Acute apical periodontitis: etiology, anatomy, clinical presentation and treatment

Acute apical periodontitis is an inflammation of periodontal tissue, mainly caused by infection in the root canal system of a tooth. It involves involvement of the alveolar bone, periodontal ligament and cementum in the area of the tooth root apex (periapical area).

Etiology

Apical periodontitis can be caused by the following factors:

• Microorganisms and their toxins: infection of the pulp as a result of caries or traumatic exposure, fractured, fractured or eroded teeth, decompensated periodontal disease, and during or after endodontic treatment without a cofferdam, through a leaky temporary restoration;
• Physical factors: rupture of the apical constriction with an endodontic instrument, expulsion of filler/syller into the periodontal tissues, traumatic injury to periapical tissues, tooth restoration in hyperocclusion;
• Chemical factors: irrigation solutions, intracanal insertions, root canal fillers/syringes, devitalizing pastes.

Bacteria are the main cause of apical periodontitis. They can exist in the root canal system as plankton, but more often they attach to dentin and form a biofilm, which provides protection against microbial competitors, the host immune system and antibacterial agents.

Contact of the pathogen with periapical tissues occurs through the root apex opening, lateral canals, or through root perforation. There is no convincing evidence to support the involvement of any particular bacterial species in the development of symptomatic apical periodontitis. In root canals that have not undergone previous endodontic treatment, the infection is a mixture of different microorganisms in which Gram-positive and Gram-negative species occur in approximately equal proportions, with obligate anaerobic bacteria predominating. The most common bacterial species are: Fusobacterium, Dialister, Porphyromonas, Prevotella, Tannerella, Treponema, Pyramidobacter, Veillonella, Campylobacter, Parvimonas, Filifactor, Pseudoramibacter, Streptococcus, Propionibacterium, Olsenella, Actinomyces, Peptostreptococcus, Eubacterium.

Acute (symptomatic) apical periodontitis develops after complete pulp necrosis; however, if the vital pulp becomes infected, periapical inflammation may develop even in the presence of living but inflamed tissue in the apical third of the root canal. This occurs because of the diffusion of inflammatory mediators, proinflammatory cytokines, chemokines, and bacterial toxins into the periapical region prior to pulp necrosis.

Signs of acute apical periodontitis are similar to those of an acute inflammatory reaction, including vascular dilation, increased permeability, and leukocyte egress from blood vessels. Leukocyte infiltration, accumulation and activation of immunoglobulins, complement factors and plasma proteins occur in the damaged tissue. Polymorphonuclear neutrophils are the main cells in acute apical periodontitis. In the process of fighting microbial infection, they die, releasing proteolytic lysosomal enzymes, active oxygen metabolites, nitric oxide, cytokines, eicosanoids and matrix metalloproteinases, which increases inflammation and tissue damage.

Although apical periodontitis is primarily an infectious disease, bacteria are usually found in the root canal system rather than in the periapical tissues.

In the acute process, apical bone destruction is not observed because the duration of acute inflammation is short and activated neutrophils and macrophages are unable to destroy bone.

Process outcome: restoration of periapical tissues, if the cause of inflammation is eliminated by root canal treatment; abscission in case of massive invasion of pyogenic bacteria; development of chronic periapical inflammation, if the irritant is preserved.

Anatomy

Depending on the etiologic factor, the affected tooth may exhibit:

• A deep carious cavity that penetrates the pulp of the tooth;
• Tooth restorations adjacent to pulp tissue may show signs of compromised seal (defects, cracked restorations, pigmentation around the margin, secondary caries);
• Signs of trauma (cracks, chipped dentin, exposed part of the pulp).

The pulp of the tooth is completely or partially necrotic, yellowish-gray or grayish-black in color, in the area of root tips there may be edematous, hyperemic, bright red pulp. The space of periodontal ligament in the area of root apex is dilated, filled with exudate of serous-hemorrhagic or purulent character.

Diagnosis

• Collection of complaints and anamnesis (presence, localization and intensity of pain, duration of the disease, presence of previous trauma or dental procedures);
• Visual inspection – the crown of the tooth may be grayish due to the penetration of pulp decay products into the dentinal tubes;
• Percussion of the tooth is painful;
• Palpation on the transitional fold – may be painful, in the area of the transitional fold in the projection of the root apex may be swelling and hyperemia of the mucosa;
• Thermoprobe and electroodontodiagnosis – no response to thermal and electrical stimuli;
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, cone beam computed tomography): carious cavity, restoration or traumatic defect penetrating into the pulp chamber, expansion of the periodontal ligament space at the root apex.

Clinical manifestations

The patient complains of a constant localized aching pain that increases with biting, a “grown tooth” sensation and sometimes tooth discoloration. From the history, it can be learned that previously there was a prolonged reaction to thermal stimuli and/or spontaneous pain, which has passed with time.

Find more science-based content on our social media channels

Subscribe and don’t miss out on the latest resources

Treatment of acute apical periodontitis

Endodontic treatment of the tooth is performed: extirpation of necrotic pulp, mechanical treatment and irrigation of root canals. In case of exudation from the root canals it is recommended to use temporary pastes based on calcium hydroxide. Subsequently, root canals are obturated with subsequent restoration.

If the prognosis of endodontic treatment is unsatisfactory, tooth extraction is recommended.

In the presence of premature contact of the restoration or mechanical trauma, the occlusal contacts are resurfaced and normalized, and dynamic follow-up is performed.