Apical Abscess: Causes and Treatment

An apical abscess, also known as a periapical abscess, is a purulent inflammation of the periapical tissues. It is typically triggered by a massive release of virulent bacteria from the root canal system.

Etiology

Acute apical abscess may develop primary as an outcome of acute apical periodontitis, be the result of exacerbation of chronic inflammation in the periapical area.

The etiologic factor is invasion of pyogenic microflora from the root canals of the tooth into the inflamed periapical tissues (extra-radicular infection). The mixed microflora of an apical abscess is dominated by gram-negative anaerobic rods and Peptostreptococci.

Polymorphonuclear neutrophils serve as the main effector cells in acute apical abscesses. After phagocytic activity of these cells and their death, a large number of tissue-destroying elements (hydrolases and oxygen radicals) appear, macrophages can no longer cope with cell cleansing and repair. This damage exceeds the reparative capacity of macrophages, resulting in the destruction of the periodontal ligament and bone tissue in the periapical region.

Bone loss is caused by activated osteoclasts, resorption is accompanied by immune cell invasion. There may also be direct invasion of microorganisms from root canals, which gradually causes tissue destruction.

Chronic apical abscess is characterized by a long-lasting purulent inflammatory process that drains through a fistulous passage. In such cases, the inflammatory process spreads to the spongy bone and one of the cortical plates, thus forming a fistula that allows continuous pus discharge.

Process outcome:

1. Healing with elimination of infection in the root canal system (removal of non-viable pulp and drainage of abscess).
2. Chronicization of the process and formation of a draining fistulous passage.
3. Destruction of the cortical plate over the abscess, penetration of purulent exudate under the periosteum of the jaw and formation of purulent odontogenic periostitis of the jaw.
4. Spread of purulent inflammation through the fascial spaces of the head and neck.

Classification

• Acute apical abscess.
• Chronic apical abscess with communication (fistula) with the oral cavity.
• Chronic apical abscess with communication with the nasal cavity.
• Chronic apical abscess with communication with the maxillary sinus.
• Chronic apical abscess with skin communication.

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).

This condition is characterized by necrotic pulp that appears yellowish-gray or grayish-black.

In cases of an acute apical abscess, a focus of destruction can be identified at the apex of the tooth, affecting the periodontal ligament and the alveolar bone. This area is filled with purulent exudate, surrounded by fibrovascular granulation tissue.

In chronic apical abscesses, the process penetrates the cancellous bone, compact lamina, mucosa or skin and a fistulous passage is formed. The opening of the fistulous passage is a convex rounded soft tissue mass with a hole in the center from which purulent exudate is released. Fistulous passage can open as close to the focus of infection, and at a distance from it: vestibularly or lingually on the mucosa of the alveolar process, on the attached gingiva. In some instances, it may run along the root of the tooth and open into the gingival sulcus or furcation area,

In this case, a deep narrow false pocket develops, masquerading as a periodontal pocket or a symptom of a vertical root fracture. Also, the opening of the fistulous passage can open into the nasal cavity, the maxillary sinus, on the skin of the face, neck.

Internally, the fistulous passage may be completely or partially lined with epithelium surrounded by inflamed connective tissue.

Diagnosis

• Collection of complaints and history.
• Clinical methods: visual inspection, percussion, palpation along the transitional fold, periodontal probing, determination of tooth mobility.
• Thermoprobe, electroodontodiagnostics.
• Radiography (intraoral contact radiography, radiovisiography, orthopantomography, cone beam computed tomography): a carious cavity, restoration or traumatic defect penetrating into the pulp chamber, a round or irregularly shaped lumen – a focus of bone destruction – is detected in the area of the root apex. A two-dimensional (2D) X-ray might only show a widened periodontal ligament space with no clear periapical radiolucency if the infection is confined to the spongy bone and the cortical plate remains intact.
• Fistula tracing: a gutta-percha pin is placed in the fistula opening until resistance is felt, then intraoral contact radiography is performed. By tracing the course of the gutta-percha pin, the source of the fistulous passage can be identified.

Clinical Manifestations

Acute apical abscess

Patients typically present with localized pain in the affected tooth, which can be moderate to severe and intensifies when biting or chewing. There is often a sensation of pressure or a feeling that the tooth is “raised” or higher than the adjacent teeth. Visualization of the tooth reveals a deep carious cavity, restoration or traumatic defect penetrating into the pulp chamber. Percussion of the tooth is sharply painful, palpation of the transitional fold can also be painful, with the involvement of the cortical plate may be present swelling and hyperemia of the mucosa in the projection of the root apex. The depth of periodontal probing is within normal limits (1-3 mm). The mobility of the tooth can be determined. There is no reaction to temperature and electrical stimuli. In addition, there may be systemic manifestations of the infectious process: increased body temperature, increased lymph nodes of the submandibular and chin area, leukocytosis.

Chronic apical abscess

In chronic apical abscess, the patient may not report any complaints, or may indicate the presence of a mass or localized swelling on the gingiva.

A tooth with a deep carious cavity, restoration or traumatic defect penetrating the pulp chamber. Percussion of the tooth is usually painless or mildly painful. Palpation of the transitional fold is painless. On the mucous membrane or skin is determined by the opening of the fistulous passage, from which purulent exudate is released. In cases where the fistula tract is blocked, localized soft tissue swelling may develop.

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Treatment of an apical abscess

Endodontic treatment of the tooth is performed: extirpation of non-viable pulp or removal of old filling material from the root canals, mechanical treatment and irrigation of root canals. In the presence of exudate in the root canals, fistulous passage, it is recommended to use temporary intracanal attachments. Drainage of purulent exudate is carried out through the root canals or through the cortical plate of the jaw in the projection of the lesion. In the future, a hermetic obturation of root canals with subsequent restoration of the tooth is performed.

If access to the infection source is challenging, adjunctive microsurgical techniques may be employed. These may include periradicular curettage, root-end resection with retrograde filling, or root amputation. Intentional replantation may also be considered.

If the prognosis of endodontic treatment is unsatisfactory, the tooth should be extracted.

Antibiotic prophylaxis during non-surgical and surgical endodontic treatment is performed in the following groups of patients:

• Patients undergoing intravenous bisphosphonate treatment (periapical surgery).
• Patients at risk of infective endocarditis (complex congenital heart disease, prosthetic heart valve, history of infective endocarditis).
• Patients with immunodeficiencies (e.g., leukemia, HIV/AIDS, end-stage renal disease and dialysis, inherited immunodeficiency disorders, uncontrolled diabetes mellitus, as well as immunodeficiencies caused by chemotherapy and post-transplant immunosuppressive or steroid medications).
• Patients after joint endoprosthesis within the first 3 months after surgery.
• Patients undergoing cranial radiotherapy.