Generally, apical periodontitis (AP) is a result of microorganisms entering the root canal system. Of course there are other causes of inflammation in the apical area, such as trauma, traumatic occlusion and foreign body reactions, but if we’re talking about common AP, then “bugs” are the cause (Abbott 2004, Harn et al. 2001).
The classic study on this topic was Kakehashi et al (1965), and this should be the starting point for any essay or exam answer. They took gnotobiotic rats (bacteria free rats) and conventional rats (with bacteria) and exposed the pulps in some teeth. In this study, the germ free rats had food, and in one case a hair forced into their long term exposed pulps, but necrosis did not occur! There was even dentine bridge formation in some cases. Conversely, all the conventional rats developed pulpal necrosis and apical periodontitis. It seems that without bacteria, rat pulps are very hardy indeed.
Sundqvist (1976) was the first to anaerobically culture and taxonomically analyse the constituent bacteria in teeth with necrotic pulps. He concluded that: AP is associated with the presence of bacteria in the root canal and that infected teeth harboured a mixture of bacteria that were predominantly obligate anaerobes (Sundqvist 1976). The significance of obligate anaerobes in endodontic infections are confirmed by a number of independent studies (Bergenholtz 1974, Wittgow et al. 1975, Kantz et al. 1974).
A study by Möller et al. (1981) compared the apical response of inducing pulp necrosis both aseptically and after contamination with indigenous oral flora in monkeys. Basically, they aseptically opened monkey pulps and used a Hedstrom file to mince the pulp. They then closed the pulp chamber so that the necrotic, uninfected tissue was inside, or they infected the tissue with plaque form the monkey’s teeth. In the teeth which contained sterile necrotic tissue, no AP formed. Those with bacteria were associated with AP. At this stage there was still a commonly held belief that necrotic tissue and stagnant tissue contributed to AP formation, but this study helps dispel this theory. In addition, this study showed that there was a variation in the ability of the various bacteria to survive and establish themselves within the root canal environment, and we start to see the concept of bacteria within root canals living in communities, rather than just as one individual strain.
There has been a significant shift away from the concept of one ‘causative pathogen’ and significant evidence exists that specificity seems to be related to the community level as certain species compositions are specifically associated with some forms of apical periodontitis (Siqueira et al. 2009a, Sakamoto et al. 2006). There is a very high level of inter-individual variation of bacterial community profiles, such that 44% of recovered taxa were isolated or detected in only one study (Siqueira et al. 2009b). Microbial ecology differs significantly between different disease forms such as chronic apical periodontitis versus acute apical abscess, suggesting the existence of a pattern associated with each one (Sakamoto et al. 2006, Siqueira et al. 2004). In addition, different magnitudes
of disease, based on intensity of signs and symptoms, may be related to the species composition of the community (Siqueira et al. 2009a).
Siqueira (2002) differentiates the types of endodontic infections into primary, secondary or persistent root canal infections. Primary infections are those that occur within a root canal system prior to any treatment being applied. A Secondary infection occurs when a root canal (RC) had been treated, and new bacteria enter the RC system. This can happen when a filling is lost, or micorleakage occurs and the root filling (RF) is exposed to bacteria which then penetrate along the RF. A persistent infection is one that remains in the canal despite treatment. That is the primary infection remains despite RCT.
An important concept to understand is the formation of biofilms. This relates to the organisation of bacteria into a protected, sessile biofilm comprised of cells embedded in a hydrated exopolysaccharide-complex in microcolonies (Nair 2006). Bacteria in root canals do form biofilms and these are much more difficult for both our immune system and current RCT methods to deal with.
Do you have a reference that should be included in this list, or a comment on what is written? Please share it with our readers.
ABBOTT, P. V. 2004. Classification, diagnosis and clinical manifestations of apical periodontitis. Endodontic Topics, 30-54.
HARN, W. M., CHEN, M. C., CHEN, Y. H., LIU, J. W. & CHUNG, C. H. 2001. Effect of occlusal trauma on healing of
periapical pathoses: report of two cases. Int Endod J, 34, 554-61.
KAKEHASHI, S., STANLEY, H. R. & FITZGERALD, R. J. 1965. The Effects of Surgical Exposures of Dental Pulps in Germ-
Free and Conventional Laboratory Rats. Oral Surg Oral Med Oral Pathol, 20, 340-9.
MÖLLER, A. J., FABRICIUS, L., DAHLÉN, G., OHMAN, A. E. & HEYDEN, G. 1981. Influence on periapical tissues of
indigenous oral bacteria and necrotic pulp tissue in monkeys. Scand J Dent Res, 89, 475-84.
NAIR, P. N. R. 2006. On the causes of persistent apical periodontitis: a review. Int Endod J, 39, 249-81.
SAKAMOTO, M., ROCAS, I. N., SIQUEIRA, J. F., JR. & BENNO, Y. 2006. Molecular analysis of bacteria in asymptomatic and
symptomatic endodontic infections. Oral Microbiol Immunol, 21, 112-22.
SIQUEIRA, J. F. 2002. Endodontic infections: concepts, paradigms, and perspectives. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod, 94, 281-93.
SIQUEIRA, J. F., JR. & ROCAS, I. N. 2009a. Community as the unit of pathogenicity: an emerging concept as to the
microbial pathogenesis of apical periodontitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 107, 870-8.
SIQUEIRA, J. F. & RÔÇAS, I. N. 2009b. Diversity of endodontic microbiota revisited. Journal of Dental Research, 88, 969-81.
SUNDQVIST G. 1976. Bacteriological studies of necrotic dental pulps. Odontological Dissertations No. 7. Department of Oral Microbiology, Umea° University, Sweden.
The Endospot Easy Study Guide on Aetiology of Apical Periodontitis
- Most AP is due to micororganisms within the RC. Other occasional causes include trauma, occlusal trauma, foreign body reaction. (Abbott 2004, Harn et al. 2001)
- Exposing pulps in rat teeth lead to AP in conventional rats (bacteria present), but no AP in gnotibiotic rats (no bugs present) (Kakehashi, 1965)
- Bacteria in infected necrotic pulps predominately obligate anaerobes. Anaerobic techniques required to culture (Sundqvist thesis, 1976)
- Monkey teeth with necrotic, uninfected pulps do not develop AP. If infected, AP develops. Different microorganisms display differing ability to survive in the root canal system. (Mollar, 1981)
- It is unlikely one microorganism causes disease in RCs. More likely that a community of mircobes exists. This community varies between people, and between various forms of disease. (Siqueira et al. 2009a, Sakamoto et al. 2006)
- Biofilms form in RCs. Biofilms protect bacteria from being destroyed. (Nair 2006)
- Primary infections (new in previously unifected RCs), secondary infections (new in previously treated RCs), persistent (remaining after treatment). Siqueira (2002)