Acute Apical Periodontitis: Etiology, Anatomic Pathology, Clinical Manifestations, and Treatment

Acute apical periodontitis (AP) is an inflammation of the periodontium that is primarily caused by an infection of the root canal system. The inflammation usually affects the alveolar bone, also known as the alveolar process, the periodontal ligament, and the cementum surrounding the apex of the tooth root (the periapical region).

Etiology

There are several possible reasons for AP:

• Microorganisms and toxins they produce in case of pulp infection resulting from caries or traumatic tissue exposure from cracks, fractures, or tooth attrition; decompensated periodontal disease; or a leaky temporary restoration. An infection can also occur during or after endodontic treatment if performed without a rubber dam.
• Physical factors: disruption of the apical constriction by endodontic instruments, extrusion of root canal filling materials (filler/sealer) into the periapical tissues, traumatic injury to periapical tissues, or tooth restoration in hyperocclusion.
• Chemical factors: irrigants, intracanal dressings, root canal filling materials and sealers, and devitalizing agents.

In the majority of cases, AP is caused by bacterial infection. Within the root canal system, bacteria can exist as planktonic organisms. However, most often, they form biofilms, which are aggregates of microorganisms attached to the dentin. For one thing, this mode of existence provides bacteria with effective protection against microbial competitors and the host immune system; for another, it makes them more resistant to a variety of antibacterial agents.

Pathogens usually enter the periapical tissues through the apical foramen, lateral canals, or root perforations. The bacteria found in untreated root canals are typically of a mixed type with approximately equal amounts of gram-positive and gram-negative species, dominated by obligate anaerobes. Notably, evidence linking certain bacterial species to distinct AP symptoms is limited. The most common bacterial pathogens include Fusobacterium, Dialister, Porphyromonas, Prevotella, Tannerella, Treponema, Pyramidobacter, Veillonella, Campylobacter, Parvimonas, Filifactor, Pseudoramibacter, Streptococcus, Propionibacterium, Olsenella, Actinomyces, Peptostreptococcus, and Eubacterium.

Acute (symptomatic) AP is a common consequence of total pulp necrosis. Nevertheless, it can also develop against viable, though inflamed, pulp tissue in the apical portion of the root canal. This may happen due to an infection of the vital pulp, resulting in the diffusion of inflammatory mediators, proinflammatory cytokines, chemokines, and bacterial toxins into the periapical region prior to complete pulp necrosis.

The pathophysiology of acute AP resembles that of a typical acute inflammatory response, involving vasodilation, increased vascular permeability, and the migration of leukocytes from the bloodstream into the perivascular space. These reactions lead to leukocyte infiltration, accumulation of immunoglobulins and plasma proteins, and complement activation in the damaged tissue. In acute AP, the primary effector cells are polymorphonuclear neutrophils, which are known as the first line of defense against bacterial infection. Neutrophil death results in the release of lysosomal proteolytic enzymes, reactive oxygen species (such as nitric oxide), proinflammatory cytokines, eicosanoids, and matrix metalloproteinases, which further intensify the inflammatory response and contribute to tissue damage.

Although AP is predominantly an infectious disease, bacteria are typically found within the root canal system rather than in the periapical tissues.

Destruction of the apical bone is uncommon in AP. Since the condition is associated with a short-term acute inflammatory response, neutrophils and macrophages are not able to resorb bone tissue.

The possible outcomes of acute AP include:
– repair of periapical tissues (if the causative factor is eliminated by root canal treatment);
– abscess formation (in cases of extensive invasion of pyogenic bacteria);
– progression to chronic periapical inflammation (if the causative factor persists).

Anatomic Pathology

Depending on the underlying etiology, the following anatomical changes may be observed in the affected tooth:

• a deep carious lesion penetrating into the dental pulp;
• signs of compromised sealing in a restoration adjacent to the pulp tissues (e.g., defects, cracks, marginal pigmentation, or secondary caries);
• signs of trauma, such as cracks, dentin chipping, or pulp exposure.

The yellow-gray or gray-black pulp may be partially or completely necrotic. At the apex of the roots, the pulp may appear edematous, hyperemic, and bright red. The periodontal ligament space near the root apex is typically widened and filled with serous-hemorrhagic or purulent exudate.

Diagnosis

• Medical history: complaints regarding pain (its presence, location, intensity), duration of the condition, and any history of trauma or prior dental interventions.
• Visual examination: the dental crown may appear grayish due to the penetration of pulp breakdown products into the dentin tubules.
• Tooth percussion: usually painful.
• Palpation along the mucobuccal fold: may also be painful, with edema and hyperemia of the mucosa observed in the projection of the root apex along the fold.
• Pulp sensibility tests (thermal and electrical): no response to thermal or electrical stimuli.
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, or cone-beam computed tomography): may reveal a carious lesion, restoration, or traumatic defect penetrating into the pulp chamber, as well as the widening of the periodontal ligament space near the root apex.

Clinical Manifestations

Patients with acute AP often complain of prolonged, dull, localized pain that intensifies when biting on the affected tooth, along with a sensation that the tooth feels “raised” or higher than the adjacent teeth. There may also be a noticeable change in tooth color. Past medical history may include a prolonged response to thermal stimuli and/or spontaneous pain that has subsided over time.

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Treatment of Acute Apical Periodontitis

The primary treatment for acute AP is endodontic therapy. This is when the necrotic pulp tissue is removed, followed by mechanical and chemical debridement of the root canals. If exudate is present in the canals, temporary intracanal dressings (calcium hydroxide paste) are recommended. Subsequently, the root canals are hermetically sealed, and the tooth is restored.

In cases where endodontic treatment may have unfavorable outcomes, tooth extraction is indicated.

For cases involving a premature contact of a restoration or mechanical trauma, occlusal adjustment through selective grinding may be performed, followed by regular monitoring.