrum as penicillin and is useful when there is hypersensitivity to penicillin, but many anaerobesare resistant, or rapidly develop resistance, to erythromycin. 15, 23, 25, 21,46,49 Cephalosporins tend to be less active against anaerobes than is penicillin, and they offer little advantage15,25,27 (Table I). Clindamycin has excellent activity against both oral aerobes and anaerobes as well as penetrating bone,56but its use is strictly limited because of the danger of inducing pseudomembranous colitis* and the fact that it is no more effective than penicillin against anaerobes.58 Tetracyclines can also be effective against oral anaerobes but some microorganisms are resistant or develop resistance,23*46and tetracyclines are not especially effective therapy for oral bacterial surgical infections.59 Comprehension of the microbiology of oral bacterial surgical infections has increased over the past decade,‘jO* 61and the polymicrobial etiology and role of anaerobes.are now established. The antimicrobial treatment has changed little over this time though it is now more appreciated that penicillins are effective against most oral aerobes and anaerobes, that oral amoxicillin gives high blood levels rapidly, and that metronidazole is, in most circumstances, the best alternative when a patient is allergic to penicillin. Bacterial culture and antimicrobial sensitivity testing is indicated, particularly in more severe infections. REFERENCES

1. Sundqvist GK, Eckerbom MI, Larsson AP, Sjogren UT. Capacity of anaerobic bacteria from necrotic dental pulps to induce purulent infections. Infect Immun 1979;25:685-93. 2. Brvan CG. Kina BG. Retronbarvnneal infection in adults. Arch Intern Med 1974;134:127-34.3. Osigi PO, Osammor JY. Osteomyelitis of the maxilla secondary to odontogenic maxillary sinusitis, case report. East Afr Med J. 1983;60:270-2. 4. Sabiston CB, Gold AW. Anaerobic bacteria in oral infections. ORAL SURG ORAL MED ORAL P~THOL 1974;38:187-92.

5. Busch DF. Anaerobes in infection of the head and neck and ear, nose, and throat. Rev Infect Dis 1984;6(supp l):SllS-Sl21. 6. Tshiassny D. Ludwig’s angina: anatomic study of role of lower molar teeth in its pathogenesis.Am J Orthod 1944;30:133-45. 7. Bauer WH. Maxillary sinusitis of dental origin. Am J Orthod 1943;29:133-51. 8. Balm AJM, Tiwari RM, De Rijcke Th BM. Osteomyelitis in the head and neck. J Laryngolbtol 1985;99:1059-65. 9. Evans BE, JacobsonJH. Pierce EC. Friedman EW. Schwartz AE. Chronic osteomyelitis of the mandible: hyperbaric oxygenation treatment. NY State J Med 1976;76:996-7. 10. Von Konow L, Nord CE, Nordearan MA. Anaerobic bacteria in dentoalveolar infections. Int J Oral Surg 1981;313-22. *References 15, 23, 25, 27, 46, 49, 57

Orofacial odontogenic infections I 57 11. Sabiston CB, Grigsby WR. The microbiology of dentopyogenie infections. Crit Rev Clin Lab Sci 1977;8:213-40. 12. Chow AW, Roser SM, Brady FA. Orofacial odontogenic infections. Ann Intern Med 1978;88:392-402. 13. Bartlet JG, O’Keefe P. The bacteriology of perimandibular space infections. J Oral Surg 1979;37:407-13. 14. Kannangara DW, Tbadepalli H, Mcqvirter JL. Bacteriology and treatment of dental infections. ORAL SURG ORAL MED ORAL PATHOL 1980;50:103-9.

15. Aderhoid L, Knathe H, Frenkel G. The bacteriology of dentogenous pyogenic infections. ORAL SURC ORAL MED ORAL PATHOL 1981;52:583-7.

16. Sabiston CB, Grigsby WR, Segerstrom N. Bacterial study of pyogenic infections of dental origin. ORAL SURG ORAL MED GR,L PATHOL 1976;41:430-5.


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158 Gill and Scdly 40. Heimdahl A, von Konow L, Satoh T, Nord CE. Clinical appearance of orofacial infections of odontogenic origin in relation to microbiological findings. J Clin Microbial 1985;22:229302. 41. Ayoub P. The anatomical basis for the propagation of odontogenic infections. J Dent Quebec 1981;18:53-6. 42. Gaustad P, Wilhelmsen KW. Anaerobic infections of the oral cavity and the ears, nose, and throat. Stand J Gastroenterol 1983;84:68-73. 43. Shaw RE. Cavernous sinus thrombophlebitis. A review. Br J Surg 1952:40:4-48. 44. Murray PM, Finegold SM. Anaerobic mediastinitis. Rev Infect Dis 1984;6(supp l):S123-S126. 45. Heimdahl A, von Konow L, Nord CE. Clinical significance of penicillin-resistant fi-lactamase-producing Bacteroides species in human orofacial infections. In: Ullman U, ed. p-lactamasen. Stuttgart: Gustav Fisher Verlag, 1983:49-56. 46. Heimdahl A, Nord CE. Orofacial infections of odontogenic origin. Stand J Infect Dis [Suppl] 1983;39:86-91. 41. Heimdahl A, Von Konow L, Nord CE. Isolation of plactamase producing bacteroides strains associated with clinical failures with penicillin treatment of human orofacial infections. Arch Oral Biol 1980;25:689-92. 48. Brock I, Calhoun L, Yocum P. fl-lactamase-producing isolates of bacteroides species from children. Antimicrob Agents Chemother 1980;18:164-6. 49. Quayle AA, Russell C, Hearn B. Organisms isolated from severe odontogenic soft tissue infections: their sensitivities to cefotetan and seven other antibiotics and implications for therapy and prophylaxis. Br J Oral Maxillofac Surg 1987;25:3444. 50. MacGregor AJ, Hart P. Increased resistance to penicillin of oral streptococci in dental students. J Antimicrob Chemother 1986;17:815-9. 51. MacGregor AJ, Hart P. The effect of a single large dose of amoxycillin on oral streptococci. J Antimicrob Chemother 1986;18:113-7.

ORAL SURC ORAL MED ORAL PATHOL August 1990 52. Southall PJ, Nahy NJ, Davies RM, Speller DCE. Resistance in oral streptococci after repeated two dose amoxycillin prophylaxis. J Antimicrob Chemother 1983;12:141-6. 53. Harrison GAT, Tubin MP, Davies RM, Speller DCE. Resistance in oral streptococci after repetition of a single dose amoxycillin prophylactic regimen. J Antimicrob Chemother 1985;15:501-3. 54. Von Konow L, Nord CE. Ornidazole compared with penicillin in treatment of acute orofacial infections. J Antimicrob Chemother 1983;11:207-15. 55. Hood FJC. The place of metronidazole in the treatment of acute orofacial infection. J Antimicrob Agent Chemother 1978;4(suppl C):71-3. 56. Nord CE, Heimdahl A, Kager L, Malmborg AS. The impact of different antimicrobial agents on the normal gastrointestinal microflora in humans. Rev Infect Dis 1984;6(suppl 10: 270-5. 57. Bystedt H, Dahlback A, Dornsbusch K, Nord CE. Concentrations of azidocillin, erythromycin, doxacyclin, and clindamytin in human mandibular bone. Int J Oral Surg 1978;7:442-9. 58. Schuen NJ, Panzer JD. A comparison of clindamycin and penicillin V in the treatment of oral infections. J Oral Surg 1974;32:503-5. 59. Epstein S, Scopp IW. Antibiotics and the intraoral abscess. J Pericdontol 1977;48:236-8. 60. Hunt DE, King TJ, Fuller GW. Antibiotic susceptibility of bacteria isolated from oral infections. J Oral Surg 1978;36: 527-9. 61. Hunt DE, Meyer RA. Continued evolution of the microbiology of oral infections. J Am Dent Assoc 1983;107:52-5. Reprint requests to: Dr. Yehuda Gill Hospital Dentistry Unit Poriya Government Hospital Tiberias, Israel