What was the diagnosis?

The diagnosis was asymptomatic apical periodontitis associated with pulp necrosis. The pulp became necrotic as a consequence of frank exposure to the bacterial biofilm associated with the recurrent/secondary caries.

What treatment should be carried out in this case?

Diet advice and caries removal with replacement of discoloured and deficient coronal restorations in the maxillary incisor teeth and endodontic treatment on the UL2.

What are the goals of antimicrobial endodontic treatment?

The ultimate goal of the endodontic treatment is to maintain or restore the health of the periradicular tissues. The treatment of teeth with irreversibly inflamed pulps is essentially a prophylactic approach, since the radicular vital pulp is usually free of infection and the rationale is to treat so as to prevent further pulp necrosis and infection, with consequent emergence of apical periodontitis. On the other hand, in cases like the one reported here, an intraradicular infection is already established and, consequently, endodontic procedures should focus not only on prevention of introduction of new bacteria in the canal, but also on elimination of those occurring therein.

Entrenched in the root canal system, bacteria are beyond the reach of the host defences and systemically administered antibiotics. Therefore, endodontic infections can only be treated by means of professional intervention using antibacterial procedures based on mechanical, chemical, and ecological effects.

Treatment procedures should ideally render the root canal system free of bacteria. Nevertheless, given the complex anatomy of the system, it is widely recognised that, with available instruments, irrigating substances and preparation techniques, fulfilling this goal is virtually impossible for most cases. Therefore, the reachable goal is to reduce bacterial populations to levels below those necessary to induce or sustain disease. The clinician should adopt an evidence‐based antibacterial protocol that predictably disinfects the root canal and allows this goal to be accomplished.

How does caries cause pulp necrosis and subsequent apical periodontitis?

Bacteria involved with caries are organised in authentic biofilms that advance towards the pulp as the tooth structure is destroyed in the process. Diffusion of bacterial products through dentinal tubules induces pulp inflammation long before this tissue is exposed. After exposure, the pulp surface is colonised and covered by bacteria composing the caries biofilm and the subjacent tissue becomes severely inflamed (Figure 1.1.2). Some tissue invasion by bacteria may occur. As a response to direct bacterial challenge, the pulp tissue invariably undergoes necrosis and then loses the ability to contain bacterial invasion. Eventually, invading bacteria colonise the necrotic tissue. These events of bacterial aggression, pulp inflammation, pulp necrosis and pulp infection occur in the tissue compartments, which coalesce and move towards the apical part of the canal until virtually the entire root canal is necrotic and infected.

Bacteria colonising the necrotic apical root canal induce damage to the periradicular tissues and give rise to inflammatory changes therein (Figure 1.1.3). Bacteria exert their pathogenicity by wreaking havoc on the host tissues through direct and/or indirect mechanisms. Bacterial virulence factors that cause direct tissue‐harmful effects include those that are toxic to host cells and/or disrupt the intercellular matrix of the connective tissue. Furthermore, bacterial structural components stimulate the development of host immune reactions capable not only of defending the host against infection, but also of causing severe tissue destruction. Pus formation in acute apical abscess and bone resorption associated with asymptomatic apical periodontitis are clear examples of tissue‐destructive effects indirectly caused by bacteria; that is, they are promoted by the host itself in defence against bacterial infection.

In addition to caries lesions, are there other avenues for endodontic infection?