1: Root Canal Infection and Endodontic Apical Disease

Chapter 1
Root Canal Infection and Endodontic Apical Disease

Nestor Cohenca and Ana Maria González Amaro

Department of Endodontics and Pediatric Dentistry, University of Washington, Seattle, WA, USA

Department of Microbiology, University Autonomous of San Luis Potosí, San Luis Potosí, Mexico

Infection control: why now?

The outcome of endodontic treatment depends on the microbiological status of the root canal. In inflamed vital pulps, the infection is commonly limited to the site of exposure causing a localized inflammatory response (1, 2). However, when aseptic technique is used, the effect of endodontic therapy is predictably high as demonstrated by several studies (3–7).

In infected necrotic pulps, microorganisms are present within the root canal system and dentinal tubules, causing a apical inflammatory lesion called apical periodontitis. In these cases, endodontic treatment should be essentially directed toward the prevention and control of pulpal and apical infections, as stated by Kakehashi, Stanley, and Fitzgerald nearly 50 years ago (8). Unfortunately, the success of the therapy for these cases is 10–15% lower when compared to non-contaminated teeth (Table 1.1) (3–7, 9–11). What is more concerning is the fact that this lower outcome has not changed or improved despite all the technological advancements the world of endodontics has seen (12). How come that despite the “art and science” of current endodontic therapy, outcome studies have failed to demonstrate an increase in endodontic success? Why do we fail to predictably control the infection after so many years of research, experiment, and treatment? The answer might be related to the fact that very few advances have ever targeted the real problem, which continues to be microorganisms, especially in the apical third. The success of the endodontic treatment is possible only with an understanding of the molecular biology of the pathogens, their structures, synergies, and weaknesses. No file will ever disinfect a root canal, nor is it designed for that purpose. Recognizing that our endodontic therapy will end in failure if we do not find a method to completely destroy the microbes within the root canal system, infection control must be our main goal and concern. Therefore, we should focus our research and development on efficient and predictable methods to control the infection and improve the endodontic treatment and healing of apical periodontitis.

Table 1.1 Outcome of endodontic therapy based on the presence or absence of apical periodontitis.

Author and year Cases/cohort Recall Without apical periodontitis (%) With apical periodontitis (%)
Strindberg (1956) 258 6 months to 10 years 93 80
Kerekes and Tronstad (1979) 491 Norway, Dental school 3–5 years 92 89
Sjogren et al. (1990) 96 Sweden, Dental school 8–10 years
96 86
Friedman et al. (2003) 92 4–6 years
92 74
Farzaneh et al. (2004) 94 Toronto, Grad students 4–6 years
94 81
Orstravik et al. (2004) Norway, Dental school 0.5–4 years
94 79
Ng et al. (2011) 702 London
Grad students
4 years
Ricucci et al. (2011) 816 Italy
5 years
92.3 82.7

Terminology and apical definitions

The term apical periodontitis has gained increasing support and is used widely in current literature. The American Association of Endodontists recently published the revised Glossary of Endodontic Terms (13). Some of the terms defined in the glossary are as follows:

  1. Normal apical tissues Teeth with normal apical tissues that are not sensitive to percussion or palpation testing. The lamina dura surrounding the root is intact and the periodontal ligament space is uniform.
  2. Symptomatic apical periodontitis Inflammation, usually of the apical periodontium, producing clinical symptoms including painful response to biting and/or percussion or palpation. It may or may not be associated with an apical radiolucent area.
  3. Asymptomatic apical periodontitis Inflammation and destruction of apical periodontium that is of pulpal origin, appears as an apical radiolucent area and does not produce clinical symptoms.
  4. Acute apical abscess An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus formation, and swelling of associated tissues.
  5. Chronic apical abscess An inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little or no discomfort, and the intermittent discharge of pus through an associated sinus tract.

In biological terms, apical periodontitis means “inflammation of the periodontium.” This is a broad term to describe an inflammatory reaction in the tissues, including lateral and furcal locations of inflammation; it does not distinguish etymologically pulp-induced periodontitis from marginally derived periodontitis. More specific pathologies such as granulomas and cysts were excluded because they do not represent a “clinical or radiographic” diagnostic reality, but rather a diagnosis based on histological findings. The prevalence of apical periodontitis has increased throughout the years (14, 15), even in the low caries-rate adult Danish population (16).

The evolution of endodontic microbiology

Miller, in 1890 (17), was the first to demonstrate the presence of bacteria in necrotic human pulp tissue. However, the cause and effect relationship is attributed to Kakehashi et al. (8) who experimented with gnotobiotic (germ-free) and normal rats. Bacterial contamination in the orally exposed pulp tissue caused necrosis and apical pathoses in normal rats. The study is considered a classic reference as it initiated a new and bright era in endodontic microbiology.

In 1966, Moller (18) established the importance of adequate isolation for microbiological sampling and various culture media for the recovery and identification of anaerobic microorganisms, providing more relevant information regarding the type of bacteria present in root canal systems. Bergenholtz then demonstrated the presence of bacteria in the traumatized teeth. Despite the fact that pulp chambers were not exposed, bacterial growth was observed in 64% of all samples. The flora was dominated by anaerobic microorganisms including Bacteroides, Corynebacterium, Peptostreptococcus, and Fusobacterium (19). Two years later, Sundqvist (20) demonstrated the prevalence of anaerobic bacteria in root canals, supporting the results obtained by Bergenholtz.

In the 1980s, the studies were more focused on understanding the colonization and interactions within the endodontic microflora. Moller investigated the relationship between uncontaminated necrotic pulp and apical tissues. The study maintained uncontaminated necrotic pulp in the root canal during a period of at least 6 months, and evaluated changes in the microbial flora enclosed in the root canal and its capacity to induce apical periodontitis (21). Using 9 monkeys (Macaca fascicularis), the pulp of 78 teeth was aseptically necrotized. Twenty-six of the pulp chambers were sealed and the pulp chamber remained free. Fifty-two teeth were infected with the indigenous flora. Clinical, radiographic and microbiological data was recorded before and after the completion of the study. The root canals were initially uninfected sterile in the final samples. No inflammatory reactions were found on the 26 control teeth. On the experimental teeth inflammatory reactions were observed clinically (12/52 teeth) and radiographically (47/52 teeth). An average of 8 to 15 bacterial strains were identified as facultative anaerobic bacteria including enterococci, coliforms, and anaerobic bacteria such as Bacteroides, Eubacterium, Propionibacterium, and Peptococcus, Peptostreptococcus. Some anaerobic bacteria not present on the initial microbiological test were isolated on the final samples. Histological examination of the apical tissue confirmed the presence an inflammatory reaction to the bacterial contamination (21).

In 1982, Fabricius et al. investigated the pulps of 24 root canals, 8 in each of the 3 monkeys that were experimented on. Teeth were mechanically devitalized and exposed to the oral flora for about 1 week and thereafter sealed. Microbiologic sampling and analysis was performed in 16 teeth (of 2 of the monkeys) after 7 days of closure (initial samples). Afterward, inoculation pulps were sealed for a period of 6 months. Final sampling was taken from the main root canal, the dentin, and the apical region at the same sampling session. All microbiologic analyses were carried out quantitatively. Final root canal samples from the apical region showed a predominance of obligate anaerobic nonsporulating bacteria; in fact 85–98% of the bacterial cells were anaerobic. The most frequently found species were Bacteroides and Gram-positive anaerobic rods. A lower proportion of facultative anaerobic bacteria were found; this was most pronounced for coliform rods in comparison with the strains of Bacteroides melaninogenicus.

Today, electron microscopy has become a great technology in many areas of science. Nair (22) studied the structure of the endodontic flora, its relationship to the dentinal wall, microbial interactions, and dynamics of apical inflammatory response. The study was performed on human teeth with granulomas and cysts. The results showed the presence of microorganisms in all the samples. The flora consisted of cocci, bacilli, and spirochetes filamentous organisms. In most cases, the bacteria were restricted to the canal, but in 4 granulomas and 1 cyst, the bacteria were found in the lesion. There was a distinct bacterial plaque adhering to the dentinal wall at the apical foramen. Nair describes this finding as a group or community of one or more types of microorganisms as well as bacterial condensate, suggesting the formation of plaque in the dentinal wall by the flora of the root canal. This finding is considered to be the subject that currently occupies many researchers: the presence of biofilm on root canal walls.

In 1990, Nair (23) analyzed nine therapy-resistant and asymptomatic human apical lesions (4–10 years) removed during surgery using light and electron microscopy. Six out of nine lesions revealed microorganisms in the apical root canal. Four contained bacteria and two contained yeasts. Of the three cases with no microorganisms, one revealed a foreign body giant cell granuloma. In the majority of therapy-resistant apical lesions, microorganisms (bacteria, yeast) and foreign body giant cell granulomas play a significant role in treatment failures.

Although endodontic microbiology has evolved significantly, it still lacks an understanding of the ecology of the root canal and requires an analysis of the bond that develops between microorganisms and their surroundings. This relationship is an essential element that provides a glimpse into the understanding of their behavior and ability to invade an area that is rich in nutrients and whose abiotic and biotic factors determine the distribution and quantity of living organisms that may share the root space. In the early 1990s, Sundqvist (24, 25) published a couple of reviews summarizing the available data. Bacterial flora of the root canal is dominated by obligate anaerobes, comprising up to 90% of the total population. Aerobic bacteria are rarely found initially in the infected root canals but could have been introduced during the treatment. During the course of an infection, interrelationships develop between microbial species, based on their nutritional demands and nutritional interactions, and the pathogenicity of the polymicrobial root flora is dependent on bacterial synergy. Bacteriocins proteins produced by a microorganism enhance their ability to inhibit growth of some species competing for the same ecological niche. Additionally, they promote bacterial coaggregation and interactions establishing the ecology of the apical tissues.

The identification of the endodontic microbiota in the apical third was reported in 1991 by Baumgartner (26) who employed both aerobic and anaerobic cultures in the same study, in order to isolate and identify the microflora of the apical portion of root canals of teeth with carious pulpal exposures and apical lesions. Ten freshly extracted teeth with carious pulpal exposures and apical lesions contiguous with the root apex were placed inside an anaerobic chamber and the apical 5 mm of the root canals cultured. In addition to anaerobic incubation, duplicate cultures were incubated aerobically. Fifty strains of bacteria from the 10 root canals were isolated and identified. The most prominent bacteria cultured from the 10 root canals were Actinomyces, Lactobacillus, black-pigmented Bacteroides, Peptostreptococcus, nonpigmented Bacteroides, Veillonella, Enterococcus faecalis, Fusobacterium nucleatum, and Streptococcus mutans. Of the 50 bacterial isolates, 34 (68%) were strict anaerobes. Baumgartner’s study demonstrated the presence of predominantly anaerobic bacteria in the apical 5 mm of infected root canals in teeth with carious pulpal exposures and apical lesions.

Advancements in the identification of endodontic flora by Molander et al. in 1998 correlated the clinical outcome, refractory lesions, and the presence of certain strains. Molander and coworkers examined the microbiological status of 100 root-filled teeth with radiographically verified apical periodontitis and 20 teeth without signs of apical pathoses. In teeth with apical periodontitis, 117 strains of bacteria were recovered in 68 teeth. Facultative anaerobic species predominated among these isolates (69% of identified strains). Enterococci were the most frequently isolated genera, showing “heavy” or “very heavy” growth in 25 out of 32 cases (78%). In 11 teeth without signs of apical pathoses, no bacteria were recovered while the remaining 9 yielded 13 microbial strains. Eight of these grew “very sparsely.” It was co/>

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Jan 2, 2015 | Posted by in Endodontics | Comments Off on 1: Root Canal Infection and Endodontic Apical Disease
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