Microbiology of Odontogenic Infections

Odontogenic infections are usually caused by normal endogenous flora. The mouth contains many microenvironments, allowing for colonization of many bacterial species. Once this environment is established, which varies with factors such as age, immune status, type of diet, and preferred environment, it can and does change over a lifetime. Table 12-1 lists many of the common “normal” aerobic, facultative, and anaerobic species of bacteria (several fungal species, viruses, and even protozoans can also be found in the “normal oral flora”). In most patients, these normal oral bacteria are the cause of most odontogenic infections. Other organisms can be implicated, however, if there is a compromised host or unusual oral environment, such as that found in chronic osteomyelitis. Facultative streptococci are the most numerous group of organisms in the oral cavity and members of the viridans group are the most abundant; these are classically based on their type of hemolysis on agar. Noticeably absent from these normal organisms are the staphylococci, although they are present in nearly every mouth, but in small numbers. Staphylococcus aureus, in particular, is much more common in the nose and throat, and may participate in mixed odontogenic infections. Gram-negative anaerobes comprise much of the rest of the mouth’s normal flora, and these organisms can increase in numbers, especially in patients with chronic periodontal disease.³

Table 12-1 Normal Mouth Flora

Adapted from Peterson LJ. Odontogenic infections. In: Cummings CW, ed. Otolaryngology Head and Neck Surgery. Vol 2. 2nd ed. St. Louis: Mosby; 1993:1199.

In a recent study describing the microbiology of head and neck infections of odontogenic origin by Rega and colleagues,⁴ the most common bacteria isolated were viridans streptococci, Prevotella, staphylococci, and Peptostreptococcus. This finding has been consistent for many years, even as name changes (especially for Bacteroides) have taken place to better reflect more recent genetic information.^5–9

Based on the results of many studies in the literature and much clinical anecdotal evidence, two important conclusions can be drawn regarding the microbiology of odontogenic infections: First, almost all odontogenic infections are due to mixed flora. Peterson states that the average number of different organisms is five, but can be as great as 10 or more.¹⁰ Second, between one third and two thirds of these infections are primarily anaerobic,^4,10 which probably has to do with the timing of obtaining the cultures.

The most commonly implicated organisms in mixed infections are viridans streptococci, Peptococcus, Peptostreptococcus, Eubacterium, Prevotella, and Fusobacterium. Notably absent from this list are the enteric gram-negative cocci and rods, such as group D streptococci, Escherichia coli, Pseudomonas, and Bacteroides fragilis, among others. This fact has profound implications for treatment when any of these non-normal organisms are cultured from an odontogenic infection.

The anaerobic bacteria seen in odontogenic infections are not usually acknowledged to be pathogenic themselves. The most commonly isolated anaerobe is probably Prevotella (Bacteroides). Entry of bacteria into deeper tissues to cause an infection is probably the result of invasive aerobic bacteria giving access through a necrotic dental pulp. The aerobes then serve as the initiators of the infection, preparing the local environment for anaerobic bacterial invasion and subsequent proliferation. The anaerobes then predominate because the reduction-oxidation potential favors anaerobic growth. The clinical picture is as follows: aerobic or facultative streptococci release exotoxins and lytic enzymes to cause a spreading cellulitis. As the infection progresses, a mixed streptococcal/anaerobic infection ensues. As the hypoxic state increases, the predominance of anaerobic bacteria becomes evident.

Implications of Microbiology for Antibiotic Therapy

For centuries, the primary treatment of odontogenic infections has been surgical, and it will continue to be so in the future. Endodontic therapy or extraction of the tooth, surgical drainage of the abscess, and release of pressure to improve vascularity are all fundamental in the management of these infections.

Antibiotics are a necessary adjunctive therapy in many of these infections to allow for faster and complete resolution. The choice of antibiotic should be based, at least initially, on the susceptibility of the organisms likely to be the cause of the infection. In an uncomplicated infection, an empirical choice can be made without the delay of obtaining a specimen for culture and sensitivity testing.

Two microbiologic factors must be kept in mind, however, when making this choice: first, the antibiotic must be effective against Streptococcus, because these bacteria are ubiquitous in odontogenic infections; second, the antibiotic should be effective against a wide range of anaerobes, because up to 90% of infections involve some of these bacteria. Fortunately, oral anaerobes are still very susceptible to available antibiotics.^11,12

The following list summarizes the effectiveness of commonly used antibiotics for odontogenic infections:

The very effective drugs can be used with confidence empirically to treat most odontogenic infections. The effective and less effective drugs are less predictable and should not be used as first-line drugs unless allergy dictates their use or specific culture and sensitivity data are subsequently available. The drugs listed as not effective are not effective against either Streptococcus or anaerobes. They should only be used in specific circumstances when indicated by culture results and then in combination with a beta-lactam antibiotic.

In certain infections, other antibiotics may be used. Drugs such as ampicillin, ticarcillin, piperacillin, azlocillin, mezlocillin, moxalactam, third-generation cephalosporins, and chloramphenicol are generally reserved because of their greater toxicity, excess expense, or extended spectra. However, these may be useful in a life-threatening situation, in which case an infectious disease control agency may become involved with the care.

Regarding recommendations for antibiotics, first, it is most useful to use a bactericidal antibiotic rather than a bacteriostatic, if available. The advantages of a bactericidal antibiotic are (1) less reliance on host resistance, (2) killing of the bacteria by the antibiotic itself, (3) faster results, and (4) greater flexibility with dosage intervals.¹³ Second, use of the most narrow-spectrum antibiotic first should be considered to allow less opportunity for development of resistant strains. Third, the addition of metronidazole to a beta-lactam antibiotic can add a significant benefit in the treatment of odontogenic infections, especially those considered to be mostly anaerobic. As always, the treating clinician must follow the clinical course of the patient and make the appropriate adjustment in antibiotic therapy as circumstances warrant.^14–17

Natural History of Odontogenic Infections

The usual cause of an odontogenic infection is necrosis of the pulp of a tooth, which is followed by bacterial invasion through the pulp chamber and into the deeper tissues. Necrosis of the pulp is the result of deep caries in the tooth, to which the pulp responds with an inflammatory response. Vasodilatation and edema cause pressure in the tooth and because the walls of the pulp canal are rigid and cannot expand, severe pain results. If left untreated, blood supply is lost and necrosis results, which then provides a perfect avenue for bacterial invasion into the bone and possibly deeper tissues.

Once the bacteria have invaded the bone, if left unchecked, the infection will spread equally in all directions, but ultimately will seek the path of least resistance until a cortical plate is encountered. During this time, pain continues until the patient seeks treatment, wherein endodontic therapy or extraction results in resolution of the symptoms and the infection.

Direction of Spread of Infection

The direction of spread of the infection from the tooth apex depends on the path of least resistance, considering the thickness of the overlying cortical bone and the relationship of the bone’s site of perforation to the muscle attachment of the jaws.

If no treatment is instituted, the infection erodes through the thinnest, nearest cortical plate of bone and into the overlying soft tissues (Fig. 12-1). Fig. 12-1A shows the root apex to be nearest the labial cortex; Fig. 12-1B shows the root apex to be nearest the palatal plate; Fig. 12-1C is a clinical photograph of a patient with a lip swelling, reflecting Fig. 12-1A. Clinical experience reveals that in the maxilla, Fig. 12-1A, is more common in that generally the labial-buccal cortex is thinner. If the root apex is centrally located, the infection erodes through the thinnest bone first, that is, the path of least resistance.

Figure 12-1. When the infection process is allowed to progress, it erodes through the nearest cortical plate. A, Tooth apex is near thin labial bone, so infection erodes onto labial side. B, Apex is near palatal side and erodes through that side. C, Patient with a lip abscess, reflecting A.

Once the bone has been perforated, local muscle attachments determine the location of the soft tissue abscess (Fig. 12-2). The most common pathway for the abscess is through the labial or buccal bone, occlusal to the muscle attachments, resulting in a vestibular swelling (Fig. 12-3). The vestibular abscess is seen as a fluctuant swelling, literally a “pus pocket,” adjacent to the affected tooth or teeth. If no treatment is provided, this pouch of pus usually ruptures and a sinus tract or fistula is established. At this point, the patient’s pain is relieved and he or she may believe that all is okay, especially because there are few, if any, systemic symptoms. However, if the tooth continues to be neglected, one of several things can happen. Slowly over time the bone involvement with the abscess can increase with more dissolution, possibly involving adjacent teeth. The patient may develop the classic “gum boil” or parulis, which is the body’s attempt at healing the sinus tract with ever-increasing amounts of granulation tissue. Occasionally the tract becomes congested and the pain and swelling may briefly return, until the built-up pressure causes release and relief. This cycle may repeat many times. The one meaningful consequence of continued neglect is development of an osteomyelitis, which may be more severe and more difficult to eradicate. Another unusual possibility is development of an orocutaneous fistula, which is much more common when it occurs in a longstanding mandibular infection (Fig. 12-4).

Figure 12-2. As infection erodes through bone, it can express itself in a variety of places, depending on thickness of overlying bone and relationship of muscle attachments to the site of perforation. This illustration notes six possible locations: 1, vestibule; 2, buccal space; 3, palate; 4, sublingual space; 5, submandibular space; and 6, maxillary sinus.

Figure 12-3. Fluctuant swelling in the right maxillary vestibule.

Figure 12-4. A, Periapical radiograph of a patient with an abscess on a mandibular molar which shows a tract through the inferior border of the mandible. B, Patient with an orocutaneous fistula, which may result from a longstanding infection caused by a molar infection similar to that in A.

(From Goldberg MH, Topazian RG. Odontogenic infections and deep fascial space infections of dental origin, Figure 8-2. In: Topazian RG, Goldberg MH, Hupp JR, eds. Oral and Maxillofacial Infections. 4th ed. Philadelphia: WB Saunders; 2002:162.)

If the infection perforates the bone above the muscle attachment (see Fig. 12-2, points 2, 4, and 5), fascial space involvement occurs. When this happens, the potential for more severe infection and more significant systemic symptoms becomes greater. A rare occurrence, in my experience, is an odontogenic infection creating a sinusitis, reflected in Fig. 12-2, point 6. The sinus membrane provides a modicum of protection to the spreading infection and allows the body’s defenses to “wall off” the abscess, most commonly.

As previously stated, once the infection extends beyond the local muscle attachments, fascial space involvement is possible. Spread of infection along these potential spaces is determined by the presence of loose connective tissue. Fasciae develop in planes covering musculature that is subjected to movement. Surrounding or separating muscles, fascial planes offer an anatomic roadmap for infection to develop from the superficial to deep tissues of the face and neck. It is important to remember that these are potential spaces until separated by pus, blood, or dissection. Other features of these spaces are:

It is my opinion that open incision and drainage is the best course of treatment for a fascial space infection, particularly when the mandibular spaces are involved. Although needle aspiration can remove pus, it usually delays recovery because dependent drainage is not accomplished and irrigation of the wound is not possible. Anaerobic bacteria can cause significant tissue destruction and this debris is better cleared with an open wound. Trismus also resolves more quickly and early return to function is a desirable end point. Clearly, clinical judgment and experience play a large role in this treatment decision.

Fascial Space Involvement

Maxillary Spaces

As previously stated, most maxillary tooth infections manifest as vestibular abscesses, more often on the labial-buccal surface, but occasionally on the palatal surface (especially if the palatal root of a maxillary molar is the cause). If the path of infection breaks out above the muscle attachments, then a space infection is possible. The two primary maxillary spaces that may be involved are the canine space and the buccal space.

The canine space becomes infected almost exclusively as a result of apical infection of the root of the maxillary canine tooth. The root must be long enough to ensure that the apex is superior to the insertion of the levator anguli oris muscle. The canine space is located between the anterior surface of the maxilla and the levator labii superioris. When infected, there is usually swelling lateral to the nose and loss of the ipsilateral nasolabial fold. Drainage is most often accomplished with an intraoral stab incision (Fig. 12-5).

Figure 12-5. Patient with a canine space abscess. Note the swelling and obliteration of the nasolabial fold.

(From Goldberg MH, Topazian RG. Odontogenic infections and deep fascial space infections of dental origin, Figure 8-9. In: Topazian RG, Goldberg MH, Hupp JR, eds. Oral and Maxillofacial Infections. 4th ed. Philadelphia: WB Saunders; 2002:169.)

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