Principles of Management and Prevention of Odontogenic Infections


Odontogenic infections are commonly encountered clinical problems that may have serious consequences if not managed promptly and properly. Although a wide range of clinical practitioners, including emergency medicine and primary care physicians and nurse practitioners, encounter odontogenic infections, the role of the dentist is crucial and indispensable. It is imperative to thoroughly understand the pathogenesis and natural progression of infections in the head and neck region and be able to recognize risk factors, as well as signs and symptoms of each stage of progression, to render proper diagnosis and management, regardless of one's level of training or expertise. It is equally crucial to understand that management of odontogenic infections is primarily surgical in nature.

This chapter focuses on two broad sections. The first discusses the microbiology and pathophysiology of odontogenic infections, along with basic principles of nonsurgical and surgical management. Special emphasis is placed on the general dentist's role in the management of odontogenic infections. The second section focuses on recognition and prevention of odontogenic infections, specifically on prophylactic antibiotic therapy that may be indicated in various clinical scenarios.

Microbiology of Odontogenic Infections

Odontogenic infections are primarily caused by normal oral bacterial flora, which include aerobic and anaerobic gram-positive cocci and anaerobic gram-negative rods. Odontogenic infections are almost invariably polymicrobial, involving multiple bacteria, and the identification of a single primary organism is usually not possible via routine culture and sensitivity testing. Approximately 50% to 60% of all odontogenic infections involve a combination of both aerobic and anaerobic bacteria.

The most commonly isolated aerobic bacteria from odontogenic infections are the viridans- type Streptococci . These bacteria are facultative organisms that possess the ability to survive with or without oxygen. These bacteria are believed to initiate the progression of a superficial infection into the deeper tissues. The most commonly isolated anaerobic bacteria from odontogenic infections include Bacteroides spp., followed by Prevotella and Peptostreptococcus spp. ( Table 16.1 ).

TABLE 16.1
Major Organisms Isolated in Odontogenic Infections
Data from Bahl R, Sandhu S, Gupta M. Odontogenic infections: microbiology and management. Contemp Clin Dent . 2014;5(3):307–311.
Organism Occurrence
Aerobic
Staphylococcus aureus 20%
Coagulase-negative staphylococci 10%
Streptococcus viridans 45%
Corynebacterium spp. 5%
Pseudomonas aeruginosa 5%
Anaerobic
Prevotella 30%
Bacteroides 30%
Peptostreptococcus 20%
Porphyromonas 5%

Once bacteria infiltrate the deeper soft tissues, they penetrate throughout the fascial spaces, or potential spaces, and spread by producing hyaluronidase, an enzyme that cleaves hyaluronic acid and allows the spread of the infection through the subcutaneous tissues. As the infection spreads into the deeper tissues, byproducts of bacterial metabolism create an acidic environment, facilitating the growth of anaerobes. As anaerobes predominate, there is further tissue breakdown and liquefaction necrosis as well as the breakdown of white blood cells (WBCs). This results in microabscesses, which may coalesce and clinically manifest as an abscess . In addition, the pressure from the expanding abscess increases the hydrostatic pressure on the surrounding blood vessels, preventing compromising blood flow leading to ischemia, and thereby further increasing the zone of necrosis within the abscess cavity.

Pathophysiology of Odontogenic Infections

Odontogenic infections, as the term implies, arise from tooth-related endodontic or periodontal sources. These etiologies may include a necrotic pulp from a carious or fractured tooth, pericoronitis from a partially impacted tooth, or deep periodontal pockets. Regardless of the source, when inadequately managed, an infection will progress and spread through the path of least resistance . For an odontogenic infection of endodontic origin, the infection in the periradicular region will gradually erode through the facial or lingual cortex of the bone of the maxilla or mandible. The location of this erosion through bone largely depends upon the faciolingual location of the source of the infection, as well as the thickness of the cortical bone ( Fig. 16.1 ). For example, an odontogenic infection arising from a necrotic pulp of a mandibular molar will generally erode through the lingual cortex, because the apices of these teeth tend to be on the lingual aspect of the mandible and the cortex tends to be thinner on the lingual than on the buccal surface ( Fig. 16.2 ). Infection from a necrotic pulp of a maxillary molar will tend to erode through the facial cortex because the facial bone is thin, which offers little resistance to erosion, and represents the path of least resistance.

Fig. 16.1, (A) Periradicular infection in a maxillary incisor with the root apex close to the facial bone results in erosion of the facial cortex and vestibular abscess. (B) Maxillary incisor with the root apex closer to the palatal cortex, increasing the likelihood of palatal cortical erosion and palatal abscess.

Fig. 16.2, Periapical infections arising from mandibular molars generally erode through the lingual cortex (left), whereas infections from maxillary molars generally erode through the thin buccal cortex (right).

Once the infection erodes through bone, it continues to spread through the path of least resistance via potential spaces. These spaces, as the term implies, are not actual “spaces” that exist in healthy tissues; they are only created when infiltrated by an infection or surgical manipulation. The location of the involved potential space depends primarily on the location of the bony erosion relative to adjacent muscle attachments on the bone. When the erosion is superior (or cranial, or coronal) to the buccinator muscle attachment, infection will involve the vestibular space in the mandible; it will involve the buccal space in the maxilla if the cortical perforation occurs facially ( Fig. 16.3 ). When the facial erosion is inferior (or caudal, or apical) to the buccinator attachment, infection will involve the buccal space in the mandible, and the vestibular space in the maxilla. When the erosion is lingual, involvement of the palatal space (maxilla) or sublingual space (mandible) will occur. For the mandible, a lingual perforation superior to the mylohyoid muscle will lead to the sublingual space, and to the submandibular space if inferior to the mylohyoid muscle ( Fig. 16.4 ). Such infections will invariably progress to deeper spaces unless managed promptly and properly. Infections of periodontal origin will seldom involve severe bony erosion, and will typically spread directly through these potential spaces.

Fig. 16.3, A cortical perforation inferior to the buccinator attachment from a maxillary molar will lead to involvement of the vestibular space. When the cortical perforation is inferior to the buccinator attachment in the mandible, the buccal space will be involved.

Fig. 16.4, Lingual perforation superior to the mylohyoid attachment will result in involvement of the sublingual space (shown in orange). When the cortical perforation is inferior to the mylohyoid attachment, the submandibular space will be involved (shown in green).

When infections reach the soft tissues, it generally manifests in four stages: inoculation (edema), cellulitis, abscess, and resolution ( Table 16.2 ). The inoculation (edema) stage refers to the stage in which the invading bacteria begin to colonize and typically occurs in the first 3 days of onset of symptoms. This stage is characterized by diffuse, soft, doughy red swelling that is mildly tender. The cellulitis stage occurs between days 3 and 5 and represents the intense inflammatory response elicited by the infecting mixed microbial flora. This stage is characterized by poorly defined diffuse firm red swelling that is exquisitely painful to palpation. As the infection evolves and anaerobes begin to predominate, liquefaction of tissues occurs with the formation of purulence, which is the hallmark of the abscess stage . As purulence is formed, the swelling and redness become better defined and localized, and the consistency changes from firm to fluctuant. When an infection is drained, either spontaneously or via surgery, the host defense mechanism destroys the involved bacteria and healing begins to occur; this is the hallmark of the resolution stage .

TABLE 16.2
Characteristics of Inoculation, Cellulitis, and Abscess
Characteristic Inoculation Cellulitis Abscess
Duration 0–3 days 1–5 days 4–10 days
Pain, borders Mild, diffuse Diffuse Localized
Size Variable Large Smaller
Color Normal Red Shiny center
Consistency Jelly or dough-like Board-like Soft center
Progression Increasing Increasing Decreasing
Purulence Absent Absent Present
Bacteria Aerobic Mixed Anaerobic
Seriousness Low Greater Less

In clinical practice, the most commonly encountered odontogenic infection is a vestibular space abscess of endodontic origin ( Fig. 16.5 ). These infections may occasionally rupture and drain spontaneously, which results in temporary resolution, preventing spread to deeper potential spaces. Spontaneously draining infections may continue to drain and form a fistula to the oral cavity or a sinus tract to skin, or reclose and result in the reforming of an abscess.

Fig. 16.5, Fluctuant edema and erythema of the maxillary left anterior vestibule associated with necrotic pulp of the maxillary left lateral incisor.

Principles of Management

Management of odontogenic infections involves three factors: (1) controlling the source of the infection, (2) establishing drainage, and (3) mobilizing the host defense system. The practitioner's predominant role is to maximize control of the first two factors to allow the host defense system to take over and combat the infection. This involves elimination of the source of the infection and providing drainage of any accumulated infection. As long as the source of the infection (i.e., endodontically or periodontally involved tooth) is present, permanent resolution will never occur. Likewise, if a significant bacterial load (>10 5 colony-forming units/mL) is present in the form of a collection of purulence or cellulitis, the host defense system may not be able to overcome the infection. It is therefore of paramount importance to understand that management of odontogenic infections is primarily surgical in nature. In other words, odontogenic infections are managed primarily with removal of the etiology and surgical incision and drainage, and antibiotics should not be regarded as the primary or sole form of treatment for infections.

With this in mind, the following universal principles should be used in the management of odontogenic infections, regardless of the severity of the infection.

Principle 1: Determine Severity of Infection

Odontogenic infections can range from routine and localized to severe and life-threatening. The practitioner's first goal is to determine the severity and intervene accordingly. This allows control of the infection and prevention from progressing to the deeper potential tissue spaces. Determination of severity begins with a complete history, followed by physical examination, and any necessary ancillary testing (e.g., radiographic imaging studies, laboratory studies).

Complete History

The goal of history-taking is to gather as much pertinent information as possible and to guide the clinician in as accurate and efficient a manner as possible. Components of history-taking and their significance are summarized in Table 16.3 .

TABLE 16.3
Components of History-Taking and Their Significance
Component Significance
Chief complaint (e.g., symptoms)
  • Origin, etiology of infection

  • Involved anatomic space(s)

  • Severity of infection

History of present illness (e.g., onset, chronicity and duration, evolution of symptoms, treatment history)
  • Origin, etiology of infection

  • Involved anatomic space(s)

  • Aggressiveness of infection

Medical history and medications
  • Other comorbidities that may affect management

Social history
  • Social factors that may affect management (e.g., substance abuse, access to dental and medical care)

Review of systems
  • Involved anatomic space(s)

  • Severity

  • Other comorbidities that may affect management (other than those elicited on medical history)

The first step in history-taking is to thoroughly elicit the patient's chief complaint. Although it is important to document the chief complaint in the patient's own words, vague complaints such as “my tooth hurts,” “my jaw hurts,” and “my face is swollen” must be probed further to include details such as the location, severity, duration, and quality of the pain and/or swelling. Certain symptoms are associated with severe infections with involvement of deeper spaces; this should raise immediate concerns and lower the threshold for prompt, if not immediate, expert consultation or activation of the emergency medical system. These include fever and malaise, difficulty breathing (dyspnea), difficulty or pain on swallowing (dysphagia or odynophagia), change in voice (dysphonia), and limited mouth opening (trismus).

The next step is to obtain a thorough history of the chief complaint (history of present illness). This provides the clinician with valuable clues that could help determine the origin and etiology of the infection, any involved anatomic spaces, and the aggressiveness of the infection.

Common questions include:

  • “Did you have any pain or other symptoms before this occurred?”

  • “Did you have any dental treatment or injuries before these symptoms appeared?”

  • “For how long have you had these symptoms?”

  • “Did the pain change in character, intensity, or location?”

  • “Have you sought any care for this problem? If so, what treatment?”

Knowledge of the initial symptoms gives the clinician clues as to the origin of the infection. For example, if the patient had a history of chronic dental pain in the area of the chief complaint, necrosis or severe periodontal disease of this tooth could be the suspected cause. This will allow the clinician to focus on this area during the comprehensive physical examination. Changes in the character and location of pain could indicate progression of the infection. For example, if pain from a mandibular molar changed to pain in the jaw and the neck, the clinician should have a high suspicion of spread to a deeper space(s). Duration of the symptoms could help the clinician determine the aggressiveness of the infection. In general, symptoms that have been steady and persistent for an extended period of time (>30 days) indicate a chronic infection that is being contained by the host defense system. On the other hand, acute-onset symptoms with rapid exacerbation generally indicate a more aggressive infection, compromise of the host defense system, or both. Previous treatment history also provides the clinician with important clues regarding the aggressiveness of the infection. If a patient presents with an infection despite having had the cause of the infection removed and/or drainage of the infection, this could indicate an aggressive infection requiring the need for more aggressive management.

After meticulously obtaining information about the symptoms and history, a thorough past medical history and social history are elicited in the usual fashion. When using a questionnaire-based form for a health history, it is essential for the practitioner not only to review the patient's responses, but to further discuss the responses with the patient and/or caregiver to avoid missing important items or miscommunication. If the patient is a poor historian, it is often necessary to contact the patient's primary care provider or specialist to obtain a complete medical history via medical consultation.

The next step is a thorough review of systems. This is the step in the history-taking when further symptoms are elicited, including not only those of the oral cavity and head and neck, but those of the entire body (such as constitutional symptoms, chest pain, shortness of breath, polyuria, polydipsia, and polyphagia). This step is crucial in identifying pertinent positive and negative symptoms that could help either rule in or rule out severe infections. It is also crucial in finding potential medical problems (comorbidities) that could impact the healing and resolution of the infection, not elicited in the medical history (such as undiagnosed diabetes mellitus or a human immunodeficiency virus [HIV] infection or other immunocompromised state).

Physical Examination

Physical examination must be performed in a comprehensive and organized fashion, and the clinician should avoid examining the oral cavity first, which makes it easy to miss obvious yet extremely important findings that have a direct impact upon management. It is recommended that the clinician begin from “big to small,” or “outside then inside.” This begins with obtaining vital signs (temperature, blood pressure, heart rate, and respiratory rate). Patients with odontogenic infections often have an elevated heart rate of more than 100 beats/min (tachycardia), a respiratory rate of more than 20 breaths/min (tachypnea), and increased blood pressure (hypertension). Although pain and anxiety can elevate these vital signs, such findings should raise concerns for the practitioner. An elevated temperature to 101°F (38.3°C) or higher strongly indicates bacteremia and systemic involvement and invariably requires immediate intervention, typically by an oral and maxillofacial surgeon. In addition to vital signs, oxygen saturation (SpO 2 ) should be determined with pulse oximetry to ensure adequate tissue oxygenation. Decreased oxygen saturations below 95% in an otherwise healthy patient should raise concerns for the possibility of airway compromise or obstruction.

After obtaining vital signs, the patient should be examined for general appearance. This could occur as early as the moment the patient enters the examination room. If the patient does not appear distressed and is ambulating and speaking without difficulty, the likelihood of a severe infection is not very likely. On the other hand, if the patient appears fatigued and lethargic ( Fig. 16.6 ), has an increased work of breathing, has a change in their voice pattern, and is unable to handle secretions (drooling), it is highly likely that a severe infection is present. The clinician should also listen for any signs of high-pitched breath sounds (stridor), which could indicate obstruction of some part of the airway.

Fig. 16.6, Patient with left canine space infection with periorbital space extension, with malaise and characteristic “toxic appearance” indicating compromised host defenses.

Next, a focused head and neck examination should be performed, beginning with inspection. The clinician should carefully look for any swelling or asymmetry, as well as erythema (redness) of the head and neck region. If any of these findings is present, it could indicate involvement of the surrounding space(s), especially if it corresponds to the area of the patient's symptoms. Common areas of head and neck swelling include the temporal, orbital, nasolabial, cheek, and mandibular angle regions and along the inferior border of the mandible ( Table 16.4 ). Any areas of swelling must be examined with gentle palpation and characterized accordingly. The consistency may be soft and normal, doughy, firm and hard (indurated), or fluctuant. A doughy consistency is commonly seen in the inoculation (edema) stage of the infection. At this stage, tenderness is generally mild and diffuse. Induration is usually a hallmark of cellulitis and is diffuse and exquisitely tender to palpation. Fluctuance indicates a fluid (e.g., purulence) collection, which is characteristic of the abscess stage. At this stage, the infection is better localized than the cellulitis stage and less tender due to less tissue pressure. It must be noted that an odontogenic infection is an ongoing spectrum of stages; therefore all of these various consistencies could overlap and be present at the same time.

TABLE 16.4
Common Areas of Extraoral Swelling in Odontogenic Infections
Region Commonly Involved Space(s)
Temple Superficial temporal space, deep temporal space
Orbit Periorbital space
Nasolabial Canine space
Cheek Buccal space
Angle of mandible Masseteric space, lateral pharyngeal space
Inferior border of mandible and neck (lateral) Submandibular space
Inferior border of mandible and neck (midline) Submental space

Mandibular mouth opening should be assessed; this is of particular importance for three main reasons. The first is that limited mouth opening (trismus) may indicate involvement of deep spaces, in particular the masticator spaces (spaces involving the muscles of mastication), which require prompt aggressive treatment by an oral and maxillofacial surgeon to prevent progression to deeper spaces and airway compromise. The degree of trismus generally corresponds to the severity of the infection. It must also be noted that swelling is not a prominent finding in such infections (in fact, it may not be present at all), which further highlights the significance of trismus. The second reason that mouth opening is important is for intraoral access. Limited mandibular opening precludes a thorough intraoral examination or intraoral surgical intervention. Therefore patients with severe trismus secondary to an odontogenic infection often require surgical drainage and elimination of the infection source under general anesthesia in a hospital setting. The third reason trismus is important is that when a patient with limited mouth opening undergoes general anesthesia, special considerations and measures must be made to protect the airway with an endotracheal tube, usually via endoscopically guided fiberoptic nasal intubation techniques. It must be noted that although trismus may be due to guarding (self-protection) secondary to pain or anxiety, the clinician should nevertheless have a heightened sense of awareness when encountering trismus. Using a maximum interincisal opening of 40 mm as the norm, the clinician can measure the distance between the maxillary and mandibular incisors without assistance (active) and with gentle assistance (passive). Ideally a ruler should be used to measure the interincisal distance; however, the use of fingerbreadths (three fingerbreadths generally corresponds to 40 mm) is a common and acceptable method. A limited mouth opening may indicate involvement of the masticator spaces, and trismus of less than 15 mm usually indicates the presence of a severe infection.

After examining the head and neck, attention is directed to the oral cavity. This examination should also be performed in a systematic fashion, progressing from general to specific areas. The clinician should avoid the temptation of examining the swelling or dentition first. Areas such as the pharyngeal walls, uvula, and the floor of mouth must be examined. Infections extending to such areas could compromise the airway, and abnormalities must be recorded and further investigated. Then, the hard and soft palate, the facial vestibule, and the gingiva should be carefully inspected, palpated, and characterized. Next, the dentition should be examined for caries, periodontal disease, large restorations, any defects around existing restorations, tooth fractures, mobility, percussion sensitivity, and vitality (for involved teeth only). When a severely carious or periodontally involved tooth is in the immediate vicinity of an intraoral swelling, it can oftentimes be deemed the source of the infection. However, when multiple problematic teeth are present or the physical examination is equivocal, ancillary testing such as vitality testing and radiographic examination is warranted.

Imaging Studies

In a general dental or oral and maxillofacial surgery office, common imaging studies used for odontogenic infections include periapical radiographs, panoramic radiographs, and cone-beam computed tomography. Bitewing radiographs, which are frequently obtained for routine caries surveillance and restorative purposes, have no significant role in the assessment of odontogenic infections because they do not capture the periapical region, which is the most common and important area from which odontogenic infections originate. Panoramic radiographs allow a general overall view of the jaws, nasal cavity, maxillary sinuses, and dentition, and have the benefit of simple acquisition with minimal discomfort for the patient (especially if trismus is present). Periapical views allow a more detailed assessment of the teeth and their periapical regions and have the benefit of less radiation dosage. A cone-beam computed tomography scan allows a three-dimensional view of the maxillofacial skeleton and teeth and is useful if the source of the infection is unclear based upon the history and clinical examination (e.g., multiple adjacent carious teeth, suspected jaw fracture, or osteomyelitis). The clinician must weigh the risks and benefits of each imaging modality and provide the most comprehensive assessment with the least morbidity to the patient (ALARA rule: as low as reasonably achievable). Adjunctive techniques could be used such as insertion of a radiopaque material (such as gutta percha) through an existing parulis, fistula, sinus tract, or periodontal pocket to localize the precise source of the infection. This technique is useful when multiple defective teeth are adjacent to an area of infection. Deep fascial space infections that either pose a risk for airway compromise (such as the lateral pharyngeal space or retropharyngeal space) or are not easily identified on physical examination (such as the infratemporal space) may benefit from obtaining medical-grade computed tomography imaging in a hospital setting. It must be emphasized that radiographic examination can never substitute for a thorough history and physical examination.

Laboratory Studies

Laboratory testing may be used to assist in the patient evaluation. However, for odontogenic infections, these are invariably limited to use in a hospital setting. The main purpose of this ancillary testing is to assess the host's systemic response to the infection, via bacteremia, as well as to monitor recovery following any treatment provided. Since localized infections (e.g., vestibular abscesses) generally do not result in significant constitutional symptoms, laboratory tests are rarely, if ever, required. However, deeper space infections, such as infratemporal lateral pharyngeal and retropharyngeal space abscesses are difficult to examine clinically and are typically associated with significant constitutional symptoms such as fever and malaise. In such infections, laboratory studies also serve as adjuncts to the physical examination when assessing response to treatment.

The most commonly used laboratory study is the complete blood count, with focus on the white blood cell (WBC) count, and more specifically, the WBC differential count. The rationale for this test is that an elevated WBC represents a strong immune response to the infection in the form of increased WBC production and mobilization into the bloodstream. It is important to understand that in an acute setting, the WBC count may be affected by noninfectious factors such as medications (e.g., corticosteroids) and stress and should always be correlated within the overall clinical context. A differential WBC count can help mitigate the effects of such factors by focusing on the immature granulocytes (polymorphonuclear leukocytes and neutrophil band cells, or a “left shift” in the differential WBC count), which serve as better indicators of an infectious process; an increase in these immature cells indicates that the bone marrow is increasing production of these cells in order to combat a systemic infection. Following resolution of the bacteremia and infection, the WBC count will gradually return to baseline; this can be a useful study to monitor progression of the infection.

Similar to any other ancillary testing, laboratory studies are intended to complement the history and physical examination and, more importantly, affect management of the patient. Indiscriminate radiologic or laboratory testing cannot be justified if it is not expected to impact upon the overall management of the patient.

Overall Assessment

Once a thorough patient history is obtained and a comprehensive physical examination is performed followed by any indicated ancillary testing, the clinician should be able to determine the location and stage of the infection as well as the etiology and severity of the infection. As discussed previously, the majority of the assessment could be determined based upon a thorough history and physical examination, and any necessary ancillary tests such as imaging and laboratory studies may help the clinician formulate an accurate diagnosis. The location of the infection may be confirmed based on an accurate physical examination as well as imaging studies, when necessary. The specific stage of the infection (inoculation, cellulitis, abscess, resolution stages) is based largely on the history as well as clinical presentation. In general, cellulitis, which appears in the initial stages of infection, indicates greater severity with uncertain progression, whereas an abscess indicates that the host defense system has effectively localized the infection via containment. The etiology of the infection is determined by integrating the history, physical examination, and imaging studies. It is important to note that the clinician should always consider nonodontogenic etiologies (e.g., tumor) in the differential diagnosis and not assume that all swellings or pain around the head, neck, and oral region are odontogenic in nature.

Principle 2: Evaluate State of Patient's Host Defense Mechanisms

A crucial part of healing following an odontogenic infection is the presence of an intact host defense system, because it is ultimately the patient's host defenses that combat an infection following surgical management, when indicated. Therefore the importance of accurately assessing the patient's host defenses, and optimizing them, cannot be overemphasized. This underscores the importance of obtaining a thorough history on patient presentation. When the host defense mechanism is compromised, it must be compensated for by aggressively managing the infection with surgical treatment and, in most cases, adjunctive antibiotic therapy.

Medical Comorbidities

Two main categories of medical comorbidities that adversely affect the host defense system are inadequately controlled metabolic diseases and conditions that directly affect the immune system.

Poorly controlled diabetes mellitus is strongly associated with impaired healing. Hyperglycemia causes decreased leukocyte chemotaxis and phagocytosis and severely impairs one's ability to resist and combat infections. Patients with severe infections, especially in a hospital setting, require careful control of blood glucose levels in order to optimize the host defense system after appropriate surgical management. Severe alcoholism, which is frequently accompanied by malnutrition, also severely impairs the body's ability to defend against infections.

Hematologic cancers such as leukemia and lymphoma adversely affect the function of leukocytes and therefore the ability to defend against infections. In addition, in severe HIV infections, both the B and T lymphocytes are affected, making the patient particularly susceptible to infections and a poor response to treatment. However, HIV seropositivity alone does not indicate a lack of ability to defend against odontogenic infections, because odontogenic infections are caused mostly by extracellular pathogens, not intracellular pathogens, against which T lymphocytes are primarily responsible to combat.

Certain medications depress the immune system and increase the risk of odontogenic infections and poor treatment response despite appropriate management. Chemotherapeutic agents for malignant conditions commonly cause bone marrow depression, thereby weakening the immune system. In some chemotherapeutic agents, these effects can last for up to 1 year or more. Immunosuppressants and corticosteroids used for various indications (such as autoimmune diseases and organ transplantation) impair the function of lymphocytes and decrease immunoglobulin production.

Principle 3: Determine Whether Patient Should Be Treated by General Dentist or Oral and Maxillofacial Surgeon

When detected early, the vast majority of odontogenic infections may be safely managed by the general dentist; however, several factors must be considered in determining whether an infection should be managed by a specialist. The decision should be based upon location, severity, surgical access, and status of host defenses ( Box 16.1 ). It must be stressed that accurate assessment is a prerequisite to management of any infection, regardless of one's level of training. Two examples of case selection are illustrated in Box 16.2 and Figs. 16.7 and 16.8 .

Box 16.1
Criteria for Referral to an Oral and Maxillofacial Surgeon

  • Difficulty breathing

  • Difficulty swallowing

  • Dehydration

  • Moderate to severe trismus (interincisal opening <25 mm)

  • Swelling extending beyond the alveolar process

  • Elevated temperature >101°F (38.3°C)

  • Malaise and toxic appearance

  • Compromised host defenses

  • Need for general anesthesia

  • Failed prior treatment

Box 16.2
Examples of Mild and Moderate Odontogenic Infections

Case 1: Right Vestibular Space Abscess Case 2: Left Buccal Space Abscess
Key Findings (Clinical Significance)
  • Well-appearing and in no acute distress (intact host defense system)

  • Subtle to mild extraoral swelling (early stages)

  • Mild intraoral swelling (early stage)

  • In mild distress (mild compromise in host defense system)

  • Moderate extraoral swelling (advanced stage)

  • Induration and severe tenderness of left cheek (cellulitis changes)

  • Involvement of infratemporal space on imaging (advanced stage, difficult region to examine clinically)

Management and Rationale
  • Incision and drainage with elimination of source (tooth #30) in office setting.

  • Reevaluation of patient in 2–3 days.

  • Superficial location with mild symptoms indicate early stages, with no evidence of host defense compromise. Sufficient access allows immediate surgical treatment with source control (pulp extirpation with subsequent root canal treatment or extraction of tooth) and incision and drainage.

  • Immediate referral to oral and maxillofacial surgeon or to local hospital with oral and maxillofacial surgery coverage.

  • Further imaging studies required (CT with contrast [see Fig. 16.8B ]).

  • Incision and drainage under general anesthesia due to deep space involvement.

  • Inpatient monitoring with clinical examination and laboratory studies. The inability to sufficiently examine the infratemporal space requires heavier reliance on ancillary studies such as laboratory and imaging studies.

  • Intravenous antibiotics required initially to supplement surgical drainage of deep fascial space abscess (deep temporal space).

Fig. 16.7, Right vestibular space abscess (see Case 1 in Box 16.2 ).

Fig. 16.8, (A) Left buccal space abscess (see Case 2 in Box 16.2 ). (B) Computed tomographic scan. Blue arrows indicate the buccal space; red arrows indicate the infratemporal space.

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