Sequelae

Once pus formation occurs, it may remain localized at the root apex and develop into either an acute or a chronic abscess, develop into a focal osteomyelitis, or spread into the surrounding tissues (Figs 34.2 and 34.3).

Fig. 34.3 Pathways by which pus may spread from an acute dentoalveolar abscess (coronal section, at first molar tooth level).

Direct spread

1. Spread into the superficial soft tissues may:

localize as a soft-tissue abscess (Fig. 34.4)

extend through the overlying oral mucosa or skin, producing a sinus linking the main abscess cavity with the mouth or skin

extend through the soft tissue to produce a cellulitis.

2. Spread may occur into the adjacent fascial spaces, following the path of least resistance; such spread is dependent on the anatomical relation of the original abscess to the adjacent tissues (Table 34.1). Infection via fascial planes often spreads rapidly and for some distance from the original abscess site, and occasionally may cause severe respiratory distress as a result of occlusion of the airway by oedema (e.g. Ludwig’s angina).

3. Infection may extend into the deeper medullary spaces of alveolar bone, producing a spreading osteomyelitis; this may occur in compromised patients.

4. In maxillary teeth, odontogenic infection may directly spread into the maxillary sinus, especially if the sinus lining and the tooth apex are subjacent, leading to acute or chronic secondary maxillary sinusitis (as opposed to primary sinusitis due to direct sinus infection). Such infection, if not arrested, may rarely spread to the central nervous system, causing serious complications such as subdural empyema, brain abscesses or meningitis.

Fig. 34.4 Extension of periapical infection from the left upper canine tooth to the infraorbital region in a teenager.

Table 34.1 Sites of contiguous spread of dentoalveolar infection (see also Fig. 34.3)

Site of spread	Maxillary teeth	Mandibular teeth
Palate	Palatal roots of premolars and molars; also lateral incisors with a palatally curved root	–
Buccal space	Canines, premolars and molars	Canines, premolars and molars
Infraorbital/periorbital region	Canines mainly	–
Maxillary sinus	Canines, premolars and molars	–
Upper lip	Central and lateral incisors	–
Masseteric space, pterygomandibular space, lateral pharyngeal space	–	Lower third molars
Lower lip	–	Incisors and canines
Submandibular space	–	Root apices below insertion of mylohyoid – usually molars but can also be premolars
Submental space	–	Incisors and canines
Sublingual space		Root apices above mylohyoid/geniohyoid – usually incisors, canines and premolars; rarely molars

Clinical features

Clinical signs and symptoms depend on the:

Clinical features may include a non-viable tooth with or without a carious lesion, a large restoration, evidence of trauma, swelling, pain, redness, trismus, local lymph node enlargement, sinus formation, raised temperature and malaise. The latter two symptoms are a direct consequence of increased levels of systemic inflammatory cytokines such as interleukins and tumour necrosis factor in response to bacterial products such as lipopolysaccharides (i.e. endotoxins).

Microbiology

Microbiologically, the dentoalveolar abscess is characterized by the following features:

The common species isolated from dentoalveolar abscesses are Prevotella, Porphyromonas and Fusobacterium spp., and anaerobic streptococci; facultative anaerobes are the second largest group, e.g. Streptococcus milleri (Table 34.2). There is evidence that some strictly anaerobic bacteria, especially Porphyromonas gingivalis and Fusobacterium spp., are more likely to cause severe infection than other species, and that synergistic microbial interactions play an important role in the severity of dentoalveolar abscesses.

Table 34.2 Bacteria commonly isolated from dentoalveolar abscesses