1.1
Microbiology of Primary Apical Periodontitis

José F. Siqueira Jr and Isabela N. Rôças

Objectives

Apical periodontitis is an inflammatory disease that affects the tissues surrounding the apical portion of the dental root and is primarily caused by bacteria infecting the root canal system. At the end of this case the reader should be able to recognise the infectious origin of apical periodontitis as well as understand some basic aspects of the microbiology of endodontic infections.

Introduction

A 34‐year‐old female was seeking replacement of defective and aesthetically unpleasant composite restorations in the maxillary incisors. The teeth had been restored more than five years previously. No significant symptoms were reported at the time of consultation.

Chief Complaint

The patient complained of the aesthetic appearance of the coronal restorations in all the maxillary incisors. She recalled having the restorations about five years ago due to decay in the teeth. Except for a mild sensitivity to sweet food in the UL2 a few years ago, all the maxillary incisors had been asymptomatic.

Medical History

Unremarkable.

Dental History

Last visit to a dental office for a check‐up appointment was two years previously. At that time, no apical periodontitis lesion was evident in the maxillary anterior region.

Clinical Examination

Extraoral examination was unremarkable. The patient had a moderately restored dentition, and her oral hygiene status was satisfactory. Composite restorations in all maxillary incisors were defective and discoloured.

All anterior teeth responded normally to thermal and electric sensitivity testing, except for the UL2, which was non‐responsive. No swelling or sinus tract was evident on the mucosa over the apices of the anterior teeth. The UL2 was discoloured with an existing restoration with marginal deficiencies.

Radiographic Examination

Periapical radiograph revealed (Figure 1.1.1):

• Normal bone levels.
• The UL2 with an existing restoration with secondary caries in proximity to the pulp chamber.
• A radiolucency involving the apical region of the UL2.

Diagnosis and Treatment Planning

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.

Discussion

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?

Under normal conditions, the pulp–dentine complex is isolated and protected from the oral microbiota by overlying enamel and cementum, the same way the connective tissues elsewhere in the body are segregated from the microbiota residing in body cavities and surfaces by the epithelium of mucosa or skin. Once the integrity of these natural layers is breached (e.g. as a result of caries, trauma‐induced fractures and cracks, restorative procedures, scaling and root planing, attrition or abrasion) or naturally absent (e.g. because of gaps in the cemental coating at the cervical root surface), the pulp–dentine complex is exposed to the oral environment. This complex is then challenged by bacteria present in carious lesions, in saliva bathing the exposed dentinal area and/or in the dental biofilm formed on the exposed surface. The subgingival biofilm associated with periodontal pockets may also represent a source of bacteria to reach the pulp via dentinal tubules at the cervical region of the tooth, or through lateral and apical foramina.

Whatever the route of bacterial access to the root canal, necrosis of pulp tissue is a prerequisite for the establishment of primary endodontic infections. As long as the pulp is vital, it can protect itself against bacterial invasion and colonisation by mounting an immune defence response. However, if the pulp becomes necrotic as a result of caries, trauma, operative procedures or periodontal disease, the necrotic tissue can be very easily invaded and colonised (infection). This is because host defences do not function in the necrotic pulp tissue.

Microorganisms can also have access to the root canal any time after professional endodontic intervention (secondary infection), either by a breach in the aseptic chain during treatment, by coronal leakage through temporary/definitive restorations or by tooth/restoration fracture.

Why do some traumatised teeth develop apical periodontitis even when the unrestored tooth crown looks intact?

Bacteria have been isolated from the root canal of traumatised teeth whose pulps became necrotic and apical periodontitis developed, even in circumstances where the tooth crown was apparently intact. How did those bacteria invade the pulp space? In the past, it was believed that such bacteria originated from the gingival sulcus or periodontal pockets and reached the necrotic canal via severed blood vessels of the periodontium, a phenomenon called anachoresis. This theory was never supported by scientific evidence. Actually, trauma can induce exposure of dentine by fracturing the crown or inducing the formation of enamel cracks, which can be macroscopic or microscopic. A large number of dentinal tubules...