Acute Form
Acute purulent apical periodontitis is characterized by the accumulation of a large number of neutrophils in the periodontal ligament tissues near the root apex. The inflammatory exudate causes histolysis of the periapical tissues. The process affects areas near the alveolar bone and root dentin, ultimately leading to the formation of an apical periodontal abscess.
Chronic Forms: Granulating and Fibrous Periodontitis
The chronic course of the disease manifests in several forms:
- Chronic apical granulating periodontitis. The main feature is the proliferation of granulation tissue (with focal or diffuse infiltration and impaired maturation) in the periapical region. The process is accompanied by resorption of the alveolar bone, destruction of the compact substance, periosteum, as well as cementum and dentin. A specific characteristic is lacunar resorption of dentin by macrophages and its replacement by osteodentin. Granulations can grow into neighboring soft tissues. During exacerbations, abscesses and fistulas (gingival or external, on the skin) occur, the location of which indicates the localization of the lesion.
- Chronic fibrous apical periodontitis. Coarse fibrous connective tissue proliferates in the periapical zone. This is an inactive and prognostically the most favorable form of the disease.
Chronic Granulomatous Periodontitis and Its Evolution
This form produces a periapical (simple) granuloma, which is an oval formation tightly attached to the root apex. On a radiograph, it appears as a distinct radiolucent focus in the area of bone destruction. The basis of the granuloma is granulation tissue with an inflammatory infiltrate, surrounded by a dense fibrous capsule. Cholesterol crystals, foreign body giant cells, and Russell bodies may be present inside. It is important to understand that this formation is not related to granulomas from the general pathology course.
Further development of the process can lead to the following formations:
- Epithelial granuloma. Strands of stratified squamous epithelium proliferate within the granulation tissue, originating from Malassez rests (remnants of odontogenic epithelium).
- Cystogranuloma. Arises from an epithelial granuloma against the background of dystrophy and necrobiosis. A cavity 0.5–1 cm in size forms, lined with non-keratinizing squamous epithelium. Detritus and cholesterol crystals accumulate in the cavity. The walls are represented by maturing granulations with inflammatory infiltration.
- Radicular (root) cyst. The predictable outcome of cystogranuloma development.
Outcomes and Complications
With appropriate treatment, a favorable outcome is possible: the destroyed bone tissue regenerates, and fibrous periodontitis develops. Any chronic form can exacerbate with the formation of pus.
Apical periodontitis is a frequent source of odontogenic infection (where the tooth serves as the entry portal). The infection spreads by contiguous extension and causes severe complications, most often in the chronic course:
- Purulent processes of the face and neck (phlegmon, fascial space abscesses).
- Intracranial pathologies (purulent meningitis, brain abscess, cavernous sinus thrombosis).
- Neck and mediastinal lesions (purulent mediastinitis, laryngeal edema with risk of asphyxia).
- The most severe conditions: jaw osteomyelitis, odontogenic sepsis, and Ludwig's angina (putrefactive-necrotic phlegmon of the submandibular and sublingual spaces of the floor of the mouth and neck, caused by group A streptococcus).