The Lazy Man’s Guide to the Microbial Causes of Primary Apical Periodontitis

R1This is a dry topic, so we’ll try to cover it as simply as possible. If you just want the outline, check out the study guide at the end of the blog post.

So Microorganisms cause Apical Periodontitis. How do they get into the tooth?

Primary apical periodontitis (AP) occurs when microorganisms (let’s call them bugs) enter the pulp chamber and colonise the pulp tissue. The bugs enter the pulp chamber through a variety of routes such as carious lesions, cracks, traumatic exposure of the pulp and due to dental procedures such as cavity preparation (Nair 1997). As mentioned in the previous post on the aetiology of AP, there is plenty of evidence of bugs being found in teeth that have apparently intact crowns (Bergenholtz 1974). These bugs gain access through accessory canals, exposed dentinal tubules, or microcracks adjacent to the gingival crevice or deep periodontal pockets (Nair 1997). The important message here is that we don’t require an obvious,visible path of entry to the pulp chamber. Bugs can enter through tiny, microscopic spaces such as dentinal tubules.

When the pulp tissue is necrotic, then a blood supply is lacking which means that the various immune cells that would normally repel a microbial invasion are also lacking, so the bugs can penetrate and colonise that much easier. When the tissue is vital however, there has been found to be an outflow of immunoglobulin-rich dentinal fluid which helps stop the inwards movement of microorganisms (Nagaoka et al. 1995). This explains why we might have a situation where a filling is lost, and dentine is exposed to a huge amount of microorganisms, but the pulp survives.

So how do the bugs enter a pulp that is vital?

In this case, the presence of bugs in close proximity to the pulp leads to inflammation in the pulp. Eventually, the inflamed pulp will necrose, and the bugs can then enter this part of the pulp. This process happens in a step by step manner. It’s not all or nothing…..We can find a situation where part of the pulp is still vital (although very unhealthy), and part is necrotic and infected. The progression from vital to completely necrotic and infected can happen rapidly,  or it can take some time. We’ll talk about this more in a future post on pulpal inflammation.

A quick word on anachoresis. It had been proposed that microorganisms that are circulating in the blood stream may lodge into necrotic dental pulp. This theory has been disproven and here are your references: Tziafas attempted to experimentally induce anachoresis in inflamed pulps in dogs but showed that the microorganisms did not end up in the teeth (Tziafas 1989). Aditionally, the study by Moller et al in 1981 showed that necrotic tissue was left in teeth for six months remained bug free (Moller et al 1981).

What happens after bugs enter the pulp chamber?

The average person has a huge number and variety of bugs (~500 species identified) in their mouth. The internal environment of the root canal is unique though, and selective pressures result in specific bugs flourishing. The three main things that influence which bugs survive are the supply of oxygen, nutrients and microbial interactions (Sundqvist et al. 2003). Initially, facultative bacteria colonise, then selective pressure results in a shift to a predominately obligate anaerobic community (Figdor et al. 2007).

Selective Pressure – Nutrition

Nutrition for these bugs come from the following sources (Sundqvist et al. 2003):

  • the oral cavity
  • degenerating connective tissue
  • dentinal tubule contents
  • fluid from the periapical tissues that is similar to plasma

Inside the root canal system there is a limited supply of  carbohydrates, and as a result those bacteria
capable of fermenting peptides and amino acids will tend to flourish over those capable of fermenting only
carbohydrates. For this reason, it is found that facultative anaerobic bacteria such as streptoccoci are found in the coronal portion of the root canal exposed to the oral environment and obligate anaerobes dominate the apical region (Fabricius et al. 1982, Sundqvist et al. 2003, Nair 1997). As the nutritional supply governs the dynamics of the microbial flora, the bacteria present at any time will depend on the stage of the infection.

So what bugs live in the infected root canal?

Here, we’re still talking about primary infections, so this is where the bugs have gained access to the pulp chamber and no treatment has been provided. The flora of treated canals is quite different, and will be discussed in a later post.

Overall, the bacteria domain consists of about 40 phyla, and of these, six can be found in the infected root canal. These phyla are the Spirochaetes, Fusobacteria, Actinobacteria, Firmicutes, Proteobacteria and Bacteriodetes (Siqueira 2003).  More specifically, the bacteria from the phyla Firmicutes, Proteobacteria and Bacteriodetes were more often associated with endodontic infections (Siqueira 2003 – check out table 1 in this ref for a full list).

Studies have shown that initially, there exists a mix of bugs comprising 10 to 30 species (Siqueira et al. 2009, Figdor et al. 2007). It has been found that no more than 10 different species are found in an individual canal and these are almost exclusively anaerobic (Gomes et al. 2004). There is a higher total percentage of gram positive species than gram negative.

Identifying the specific pathogens in a root canal system is complicated. The names of species are constantly being updated, and new species are being identified. Additionally, not all species can be cultured, and molecular methods (using DNA probes) have helped to identify additional species, such as many from the Treponema genus (Siqueira 2003). Who knows how many species we have not been able to identify?

OK, so get yourself a copy of the references – probably Figdor & Sundqvist 2007 if you’re only going to get one. If you’ve got any comments, or handy study hints for this topic, please help our readers out by leaving a comment.

References

BERGENHOLTZ, G. 1974. Micro-organisms from necrotic pulp of traumatized teeth. Odontol Revy, 25, 347-58.

FABRICIUS, L., DAHLEN, G., OHMAN, A. E. & MOLLER, A. J. 1982. Predominant indigenous oral bacteria isolated from infected root canals after varied times of closure. Scand J Dent Res, 90, 134-44.

FIGDOR, D. & SUNDQVIST, G. 2007. A big role for the very small–Understanding the endodontic microbial flora. Australian Dental Journal, 52, 38.

GOMES, B., PINHEIRO, E., GADE-NETO, C., SOUSA, E., FERRAZ, C., ZAIA, A., TEIXEIRA, F. & SOUZA-FILHO, F. 2004. Microbiological examination of infected dental root canals. Oral microbiology and immunology, 19, 71-76.

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.

NAGAOKA, S., MIYAZAKI, Y., LIU, H. J., IWAMOTO, Y., KITANO, M. & KAWAGOE, M. 1995. Bacterial invasion into dentinal tubules of human vital and nonvital teeth. J Endod, 21, 70-3.

NAIR, P. 1997. Apical periodontitis: a dynamic encounter between root canal infection and host response. Periodontology 2000, 13, 121.

SIQUEIRA, J. F., JR. 2003. Taxonomic changes of bacteria associated with endodontic infections. J Endod, 29, 619-23.

SIQUEIRA, J. F. & RÔÇAS, I. N. 2009. Diversity of endodontic microbiota revisited. Journal of Dental Research, 88, 969-81.

SUNDQVIST, G. & FIGDOR, D. 2003. Life as an endodontic pathogen. Endodontic Topics, 6, 3-28.

TZIAFAS, D. 1989. Experimental bacterial anachoresis in dog dental pulps capped with calcium hydroxide. J Endod, 15, 591-5.

The Endospot Easy Study Guide on the Microbial Aetiology of Primary Apical Periodontitis

  1. Microorganisms enter the pulp space through (Nair 1997):
    1. carious lesions
    2. cracks
    3. traumatic exposure
    4. accessory canals
    5. exposed dentinal tubules
    6. periodontal pockets to the apical foramen
  2. An outward flow of immunoglobulin-rich fluid opposes microbial penetration towards the pulp
  3. Anachoresis does not occur (Tziafas 1989)
  4. Selective pressures within the pulp space lead to a shift from the initially facultative anaerobic to an obligate anaerobic community (Figdor 2007)
  5. Three main factors of selective pressure are (Sundqvist 2003):
    1. Nutrition
    2. Oxygen
    3. Microbial interactions
  6. Nutritional pressure leads to microbes which can metabolise peptides and amino acids dominating (Sundqvist 2003)
  7. Six phyla are found in primary root canal infections(Siqueira 2003):
    1. Spirochaetes
    2. Fusobacteria
    3. Actinobacteria
    4. Firmicutes
    5. Proteobacteria
    6. Bacteriodetes
  8. No more than 10 species per canal, with a higher percentage of gram positive than negative, and almost exclusively anaerobic (Gomes 2004)
  9. Molecular methods have helped to identify microbes that cannot be viably cultured. (Siqueira 2003)
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