Etiology

A dental abscess arises from a bacterial infection associated with the dental pulp and tissues surrounding a tooth.

Oral bacteria are found in saliva and oral plaque. The bacteria can adhere to the gums causing inflammation (gingivitis) and to the teeth (with the development of decay), if not removed regularly with proper brushing and flossing. Tooth decay can lead to the spread of bacteria and involve the neurovascular structures within the tooth (i.e., dental pulp). If untreated, the bacterial infection can spread into the tissues surrounding the teeth causing periradicular inflammation and suppuration. Inflammation and infection can also involve the gingivae or periodontal tissues, leading to gingival or periodontal abscess, respectively.

Odontogenic infections are polymicrobial. One retrospective study found gram-positive cocci (Streptococcus viridans) to be the predominant bacteria, followed by gram-negative rods. Staphylococcus aureus is rarely involved in dental infections.[10]

Virtually any species of microorganism that inhabits, or is introduced into, the mouth can be involved with an infection. It was believed that oral infections were predominantly caused by aerobic microorganisms (e.g., streptococci, staphylococci); however, improvements in microbiologic techniques and technology have established a major role for anaerobes in acute dentoalveolar abscesses, including gram-positive anaerobes (e.g., Peptostreptococcus , Peptococcus) and gram-negative anaerobes (e.g., Bacteroides, Fusobacterium).

Pathophysiology

Oral bacteria combine with food particles and saliva to form plaque, which builds up on teeth when not removed with brushing and flossing. Bacteria in plaque transform carbohydrates into the energy they need for reproduction, resulting in the production of acids that lead to tooth decay.

Untreated decay advances through the enamel and dentin into the pulpal tissue, resulting in pulpal inflammation. Decay into the dentin will lead to symptoms of thermal sensitivity, and once into the pulp, more acute toothache-type pain. Pulpal inflammation can lead to pulpal necrosis, with the pulp chamber becoming infected with bacteria that communicate via the pulp canal to the bone under, and supporting, the tooth with the development of a periapical abscess.

If left unattended, the abscess can penetrate through the cortical bone to involve the potential spaces created by fascial attachments.

Bacteria in plaque adhering to the teeth and gums can lead to inflammation of the gums (gingivitis). Chronic gingival inflammation can lead to periodontal disease with loss of supporting periodontal bone and compromise of the periodontal ligament with bacterial invasion and development of a periodontal abscess.

When a tooth is incompletely erupted or partially impacted with incomplete access for cleansing, the overlying mucosa (operculum) acts as a trap with the accumulation of food debris and bacteria from plaque, resulting in a pericoronal abscess (pericoronitis). This is most commonly seen with partially erupted lower-third molars (wisdom teeth).

As the body’s defenses are mobilized to combat an oral/facial infection, the cellulitis progresses into a brawny infiltrative stage. In this stage, suppuration (pus) is often present, but is not localized to a specific area. A space-related abscess develops when the infection with suppuration becomes localized.

Once the infection is in the soft tissue, depending on its anatomic location, it can spread by direct extension through the mucosa, skin, or muscle, or dissect along anatomic fascial planes or layers.[11]​​​​

Fascial spaces at high risk of complications include the fascial planes of the neck, and the parapharyngeal, temporal, periorbital, pterygomandibular, or parotid spaces. These high-risk areas are at greater risk for serious potential complications such as airway involvement, eye involvement, brain abscess, or cavernous sinus thrombosis. Multiple fascial space involvement is considered high risk for complications.[11]

Classification

Clinical classification

While there is no official classification for dental abscess and odontogenic infections, the following clinical classification is generally accepted and used in clinical practice.

Periapical (dentoalveolar) abscess:

  • Most common type of dental abscess. Results from inflammation and necrosis of the dental pulp, which may be caused by untreated dental caries (the most common cause) or trauma. Traumatic etiology includes macrotrauma (e.g., sports injuries, falls, interpersonal violence), microtrauma (e.g., chronic tooth grinding), or iatrogenic damage (e.g., incomplete/failed root canal treatment, leaking fillings, thermal or chemical damage during placement of a filling).

Periodontal (lateral) abscess:

  • Occurs alongside a tooth as a complication of advanced periodontal disease, which begins in a periodontal pocket that has become obstructed.

Pericoronal abscess (pericoronitis):

  • Abscess involving the gum tissue surrounding the crown of a partially erupted tooth. It is most commonly associated with an incompletely erupted lower wisdom tooth.

Gingival abscess:

  • Abscess with localized infection that involves only the gum tissue near the gingival margin or interdental papilla. Does not affect the tooth itself or the periodontal ligament. Most develop following induction of a foreign body or injury (e.g., toothpick puncture, overly aggressive tooth brushing).

Combined periodontal-endodontic abscess:

  • When a periapical and periodontal abscess have combined.

Fascial space infection:

  • Occurs as a dental abscess spreads beyond the confines of the local bone and soft tissue to involve adjacent anatomic areas such as the maxillary sinus and fascial spaces of the head and neck. Some examples of fascial spaces include the buccal, canine, palatal, sublingual, submental, submandibular, parapharyngeal, infraorbital, and periorbital spaces.

Use of this content is subject to our disclaimer