Although most infections of the oral cavity in children are odontogenic and may be treated simply with local measures, the occasional spread of these infections to adjacent or distant fascial spaces or to the maxilla and mandible may result in life-threatening complications. Consequently, careful attention, including liberal use of the dental consultation, should be given to such infections.
Microbiologic Considerations in Dental Infections
Normal Flora
That the oral cavity provides an environment favorable to the growth of microorganisms is substantiated by reports of bacterial counts of 10 8 to 10 11 organisms/mL of saliva. More than 30 species of bacteria normally can be identified in saliva in varying proportions depending on a dynamic interaction of microbial ecosystems, including the tongue, the gingival crevice, and the presence of plaque. Age, anatomic relationships, eruption of teeth, presence of decayed teeth, diet, oral hygiene, antibiotic therapy, systemic disease, cancer chemotherapy, and hospitalization can modify the microbial population. In the older literature, emphasis was placed on the role of Streptococcus and Staphylococcus spp. in producing odontogenic infections, to the exclusion of most anaerobic bacteria. This emphasis probably was the result of failure to culture satisfactorily for anaerobic organisms, and it is now well known that the ratio of anaerobic to aerobic organisms ranges from 3 : 1 to 10 : 1.
The nomenclature of the oral flora is changing rapidly as a result of the improved understanding of the genetic makeup of these bacteria provided by molecular biology techniques. Table 8.1 summarizes changes in nomenclature among selected members of the oral flora. Molecular methods based on polymerase chain reaction allow direct identification of bacterial species to be made from the oral flora and odontogenic infections by isolation of their DNA, RNA, or both. These methods have led to appreciation of the true oral flora, for which 60% of species are unculturable. In recent years, many new species and phylotypes have been identified in the normal and pathologic oral flora.
| Older Terminology | Current Terminology |
|---|---|
| Streptococcus viridans | Streptococcus anginosus |
| Streptococcus intermedius | |
| Streptococcus constellatus | |
| Streptococcus mutans | |
| Streptococcus sanguinis | |
| Streptococcus mitis | |
| Streptococcus salivarius | |
| Streptococcus vestibularis | |
| Streptococcus (milleri) anginosus | Streptococcus anginosus |
| Streptococcus intermedius | |
| Streptococcus constellatus | |
| Bacteroides melaninogenicus | Prevotella melaninogenica |
| Prevotella intermedia | |
| Prevotella oralis | |
| Prevotella buccae | |
| Prevotella denticola | |
| Prevotella nigrescens | |
| Porphyromonas asaccharolytica | |
| Porphyromonas gingivalis | |
| Porphyromonas endodontalis | |
| Porphyromonas salivosa | |
| Porphyromonas circumdentaria | |
| Streptococcus faecalis | Enterococcus faecalis |
| Streptococcus faecium | Enterococcus faecium |
| Peptococcus species | Peptostreptococcus spp. (main oral pathogen is P. micros) |
The flora of children is similar to that of adults, with several exceptions. At birth, the oral cavity is sterile, but colonization with Streptococcus salivarius occurs rapidly. This organism has been found in 80% of cultures taken from 1-day-old infants. The percentage of Streptococcus spp. decreases from 98% at day 1 to 70% at 4 months as other organisms become established. Staphylococcus, Neisseria, Veillonella, Actinomyces, Nocardia, Fusobacterium, Bacteroides, Corynebacterium, and Candida spp. and a variety of coliforms gradually become established by the time the child reaches 1 year of age. As the deciduous dentition erupts, anaerobic organisms become well established in the gingival crevice, yet the spirochetes Bacteroides and Prevotella spp. and related oral anaerobes, which commonly are associated with the gingival crevice in adults, seem to be present in fewer numbers in patients younger than 13 to 16 years. Eruption of deciduous teeth also is associated with the establishment of Streptococcus mutans and S. sanguinis, which adhere to the enamel surface.
Pathogenic Organisms
Not all residents of the oral flora are pathogens. In the odontogenic infections caries and periodontal disease, a progression from initiating infections caused by oral streptococci toward a predominance of oral anaerobes in the more severe and long-standing infections apparently occurs. Caries is initiated primarily by Streptococcus mutans, a member of the α-hemolytic S. viridans group. As tooth decay progresses toward the dental pulp, Lactobacillus and Actinomyces spp. join the carious milieu. Severe pulpal infections generally are caused by a combination of these same oral facultative streptococci plus obligate anaerobes such as Porphyromonas endodontalis, formerly classified as Bacteroides endodontalis .
Periodontal infections also are polymicrobial; gram-positive aerobes, primarily streptococci, predominate in gingivitis, and the gram-negative anaerobic rods predominate in bone-destroying periodontitis. Juvenile periodontitis (formerly called periodontosis ), a particularly aggressive periodontal infection in children and adolescents, shows a predominance of Aggregatibacter actinomycetemcomitans (formerly known as Actinobacillus actinomycetemcomitans ) in its cultivable flora.
Orofacial odontogenic infections that spread beyond the teeth and alveolar processes are polymicrobial, yielding on average four to six isolates per case. With the use of molecular methods, even greater numbers of species can be identified in these infections, ranging from five to 18 species per case. Severe orofacial infections have been associated statistically with Fusobacterium nucleatum . The concept of the progression from aerobic streptococci to anaerobic gram-negative rods in orofacial infections is supported further by studies that have found a predominance of streptococci in early infections (in the first 3 days of symptoms) and a predominance of anaerobes in late infections. Table 8.2 lists the frequency with which the major pathogens in orofacial infections were isolated in two studies. Although the majority of bacterial identification studies are done with adult subjects, research indicates that odontogenic infections in children are caused by similar bacteria. In a recent study, S. viridans and Neisseria and Eikenella spp. were the most frequently isolated aerobic and facultative organisms. Prevotella and Peptostreptococcus spp. predominated among anaerobes.
| Microorganism | PERCENTAGE OF CASES | |
|---|---|---|
| Lewis et al. | Sakamoto et al. | |
| Streptococcus milleri | 50 | 65 |
| Peptostreptococcus spp. | 64 | 65 |
| Other anaerobic streptococci | 8 | 9 |
| Bacteroides (Prevotella) oralis | 40 | 74 |
| Bacteroides (Prevotella) gingivalis | 28 | a |
| Bacteroides (Porphyromonas) melaninogenicus | 24 | 17 |
| Fusobacterium spp. | 14 | 52 |
Infections originating from nonodontogenic causes (facial trauma, surgical manipulation, tonsillitis) are included in most studies of soft tissue and fascial space infections, and contamination from the skin or oropharynx might allow aerobic organisms, such as Staphylococcus aureus and aerobic Streptococcus spp. , to become established. In contrast, infections originating solely from the dental periapical tissues are much more likely to be predominantly anaerobic.
A pitfall in the identification of organisms as described in the older literature was the failure to culture satisfactorily for anaerobic organisms. The more current literature recognizes this fact. The preponderance of anaerobic organisms in odontogenic infections mandates the use of anaerobic and aerobic culturing techniques in situations in which cultures are indicated.
Anatomic Considerations
Most severe orofacial infections develop consequent to dental infection—periapical, periodontal, or pericoronal. Spread occurs along anatomic pathways of least resistance. Periodontal and pericoronal infections rarely have major sequelae because they generally drain from the gingival sulcus along the surface of the tooth into the oral cavity. Infections associated with the root apices generally are confined within the bony alveolar process ( Fig. 8.1 ). Should spontaneous intraoral drainage occur through either the periodontium or the pulp chamber, further spread through the 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 occur. Infections associated with root apices close to the buccal cortical plate generally spread buccally, whereas infections close to the lingual or palatal cortical plate or maxillary sinus spread in those directions ( Fig. 8.2 ). When penetration of the cortical plate occurs, infection involves the adjacent soft tissues and may manifest as cellulitis or a soft tissue abscess, which eventually may perforate the mucous membrane or skin as a sinus tract ( Fig. 8.3 ).
Perforation of periapical infections through bone follows a typical pattern that results from the position of the root apices in relation to the bony cortex and to muscle attachments ( Fig. 8.4 ). Infections involving maxillary anterior teeth and buccal roots of maxillary posterior teeth generally perforate labially or buccally, whereas infections involving palatal roots of posterior teeth perforate palatally or rarely into the maxillary sinus. The presence of the buccinator muscle attachment superior to the root apices usually confines these infections and fistulas to the oral cavity. In children, maxillary root apices often are superior to the buccinator, however, and infections may spread to the buccal or infraorbital space or to the periorbital tissues. They eventually may drain through the skin.
Infections of the mandibular incisor or canine tooth may spread either labially or lingually because the alveolar process is thin in this area. Labial perforation, which occurs more commonly, may be confined intraorally if the root apices are superior to the origin of the mentalis muscle but may spread extraorally if the apices are inferior to the mentalis attachment ( Fig. 8.5 ). Infections of the mandibular premolar and first molar often perforate buccally, whereas the second and third molars perforate lingually.
When spread of mandibular infections occurs medially, the relationship of the tooth apices to the mylohyoid muscle origin is significant ( Fig. 8.6 ). From the first molar forward, the dental root apices are superior to the mylohyoid, and these infections localize intraorally in the floor of the mouth (sublingual space). The apices of the second and third molars generally are inferior to the mylohyoid and so the submandibular space is involved, with an extraoral presentation. As in maxillary infections, the relationship of the buccinator muscle to the root apices determines whether the infection spreads intraorally or extraorally.
Two fascial spaces commonly associated with odontogenic infections are the submandibular and masticator spaces. The submandibular space is formed within the superficial layer of deep cervical fascia inferior to the mylohyoid muscle and inferomedial to the mandible. Anteriorly and posteriorly, it is limited by the bellies of the digastric muscle. Within this space lies the submandibular gland and portions of the facial artery and anterior facial vein. This space is closely approximated to the sublingual and masticator spaces. Infections of the submandibular space may originate in these adjacent spaces and in the mandibular posterior teeth.
The masticator space also is formed within the superficial layer of deep cervical fascia. Its name is appropriate because its contents include the masseter, internal and external pterygoid, and temporalis muscles, as well as the mandibular ramus and the inferior alveolar neurovascular bundle. The submandibular, lateral pharyngeal, and retropharyngeal spaces are adjacent. Infections of the masticator space may originate in adjacent spaces or spread to it from periapical or pericoronal infections of the mandibular second and third molars and maxillary third molar.
Treatment of Odontogenic Infections
Patients with odontogenic infections may present with symptoms ranging from minor to life-threatening. Too often, a patient may be given a thorough systemic and extraoral head and neck evaluation while the intraoral search for the etiologic agent is overlooked.
A thorough oral examination begins with an evaluation of the degree of mandibular opening. Interincisal distance on wide opening extends 40 mm or more, even in young children. Painful limitation of the oral opening, or trismus, is associated with inflammation of the muscles of mastication and indicates spread of the infection to the masticator space. In association with a high fever, it can represent a serious turn of events. Teeth are inspected visually for caries, by percussion for tenderness, and by electric sensitivity or hot and cold stimulation for the pulpal pain response. Gingival tissues are probed for periodontal defects, and salivary glands are palpated for tenderness and milked to observe for purulent discharge from the duct orifices.
General Therapeutic Principles
As with infections elsewhere in the body, the principles of treatment of oral infections involve surgical drainage and antibiotics. Surgical drainage may comprise standard incision and drainage of an orofacial swelling or, in the case of localized periapical infection, endodontic drainage through the pulp or extraction of the offending tooth.
Surgical treatment of odontogenic infections is primary. In a systematic review of the literature, Flynn concluded that once an abscess was drained, the usual antibiotics used for treatment of odontogenic infections worked. Dodson and colleagues, in a review of head and neck infections requiring hospitalization of children, found that facial infections of the regions at or above the level of the upper lip and teeth most frequently were upper respiratory tract– or sinus-related and that lower face infections primarily were odontogenic. Infections of the upper face resolved without surgery in 65% of cases, whereas infections of the lower face resolved without surgery in only 25% of cases. Odontogenic infections almost always required some sort of surgical intervention. This finding may be due to the fact that the portal of entry in respiratory tract infections is through the surface mucosa, whereas the tooth roots carry the invading bacterial pathogens deep into the bone of the jaw, through which the surrounding deep fascial spaces become infected.
Respiratory pathogens frequently are viral, and odontogenic infections almost uniformly are bacterial, which may explain the propensity of odontogenic infections to form abscesses that need to be drained. Odontogenic infections treated with antibiotics only almost always recur in worse form than their previous manifestation. The indications for treating with antibiotics in addition to appropriate dental surgical therapy are fever, trismus, lymphadenopathy, osteomyelitis, and compromise of the immune system. Minor infections localized to the alveolar processes can be treated by tooth extraction, gingival curettage, or root canal therapy, with or without intraoral incision and drainage, without the use of antibiotics in the nonimmunocompromised individual.
Approximately 10% of all antimicrobials prescribed in the community are for the treatment of an oral process. Misuse and overuse of antimicrobials have led to increasing resistance among many bacterial species. Oral pathogens have not been the exception. In an effort to promote the judicious use of antibiotics, the American Academy of Pediatric Dentistry (AAPD) and American Dental Association have developed guidelines intended to help reduce the inappropriate use of antimicrobial therapy in oral infections. Despite the guidelines, the adherence to the recommendations continue to be low, as demonstrated in a recent survey of 154 dentists revealing that adherence to guidelines was between 10% and 40%. In these guidelines, consideration for treatment with antibiotics involves the assessment of certain factors such as the type of infection, location and extent of infection, risk for bacterial contamination (e.g., deep crown fractures), trauma, and immunologic status of the patient.
Selecting the appropriate antibiotic should follow the basic principles of therapeutics, which include choosing the narrowest spectrum based on cultures and susceptibilities and selecting an agent that concentrates adequately in the desired tissues and that has a good safety profile, convenient dosing, and the fewest side effects. In addition, it is important to inquire about the patient’s previous antimicrobial exposures, which is a known risk factor for harboring more resistant organisms, as well as documentation of any drug allergies. In the adolescent population, asking about oral contraceptives is important because certain antibiotics used to treat dental infections, such as penicillins and tetracycline derivatives, can interfere with the efficacy of contraceptives.
Antibiotic selection for odontogenic infections, although ultimately based on Gram stain and aerobic and anaerobic cultures, generally is begun empirically before culture results are available. Odontogenic infections are usually polymicrobial, with anaerobes playing an important role. Penicillin and amoxicillin have been the first choice for outpatient infections on the basis of a good safety profile, bactericidal nature, and sensitivity of most streptococci and oral anaerobes to penicillin. However, there have been more reports of penicillin and amoxicillin resistance among oral pathogens that produce β-lactamases. Moreover, penicillin offers little or no coverage against Neisseria spp., a pathogen frequently found in odontogenic infiltrates. A study of hospitalized patients with odontogenic infections found penicillin-resistant organisms in 54% of cases and therapeutic failure of empiric penicillin in 21% of cases. The duration of previous therapy with β-lactam antibiotics also has been correlated with increased numbers of β-lactamase–producing bacteria in persisting infections. Patients with persisting infection after 3 days of treatment with a β-lactam antibiotic had a 50% incidence of β-lactamase–producing bacteria in the infection. β-Lactamase inhibitors used in combination with β-lactam antibiotics may improve their effectiveness against resistant anaerobes, and using higher doses of the amoxicillin component may overcome resistance of some oral streptococci.
Antibiotic susceptibility studies indicate that the oral anaerobes (especially Fusobacterium ) and Streptococcus spp. now are largely resistant to erythromycin. Based on these data, erythromycin should not be used as first choice in patients with odontogenic infections who are allergic to penicillin. Clindamycin, on the other hand, has an excellent track record in the treatment of odontogenic infections and can be used in patients allergic to penicillin. It concentrates well in saliva and bone and has enhanced activity against anaerobes, including bacteroides. However resistance of odontogenic flora to this lincosamide derivative is also on the rise. Poeschl and colleagues tested 73 streptococci species isolated from patients with odontogenic deep-space infections and found 16% clindamycin resistance among Streptococcus spp. and 11% resistance among oral anaerobes ( Prevotella, Bacteroides, and Peptostreptococcus spp.). Eikenella corrodens, an occasional pathogen in odontogenic infections, is uniformly resistant to clindamycin, which may explain the lack of effectiveness of clindamycin in some cases. A feared complication of the use of clindamycin is the development of Clostridium difficile colitis. This entity was first described after the use of this antibiotic and has been reported after use of clindamycin as prophylaxis for dental infections. However, more cases are reported yearly of C. difficile after the use of penicillin and cephalosporins than with clindamycin. Penetration of this drug through the blood-brain barrier is poor, and it should not be used to treat central nervous system abscesses of odontogenic origin. Azithromycin is another alternative in patients with severe penicillin allergies. It has comparable activity against oral gram positives but enhanced coverage for anaerobic gram negatives when compared to erythromycin, and it has been utilized successfully in the treatment of adult patients with periodontal disease.
Moxifloxacin, a fluoroquinolone with a spectrum of activity similar to that of amoxicillin-clavulanate, has been studied for the treatment of odontogenic infections with very good outcomes. A double-blind, phase II randomized trial comparing moxifloxacin with clindamycin in odontogenic infections found that moxifloxacin has excellent activity against Streptococcus spp. and oral anaerobes and was very effective in treatment of inflammatory odontogenic infections and abscesses. However, this trial did not include children. Fluoroquinolones, especially ciprofloxacin and levofloxacin, have been used more often in children in recent years, especially in those with cystic fibrosis. The concern of musculoskeletal adverse events (e.g., tendinitis or adverse cartilage effects) has always been the limiting factor for their use in children. Ciprofloxacin and levofloxacin are less active against oral pathogens. Moxifloxacin has been used successfully in the treatment of multidrug-resistant tuberculosis in children. Yet the optimal dosing remains to be determined. A recent pharmacokinetic study of moxifloxacin in children with tuberculosis showed that using a 10 mg/kg daily dose achieved low serum concentrations when compared to the maximum 400 mg daily adult dose, suggesting that perhaps higher doses are needed.
The second-line antibiotics in odontogenic infections are the cephalosporins, which, with the exception of the cephamycins (i.e., cefoxitin, cefotetan), have poor activity against oral anaerobes. Cephalosporins can be combined with metronidazole to enhance anaerobic coverage. Metronidazole has excellent activity against anaerobic bacteria but no activity against aerobic organisms. Moreover, it has no activity against organisms such as Actinomyces and microaerophilic streptococci, thus limiting its use as monotherapy for odontogenic infections.
Tetracycline is incorporated permanently into newly formed dentin, causing permanent disfiguring discoloration of the dentition. It should not be used in children until they are at least 9 years old, when all but the third molar teeth would have full crown formation.
Penetration into the blood-brain barrier is important when treating odontogenic infections that spread beyond the oral cavity and approach the cranial cavity. Penicillin will penetrate the barrier when the meninges are inflamed, whereas first- and second-generation cephalosporins will not. Clindamycin has poor penetration into the central nervous system and should not be used in brain abscesses. Conversely, metronidazole has excellent central nervous system penetration but needs to be combined with treatment for aerobic bacteria.
The aforementioned considerations suggest that the empiric antibiotics of choice are penicillin in mild odontogenic infections and clindamycin for severe cases or in a patient with penicillin allergy. Table 8.3 lists our recommendations for empiric antibiotic therapy in odontogenic infections.
| Type of Infection | Antibiotic of Choice |
|---|---|
| Outpatient infections | Penicillin |
| Clindamycin | |
| Penicillin allergy | Clindamycin |
| Azithromycin | |
| Inpatient infections | Clindamycin |
| Ampicillin + metronidazole | |
| Ampicillin + sulbactam | |
| Penicillin allergy | Clindamycin |
| Third-generation cephalosporin IV (if the penicillin allergy was not the anaphylactoid type—use caution) + metronidazole |
Nursing Bottle Caries
Nursing bottle caries is a pattern of tooth decay affecting mainly the primary upper incisors and frequently the upper and lower primary molars in children of bottle-feeding age. It is caused by a practice of putting the child to bed with a nursing bottle filled with a sugar-containing drink, such as milk, fruit juice, or a soft drink. The child sucks on the bottle intermittently during sleep, when salivary secretion is low, and the sugar-containing liquid stays in the mouth for extended periods. This situation provides an excellent environment for the growth of caries-producing organisms such as S. mutans . Nursing bottle caries can destroy virtually the entire primary dentition of a child as it erupts. Pediatric physicians and dentists should instruct parents to avoid putting their children to bed with nursing bottles or, if they must do so, to use water only in the bedtime drink.
Periapical Abscess
Extension of microorganisms through the root apex leads to the formation of an abscess. Early in this process, the acute abscess is indistinguishable clinically and radiographically from an acute pulpitis, particularly because radiographic evidence of bone destruction may take 7 to 14 days or more to develop. Sensitivity to heat stimulus (relieved by cold), exquisite sensitivity to percussion, and tenderness to finger pressure on the alveolar process are indications that the tooth has become abscessed. Electric pulp testing may be diagnostic if the tooth shows no response to the electric stimulus, but a positive pain response may be equivocal in multirooted teeth. Chronic abscesses are diagnosed more easily by looseness of the tooth, suppuration from draining sinuses or gingival crevice (see Fig. 8.3 ), and radiolucency on the radiographs (see Fig. 8.1 ). Depending on the path of least resistance, fluctuant areas may be noted in the buccal or lingual mucosa. Spread through the tissues, or cellulitis, may lead to the classic presentation of swollen face, pain, elevated temperature, and malaise.
In 1951, Krogh showed a 3% complication rate when 2626 infected teeth were removed at the time of initial presentation. In 1975, Martis and Karakasis published a similar study in which they treated 1376 acute dentoalveolar abscesses by immediate extraction. A 3% complication rate was found in this study as well. A complication was defined as further extension of the infection requiring additional treatment. Hall and associates published a report in 1968 in which 350 patients with odontogenic cellulitis were divided randomly into two groups. The first group had extractions performed on the day of initial presentation, whereas the second group waited (with antibiotics) until the fourth day for surgical treatment to be performed after “localization” had occurred. The investigators’ observations showed that extraction did not spread the cellulitis in either group. Patients with earlier extractions recovered more rapidly, whereas patients with delayed treatment had a greater need for incision and drainage, which was twice as likely to be extraoral than intraoral. In 1978, Martis and colleagues showed in a series of more than 2000 patients that extraction without antibiotics in the presence of periapical infection led to the same complication rate as did extraction of noninfected teeth. Current literature validates these earlier findings, indicating that infections in patients with poor oral health and a lack of preceding dental treatment produce a stronger systemic response. Extraction of involved teeth when indicated and other dental treatments lead to a less severe course of infection.
Considering the prospect of early relief of symptoms and a 97% chance that extraction (or occasionally root canal treatment) will cure the infection, early surgical intervention is mandatory. The use of antibiotics must be determined on an individual basis according to principles outlined previously ( Box 8.1 ).
Antibiotic Therapy Is Necessary
Acute-onset facial or oral swelling
Swelling inferior to the mandible
Trismus
Dysphagia
Lymphadenopathy
Fever >38.3°C (>101°F)
Pericoronitis
Osteomyelitis
Antibiotic Therapy Is Not Necessary a
a With coexisting immune system compromise, antibiotic therapy may be indicated in some of these conditions.
Asymptomatic periapical abscess
Parulis (draining sinus tract)
Dry socket (alveolar osteitis)
Periodontal disease
Dental extractions
Root canal therapy
Periodontal Infections
Surrounding the teeth is a distinctive, pink keratinized mucosa, the gingiva ( Fig. 8.7A ). Normal gingiva is attached firmly to the alveolar bone and extends between the teeth as the interdental papilla. A thin cuff of free (nonattached) gingiva surrounds each tooth, and the resulting crevice between the free gingiva and the tooth normally is 1 to 3 mm in depth. It is represented by a thin roll of tissue along each tooth in Fig. 8.7A .
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