Odontogenic Infections: Their Spread and Abscess Formation
The most frequent causes of inflammatory swellings of the jaws, the middle and lower thirds of the face, and the upper part of the neck are infections of the teeth, with the pulp canal or the periodontal membrane as the primary focus. The dentoalveolar abscess is the most frequently encountered dental infection. It is usually the end result of dental caries; more rarely, it originates in a tooth devitalized by trauma. The abscess may develop very acutely and burrow through bone to lodge under the periosteum, which it then perforates to induce an intraoral or a facial abscess. In other instances, a more chronic inflammatory process leads to an organized granuloma at the root apex, which may remain dormant for years, evolve slowly into a sterile cyst, or develop into an acute alveolar abscess. While the abscess is confined to the bone, pain and extreme tenderness of the involved tooth are the characteristic symptoms. By the pressure of edema, the tooth is extruded from its socket, so that each contact with the teeth of the opposing jaw aggravates the pain.
The periodontal abscess is the second most common odontogenic infection. It arises from an ulcerated periodontal crevice (pocket), which is created by the loss of attachment (poor contact) between the tooth on one side and the investing gingiva, periodontal membrane, and bone on the other. This periodontitis occurs with increasing severity in older age groups and is the most prominent etiologic factor in the loss of teeth. Calculous deposits, traumatic occlusion, irritating filling margins, implanted teeth, and other factors may play a contribut- ing role. A third odontogenic infection, the pericoronal abscess, originates in a traumatized or otherwise inflamed flap of gingiva overlying a partly erupted tooth, usually a lower third molar.
Odontogenic infections involve the soft tissues chiefly by direct continuity (the numbered pathways are illustrated in the drawings). Lymphatic spread plays a secondary role, and hematogenous dissemination rarely results in a facial abscess. Bacteremia, however, is common and has been demonstrated as a transient phenomenon arising from chewing or manipulation of apically or periodontally infected teeth. Local extension follows the line of minimal resistance chosen based on the tooth and its anatomic proximity to the bone, fascia, and muscle attachment. Where the muscle layers act as a barrier, extensive cellulitis may spread along the fascial planes of the head and neck. Infections from the maxillary teeth may perforate the cortical bone of the palate, the vestibule, or the regions separated from the mouth by attachments of the muscles of facial expression or the buccinator muscle. Those from the incisor teeth tend to involve the upper lip; from the cuspids and premolars, the canine fossa; and from the molar teeth, the infratemporal space or mucobuccal fold. The vestibular abscess is generally localized and is not accompanied by excessive edema, owing to the softness of the tissues and lack of tension. In the advanced stage, a shiny fluctuant swelling is visible at the region of the root apex or somewhat below it. Abscess (postzygomatic) of the canine fossa usually bulges into the buccal sulcus but is chiefly marked by swelling of the infraorbital region of the face and the lower eyelid. The upper lid, the side of the nose, and the nasolabial fold and upper lip may be involved by edema.
Infections of the mandibular teeth may give rise to swellings of the vestibule or the sublingual, submental, or submandibular space. Abscess of the submandibular region is encountered with infections of the premolar and molar teeth. The classic sign is a large visible swell- ing below the mandible, extending to the face and distorting the lower mandibular border; it is extremely tender and accompanied by trismus. A submandibular space abscess may easily pass into the sublingual space (5) along the portion of the gland that perforates the mylohyoid muscle. This results in elevation of the floor of the mouth and displacement of the tongue to one side. The submental area may be invaded by passage of pus past the digastric muscle, resulting in a general swelling of the entire submandibular region. A dentoalveolar abscess from a lower molar tooth is capable of producing the most serious and fulminating infections of the submandibular (4), pterygomandibular (8), and parapharyngeal (9) pathways. A pterygomandibular abscess results in deep-seated pain and extreme trismus, with some deviation of the jaw owing to pterygoid muscle infiltration. Infection in this space may, in exceptional cases, enter the pterygoid and pharyngeal plexuses of veins and result in a cavernous sinus thrombosis. A parapharyngeal abscess causes bulging of the pharynx, with equally marked trismus.
The onset of facial cellulitis is heralded by edema of the soft parts, often quite extensive and without discernible fluctuation. Pain increases with pressure and induration. As abscess formation progresses, the central area reveals pitting edema and eventually becomes shiny, red, and superficially fluctuant. Pain and tenderness are related to pressure and induration. A fever of 38.5° to 40° C, leukocytosis, and severe toxemia are characteristic. Trismus occurs when the elevator muscles are affected by inflammation or reflex spasm caused by pain. In some cases, rather than the typical production of an abscess, a chronic cellulitis follows the acute phase, with persistent, deeply attached swelling. A phlegmon may be apparent from the onset, with a brawny, indurated distention of muscular and subcutaneous layers, devoid of exudate and showing no tendency to localize.
Ludwig angina, a purulent inflammation, begins as a phlegmon in the submandibular space, usually after a molar tooth infection or extraction, and rapidly spreads to occupy the submandibular region, bounded inferiorly by the hyoid bone. The floor of the mouth and tongue are raised through infiltration of extrinsic and intrinsic muscles. The hard, dusky swelling descends to the larynx, where edema of the glottis, combined with the pressure of the tongue against the pharynx, interferes with respiration. In addition to the usual flora of odontogenic infections (alpha, beta, and gamma strep- tococci and, occasionally, gram-negative bacilli), the bacterial picture in true phlegmon tends toward anaer- obic organisms, or facultative anaerobes, and gangreneproducing mixed groups such as the fusospirochetal combination.
Osteomyelitis may produce cellulitis or abscess similar to the odontogenic variety. Its chief incidence is as a complication following a traumatic extraction, particularly if performed in the presence of acute infection, or a comminuted fracture involving the roots of teeth. Occasionally, it is the result of an abscess contiguous to a large area of bone, and it typically begins in the lower third molar region. Sclerotic or dense bone is more easily deprived of nutrition through trauma and at increased risk for developing an abscess following tooth extraction. Symptoms include those of cellulitis, with intermittent, deep, boring pain, and sequestrum and involucrum formation, seen on radiographic imaging in late stages. Symptom and radiographic resolution results from therapeutic intervention with abscess drainage and antibiotic therapy.
A fracture of the mandible or maxilla is always compound where teeth are present, causing the line of fracture to be contaminated by normal oral flora that seldom produces infection; however, with projection of a tooth root in the line of fracture, suppuration typically develops. An externally compounded fracture is more prone to develop sepsis than a noncomminuted or simple nondisplaced fracture.
Actinomycosis is a specific infection that occurs centrally in the jaws or peripherally in the soft tissues, where it forms an indurated swelling with multiple fistulae of the skin, resembling a chronic odontogenic abscess. Because this is an obligatory oral pathogen, inoculation is usually through damaged mucosa, most often following oral surgery or recent dental work and less often following trauma or local radiation therapy. The diagnosis is chiefly made by a smear of the exudate, which contains peculiar granular yellow bodies (sulfur granules) and the specific organism (Actinomyces bovis) that causes the disease. Culture of the organism is unreliable, and biopsy may be required to establish the diagnosis.