apical pericementitis
apical periodontitis

Another cause is due to untreated necrotic pulp (chronic apical periodontitis).

Apical periodontitis is typically the body's defense response to the threat of microbial invasion from the root canal.

Their biologic activities have been extensively researched and reviewed, and their importance in the pathogenesis of apical periodontitis is obvious.

Furthermore, concentrations of IgG antibodies have been found to be nearly five times higher in lesions of apical periodontitis than in uninflamed oral mucosa.

This is because neutrophils, which are rich sources of PGE2, are present when the majority of rapid bone loss occurs during the initial stages of apical periodontitis.

Sequelae of a necrotic pulp include acute apical periodontitis, dental abscess or radicular cyst and discolouration of the tooth that may require tooth bleaching.

Acute periapical periodontitis, also termed acute apical periodontitis, acute periradicular periodontitis, or symptomatic periapical periodontitis.

For example, it has been demonstrated that there is an association between nonresolving apical periodontitis lesions and the presence of cholesterol clefts within the periapical lesion; in fact, an incidence of up to 44% has been reported!

Indeed, most of the common oral pathologies have been reported as possible sources of barodontalgia: dental caries, defective tooth restoration, pulpitis, pulp necrosis, apical periodontitis, periodontal pockets, impacted teeth, and mucous retention cysts.

Although the neutrophils themselves rarely remain alive for more than a few days, the excessive accumulation of dead neutrophils and the enzymes they released is a major cause of tissue breakdown in the acute phases of apical periodontitis.

Periapical periodontitis (also termed apical periodontitis, AP, or periradicular peridontitis) is an acute or chronic inflammatory lesion around the apex of a tooth root which is caused caused by bacterial invasion of the pulp of the tooth.

Together, the cells of this second strike compose the bulk of the apical periodontitis lesion and serve an important role in the subsequent chronic phase of inflammation of apical periodontitis, as they can live for many months.