Infection of the dental pulp may result from microbial penetration directly through the dentin secondary to dental caries, dental drilling, or tooth fracture or by hematogenous spread. The most common cause of pulpal infection is from dental caries that begins with the formation of dental plaque. Regular oral care is needed to prevent plaque buildup. Plaque is composed of a large number of bacteria (>10⁸ colony-forming unit [CFU]/mm³), including S. mutans, which firmly adhere to the enamel of the tooth. These bacteria secrete enzymes that progressively dissolve away the tooth enamel and dentin, permitting the bacteria to access the pulp (49). Microbial infection of the pulp (pulpitis) results and manifests clinically with pain and temperature sensitivity in the tooth. If the infection is not recognized and treated, the bacteria may then migrate through the pulpal foramen at the apex of the tooth into the alveolar bone at the root of the tooth, forming a periapical abscess, or extend beyond into the medullary space of the mandible, resulting in osteomyelitis.

Gingivitis is a periodontal process. Mild inflammation of the gums is present in almost all adolescents and in most American adults (50,51). Acute and chronic gingivitis begin with the formation of plaque below the gumline. Swelling and hyperemia of the free gum margin occurs, and the gums may bleed easily with brushing. Gingivitis is increased in frequency or severity in certain patient groups such as HIV-positive patients, cancer patients undergoing chemotherapy, and young patients with type 1 diabetes mellitus (52). Cessation of dental oral hygiene results in the appearance of gingivitis within 10 to 21 days.

Periodontal infections usually begin with gingivitis. As the infection becomes chronic, it extends deeper into the junction between the tooth and gingiva. This leads to loss of the connective tissue attaching the tooth to the bone (the periodontal ligament) and resorption of the bone. The resulting periodontitis causes a pocket to form between the tooth and the gingiva. This space is ideal for the growth of anaerobes due to the very low reduction oxidation potential. Spirochetes, of many morphotypes, some uncultivable, appear to be one of the predominant bacteria in advanced lesions (53,54). The chronic infection that occurs causes loosening and then loss of teeth. Periodontal abscesses result from infection of deep periodontal gingival pockets (55,56). Needle aspiration and appropriate culture of pus from dentoalveolar abscesses reveal a polymicrobial flora with a predominance of facultatively anaerobic streptococci together with obligately anaerobic gram-positive cocci and gram-negative rods (57). Over 60% of these infections include aerobic microorganisms, whereas approximately one third have purely anaerobic isolates. In an analysis of apical abscess aspirates from 42 persons using reverse capture checkerboard hybridization assay, the most prevalent microorganisms were Fusobacterium nucleatum, Parvimonas micra, Porphyromonas endodontalis, as well as streptococci, Olsenella uli, Eikenella corrodens, and other anaerobes such as Prevotella (58).

The most extreme form of gingivitis is ANUG. ANUG represents tissue invasion and destruction by mixed anaerobes and facultatively anaerobic bacteria. Data suggest an important role for spirochetes and for Fusobacterium spp. (59). In HIV-seropositive patients, yeasts and herpes viruses may also contribute (60). ANUG manifests as a loss of the papillae between adjacent teeth and results in exposure of the roots of the tooth. There is bleeding of the gingivae with blunting and necrotic punched-out lesions of the interdental papillae. The disease is characterized by the sudden onset of pain and tenderness of the gums associated with increased salivation and a peculiar metallic taste, and it is accompanied by systemic symptoms. ANUG most frequently occurs in adolescents and young adults. Risk factors include poor oral hygiene, infrequent dental care, poor nutrition, and possibly diabetes (61). Prevalence studies have demonstrated that 4% of students using dental services at Harvard University and 6.7% of 9,203 adolescents in Chile have this condition (61,62). Stenotrophomonas bacteremia associated with ANUG in a young girl with leukemia has been reported (63).

Acute suppurative parotitis is a healthcare-associated infection that occurs after surgery or in patients who are predisposed because of malnutrition, immunosuppression, or dehydration or in whom drugs have been used that decrease salivary flow (64,65). Such drugs include anticholinergic agents, antihistamines, and tranquilizers. The pathogenesis of this infection is presumed to be retrograde movement of mouth microorganisms up the parotid duct in patients with diminished rates of salivary flow. The condition is unilateral in 80% to 90% of cases and presents clinically as the acute onset of unilateral facial swelling with pain. Physical examination demonstrates purulent fluid, which can be expressed from the parotid duct. The microbial causes reported in the older literature were Staphylococcus aureus in the vast majority (64). Newer studies using proper anaerobic culture methods demonstrate anaerobes in most patients (66). The microorganisms are the same as those recovered from the gingival sulcus. Methicillinresistant S. aureus has been reported as the cause of one outbreak in a nursing home (67).

Acute tonsillitis is rarely an institutionally related infection unless an outbreak of acute group A β-hemolytic streptococcal infection is spreading through the population. Although group A β-hemolytic Streptococcus is the most commonly recognized cause of tonsillitis, the significance of recovery of other microorganisms such as mycoplasma, chlamydia, and anaerobes from inflamed tonsils has been debated (68, 69, 70, 71 and 72). The pathogenic role of these bacteria is not known. Microbiologic studies of the core of tonsils removed from 150 children with recurrent tonsillitis due to group A ß-hemolytic Streptococcus during three periods beginning in 1977 and ending in 1993 revealed mixed flora (8.1 microorganisms per tonsil) in all tonsils and an increased rate of recovery of ß-lactamase-producing bacteria with time (73).

Erysipelas, a soft tissue infection of the cheek due to direct extension of bacteria from the mouth, is often due to group A or C streptococci. This rare complication follows 2 to 3 days after oral surgery and represents bacterial entry into soft tissues injured by instrumentation.

Noma (gangrenous stomatitis) is an acute, fulminant, necrotizing infection of the cheek and facial tissue that destroys the oral and para-oral structures and is found predominantly in malnourished children, particularly in sub-Saharan Africa. Certain groups of patients in developed countries may develop noma-like lesions that are slowly progressive. These persons are malnourished or have underlying illnesses such as leukemia (74). The antecedent lesions to noma are believed to be oral herpetic ulcers, necrotizing gingivitis, or a buccal abrasion due to the rubbing of a tooth or from surgery (75,76). Infection of these precursor lesions with synergistic bacteria, such as Fusobacterium necrophorum and Prevotella, causes progressive full thickness necrosis of the cheek, leaving a large open defect through which the mandible and tongue can be seen (76, 77 and 78).

Cervicofacial actinomycosis is a rare disease most commonly caused by Actinomyces israelii. The portal of entry is through disrupted mucosal barriers after trauma, dental manipulations, or oral and maxillofacial surgery (79,80). The infection often appears as a chronic, slowly progressive induration or soft tissue mass in the mandibular-preauricular area and is sometimes accompanied by fistulous tracts to the skin that release sulfur-like granules. Systemic signs usually are absent (81).

Primary oral tuberculous lesions are seen rarely (82, 83 and 84). Primary lesions usually occur in younger patients, are painless, and are associated with cervical lymphadenopathy. Secondary oral tuberculous lesions are more common and are seen mainly in older persons. Although the lesions are variable in appearance, the ulcerative form is the most usual, occurring on the tongue base or gingiva. These lesions are often painful. Most of these patients have accompanying active pulmonary tuberculosis (85,87).

There are many oral complications from cancer therapy, one of the most prominent of these being infection. As a result of treatment effects on the mouth and immunosuppression, the oral cavity has the potential to become a reservoir for opportunistic microorganisms. Candida microorganisms are the primary cause of opportunistic fungal disease in patients who are immunocompromised. As many as 60% of cases of fungal septicemia in cancer patients are associated with prior oral infections (88). The most common oral manifestation of a candidal infection is pseudomembranous candidiasis, manifested by removable white curd-like plaques over an inflamed mucosa. Other forms include leukoplakia-like white plaques that are not removable, referred to as chronic hyperplastic candidiasis, and chronic erythematous candidiasis that appears as patchy or diffuse mucosal erythema. Oral infections can extend to involve the esophagus. Because of the widespread use of azole prophylaxis in leukemia patients, candidiasis has become less common in this population. However, C. krusei, a fluconazole-resistant Candida species, and C. glabrata, an azole dose-dependent Candida species, now make up the majority of cases in hematology units (89).

Aspergillosis is the second most frequent fungal infection in cancer patients, particularly patients with hematologic malignancies (90). The paranasal sinuses are the most common sites of Aspergillus infection in the facial region, but there have been a few reports of primary oral
aspergillosis (90, 91, 92, 93, 94 and 95). The oral lesions initially manifest on the gingiva and then develop into necrotic ulcers covered by a pseudomembrane. Spread to the alveolar bone and facial muscles may occur rapidly.

HSV is the most common viral pathogen in patients receiving cytotoxic agents or bone marrow transplants. The vesicular lesions on an erythematous base may appear anywhere on the mucosa and in addition to the mouth can involve the respiratory and gastrointestinal tracts. In immunocompromised patients, the oral mucositis associated with HSV may be particularly painful, severe, and prolonged. The oral HSV ulcerations may act as portals of entry for bacterial and fungal microorganisms (47).

The most frequent viral infection following solid organ transplants is CMV. This infection can develop in high-risk transplant recipients despite ganciclovir or valganciclovir prophylaxis (96). Oral manifestations, when they occur, are nonspecific and require biopsy to confirm the etiology. The infection often consists of a single, large, shallow ulceration (97).

An epidemiologic retrospective study of hospitalized patients with maxillofacial infections noted differences between pediatric and adult patients. Upper face infections predominate in children (81%), whereas in adults, lower face infections, mainly odontogenic or peritonsillar, are more common (66%) (98).

Osteomyelitis of the jaw (usually the mandible) most often results from chronic infection of a tooth, either from periapical abscess or from gingivitis. Other risk factors for osteomyelitis of the jaw include compound jaw fractures, diabetes mellitus, treatment with steroids, and surgery. Infection is particularly likely to occur when surgery is performed after irradiation of the mandible for tumor removal or after compound fracture of the mandible through the socket of a molar tooth. The causative agents reflect the broad range of microorganisms in the mouth, but most often seem to be due to streptococci and anaerobes (such as Actinomyces, Prevotella, Bacteroides, Porphyromonas, and Fusobacterium) in addition to S. aureus in persons with underlying illness (81).

Peritonsillar abscesses arise by direct extension from infected tonsils and tonsillar remnants and are rarely healthcare associated in nature. It is critical to recognize and treat this infection to avoid respiratory compromise and other serious complications (99, 100, 101 and 102).

Maxillary sinusitis caused by mixed aerobes and anaerobes is recognized as a complication of periapical dental abscesses in the upper teeth and following dental/oral procedures in this region of the mouth (103,104). Sinusitis sometimes complicates extraction of the premolars and molars on the upper side, because the root tips of these teeth almost touch the lower border of the maxillary sinuses (105).

Retropharyngeal abscesses arise by direct extension from uncontrolled tonsillar infection or after perforation of the posterior pharyngeal wall by a foreign body. The foreign body may be a bone or another sharp object carried in the mouth. A retropharyngeal abscess presents initially with pharyngeal discomfort, limited neck motion, and nonspecific constitutional symptoms, including fever and chills (106). In its later stages, the abscess can be recognized by forward displacement of the posterior pharyngeal wall (107). A lateral soft tissue film of the neck or computed tomography of the neck is required for diagnosis and will demonstrate air fluid levels or pockets of air in the retropharyngeal space. Clinical differentiation between a retropharyngeal abscess and cellulitis of the retropharyngeal space is difficult and may be accomplished by performing needle aspiration of the area. A return of pus signifies an abscess (108). Prompt recognition and urgent surgical management by incision and drainage are the standard treatment, because the retropharyngeal space directly communicates with the posterior mediastinum and lifethreatening complications such as necrotizing fasciitis and carotid artery rupture may occur rapidly (109, 110, 111 and 112). There are reports of children being treated successfully without surgical intervention (106).

Carotid artery mycotic aneurysm associated with dental surgery procedures have been noted in the literature on several occasions (113). Patients develop fever and a rapidly enlarging neck mass shortly after the procedure. Prompt diagnosis and treatment are essential for an acceptable outcome.

Anaerobic pulmonary infection (“aspiration pneumonia”) due to mixed anaerobes and facultatively anaerobic microorganisms occurs after aspiration/microaspiration of oropharyngeal secretions. Clinical evidence suggests that the presence of severe gingivitis and/or oral surgery on the gums is associated with subsequent development of aspiration pneumonia. Clearly, the very large numbers of microorganisms (>10¹⁰ microorganisms per gram of tissue) found in gingival material provide a large inoculum if aspirated into the lungs. The interplay of local host defenses to clear the bacteria and the frequency of dental procedures on patients with gingivitis suggests that local host defenses usually overcome this inoculum.

Deep fascial space infections in the upper neck and underneath the jaw usually result from direct extension of odontogenic or oropharyngeal infection, and they have been associated with dental extraction (114, 115, 116, 117, 118 and 119). Ludwig’s angina is a diffuse fasciitis and cellulitis with edema of the soft tissues of the neck and floor of the mouth, originating in the submandibular and submental spaces. It is the result of a polymicrobial infection, often related to peritonsillar or parapharyngeal abscesses, mandibular fracture, or oral mucosal injuries. Airway compromise is the leading cause of death (119). Progression of infection upward may involve the whole side of the face, including the eyelids and orbit, whereas downward movement of infection can lead to necrotizing cervical fasciitis or mediastinitis. The anatomic parameters influencing the spread of infection in these areas is beyond the scope of this chapter but is covered in other works (19,50).

Many distant abscesses have been reported as complications of dental and periodontal infection, including brain abscess, meningitis, paraspinal abscess, liver abscess, suppurative jugular thrombophlebitis (Lemierre’s syndrome), septic cavernous sinus thrombosis, septic arthritis, cellulitis, and necrotizing cavernositis of the penis (39, 40, 41, 42, 43 and 44,120, 121, 122, 123 and 124). The route of migration is held to be bacteremia.