Most severe orofacial infections develop as a result of periapical, periodontal, or pericoronal dental infection (the latter surrounding the crown of an erupting tooth), with spread occurring along the anatomic pathways of least resistance. Generally, periodontal and pericoronal infections drain through the gingival sulcus into the oral cavity and rarely have major sequelae; the exception is pericoronal infections involving erupting third molar teeth, which can spread into deeper anatomic
spaces because of their posterior location in the oral cavity. Conversely, usually infections associated with root apices are confined within the bony alveolar process. Should spontaneous intraoral drainage occur through either the periodontium or the pulp chamber, further spread through marrow spaces is unlikely. If such drainage does not occur, spread through bone (osteomyelitis) or perforation of the cortical plate of the affected jaw may take place. Once penetration of the cortical plate occurs, infection will involve the adjacent soft tissues and may manifest either as cellulitis or as a soft tissue abscess that eventually may perforate mucous membrane or skin as a sinus tract (Fig. 247.1).

Usually, perforation of periapical infections through bone follows a typical pattern stemming from the position of the root apices in relation to the bony cortex and to muscle attachments (Fig. 247.2). Abscesses associated with anterior teeth and the buccal roots of maxillary posterior teeth tend to perforate labially or buccally (into the cheek) because the tooth roots are close to that cortical plate. Abscesses associated with mandibular posterior teeth may perforate either the buccal or the lingual cortical plate. When the spread of a mandibular infection occurs lingually, the relationship of the tooth apex to the mylohyoid muscle origin is significant. If the roots are superior to the mylohyoid muscle, infections will localize intraorally in the floor of the mouth (sublingual space). Usually, apices of the second and third molars are located inferior to
the mylohyoid muscle; consequently, the submandibular space will be involved, with extraoral localization.

In children, often the maxillary and mandibular root apices are located superior and inferior, respectively, to the attachment of the buccinator muscle. Consequently, dental infections in younger patients may have a greater tendency to spread into the facial soft tissues and to localize extraorally.

Two fascial spaces commonly associated with odontogenic infections are the submandibular and masticator spaces. The submandibular space is formed by a splitting of the superficial layer of deep cervical fascia, superficial to the mylohyoid muscle and inferior to the mandible. Anteriorly and posteriorly, it is limited by the digastric muscle. Within this space lie the submandibular gland and portions of the facial artery and anterior facial vein. This space is approximated closely to the sublingual and lateral pharyngeal spaces. Often, infections of the submandibular space originate from lower molar teeth, and submandibular space infections either may spread to or arise from infections in the sublingual, lateral pharyngeal, or masticator spaces.

The masticator space also is formed by a splitting of the superficial layer of deep cervical fascia to surround the muscles of mastication and the lower jaw. Its contents include the masseter muscle, the internal and external pterygoid muscles, the temporal muscle, and the mandibular ascending ramus. The temporal and infratemporal spaces are the superior extensions of the masticator space. Adjacent are the submandibular, lateral pharyngeal, and retropharyngeal spaces. Infections of the masticator space may originate in adjacent spaces or can spread to it from periapical or pericoronal infections of the mandibular second and third molars and the maxillary third molar.

Patients with odontogenic infections may have symptoms ranging from minor to life-threatening. Patients with an orofacial infection should receive thorough systemic and extraoral head and neck evaluations; importantly, the intraoral examination for a possible odontogenic cause must not be overlooked. Thorough intraoral evaluation begins with assessing the degree of mandibular opening. The interincisal distance on wide opening may be 40 mm or more, even in young children. Painful limitation of opening, or trismus, is associated with inflammation of the muscles of mastication and indicates spread of the infection to the masticator space. Teeth are inspected visually for caries, by percussion for tenderness, and by electric or hot and cold stimulation for pulpal involvement. Gingival tissues are probed for periodontal defects, and salivary glands are palpated for tenderness and are milked to observe for purulent discharge from the duct orifices.

New treatment concepts for caries and periodontal disease, the most common oral infections, are evolving. These infections are coming to be viewed as a pathologic colonization of the oral cavity by specific normally nonresident pathogens. Traditional dental therapy for caries and periodontal disease aimed at suppressing the growth of a polymicrobial flora and repairing the damage that it causes. Instead, the goal of treatment would not be to control the growth of Streptococcus mutans (the primary agent of caries) or of a variety of periodontal pathogens by oral hygiene measures alone, but rather to eliminate S. mutans entirely.

Strategies for eradicating such organisms include the elimination of colonization sites for S. mutans by sealing the pits and fissures of the teeth with acrylic resins, use of such topical antiseptics as chlorhexidine, oral hygiene measures, and periodic culturing of saliva for this caries-producing organism. Similarly effective, especially in adults, may be elimination of periodontal pathogens by periodontal surgical débridement of the entire dentition at one visit and by a course of antibiotics effective against these organisms, followed by oral hygiene measures and topical fluoride therapy. Treatment protocols using these strategies are being tested. As with infections elsewhere in the body, the principles of treatment of orofacial infections involve surgical drainage and antibiotics. In a review of serious pediatric head and neck inpatient infections, Dodson and colleagues found that infections located above the upper lip originated most frequently in the sinuses or upper respiratory tract, whereas lower facial infections were primarily odontogenic. Almost always, odontogenic infections required surgical intervention, probably owing to the abscess-producing flora of odontogenic infections and the deep intrabony portal of entry afforded to those organisms by the roots of the teeth. Dental infections treated only with antibiotics almost always recur in a manifestation worse than the previous. Surgical drainage, preferably intraoral, may include standard incision and drainage of cellulitis or abscess or, in the case of localized periapical infection, endodontic drainage through the pulp (root canal therapy) or extraction of the offending tooth. Antibiotic therapy, although not necessary for minor, well-localized periapical lesions in noncompromised patients, is indicated if cellulitis or abscess, infections of adjacent bone (osteomyelitis), systemic signs (fever, dehydration, lymphadenopathy), trismus, or immunocompromise are present.

Generally, antibiotic selection for odontogenic infections, although based ultimately on Gram stain and aerobic and anaerobic cultures, is begun empirically before culture results
are available. Penicillin is the logical first choice for oral therapy of outpatient odontogenic infections because of its lack of toxicity, its bactericidal nature, and the sensitivity of most streptococci and oral anaerobes to this drug. Such aminopenicillins as ampicillin and amoxicillin with or without clavulanate have not demonstrated significantly better clinical success than that of penicillin V. If clinical signs or Gram stain results suggest the presence of Staphylococcus aureus, a penicillinase-resistant drug, such as oxacillin or dicloxacillin, may be added to the penicillin until the culture results are available. Alternately, a first- or second-generation cephalosporin, such as cephalexin or cefuroxime, may be used. In the case of penicillin allergy, clindamycin may be substituted, but it remains the drug of second choice for outpatient infections because of its greater toxicity. The macrolide antibiotics should be considered as tertiary selections for orofacial infections because of the high rate of resistance found among the oral streptococci and anaerobes. Among the macrolides, azithromycin would be the best choice, because of its ability to concentrate above serum levels in phagocytes. Tetracycline may result in severe staining of teeth in children younger than age 12 years and should be avoided, except when given specifically for Actinobacillus actinomycetemcomitans in cases of severe juvenile periodontitis. Similarly, the safety of using metronidazole in children has not been established, even though it is highly effective against obligate anaerobic bacteria. The fluoroquinolones are chondrotoxic in children, and their bacterial spectrum is not highly effective against most oral pathogens. Among the fluoroquinolones, however, moxifloxacin appears to have the optimum antimicrobial spectrum for odontogenic infections. However, orofacial infections severe enough to warrant hospital admission may differ microbiologically from less severe infections. Resistance to penicillin among the oral pathogens is increasing. In one study in the United Kingdom, 55% of the strains isolated were resistant to penicillin. Therefore, parenteral clindamycin, which remains highly effective against oral pathogens, is the antibiotic of first choice in severe odontogenic infections.