The Source of Infection Problems with Root Canal Treatment in Dentistry.

The Source of Infection Problems with Root Canal Treatment in Dentistry.

Partial source material: The Silent Saboteur

Posted by William D. Nordquist DMD MS

 

When a tooth decays or periodontal disease occurs to the extent that infection enters the pulp chamber of a tooth, the traditional treatment involves the mechanical removal of infected pulpal tissue and replacement with an inert root canal filling. If done properly, this form of treatment is usually quite effective from a clinical standpoint in that the area in question usually becomes asymptomatic, and all clinical means of assessment available to the treating dentist usually reveal local osseous regeneration and healing in addition to restoration of function. In spite of the apparent success of this form of treatment, there is recent suspicion that this might represent an over-simplification of this common clinical situation. In fact, if one examines the situation from strictly a biologic point of view, there is little question that, in spite of the many forms of clinical measurement to the contrary, traditional root canal treatment (RCT) is far from ideal. We  know this to be the case since even when root canal debridement is accomplished in the best manner possible, subsequent analysis of treated teeth reveals small foci of bacterial debris that are nonetheless left behind within tiny irregularities of the root canal or apical surface of the tooth. (1 & 2) These foci, even though clinically innocuous in most cases, can and sometimes do represent the source of infection of adjacent contiguous bone that later causes subsequently placed adjacent implants to fail (3-6). If such infection is capable of causing a nearby implant to fail, it begs a larger and much more important question: that is, can these apparently innocent but persistent dental foci of infection at the apices of teeth also represent the source of distant infection or chronic inflammatory processes elsewhere in the body that occur via blood-borne spread? If so, this would represent a potentially serious problem.

It is generally accepted fact that once being diagnosed, infections that occur elsewhere in the body (e.g., the appendix or the skin etc.) are ordinarily treated aggressively in order to prevent further damage to adjacent tissues and spread of infection to vital organs. Yet low grade, chronic dental infection, because it is usually clinically silent and apparently innocuous, is commonly tolerated by the dental profession and is usually passed over lightly or is basically ignored. It has been common practice for dentists to assume this practice since, in reality, there has been no real impetus to pursue any therapeutic solution since the presence of a few bacteria surrounding RCT-treated teeth was generally assumed to be less than clinically significant and thus, for all practical purposes, a non-problem. In any case, there was certainly not enough rationale to consider more aggressive treatment (such as the sacrifice an otherwise good tooth), and further still, there were no good alternatives to root canal therapy short of apical surgery or extraction. In spite of the fact that clinically silent root canal fillings are usually deemed clinically acceptable, the assumption of innocence with regard to apparently normal, apical tissues following RCT has not always been the case.

Looking back into history, we note that the efficacy of root canal treatment has, at times, been called into question, but the politics of practice were usually sufficient to silence such critics. One prominent example of such is the case of Weston A. Price, DDS (1870–1948), a prominent dentist and also a nutritionist. Price was the chairman of the Research Section of the American Dental Association from 1914–1923 but was later marginalized by the ADA for his outspoken views on what he considered the detrimental aspects of  root-canal therapy. In our opinion, however, after a thorough reading and review of Price’s work, it is clear that he practiced and understood the concept of infection associated with root canal treatment therapy far better than we do today.  One only has to examine his research to make this point. For example, in one experiment performed nearly 100 years ago, Price(7) took infected teeth or extracts of such from patients suffering from a wide range of serious “medical” problems, and implanted these samples under the skin of laboratory animals. Subsequent examination revealed that the laboratory animals quickly came down with infections in distant parts of their bodies. Expected results from such an experiment would be that an infection from the implanted infected tooth material might go anywhere in the body of the experimental animal to cause disease in more or less a random distribution pattern. However, that was not the effect that Price observed. What was observed was that if the donor patient had infected kidneys and his infected dental material was implanted into several lab animals, essentially all the animals developed infected kidneys, and did so with rapidity(8). As a result of his experiments, Price claimed that as many as 95% of focal infections in distant tissues started in the teeth and tonsils (9)! Price theorized that ordinarily harmless bacteria normally found in the mouth get trapped in the dentinal tubules or root surfaces of infected teeth or tonsils and somehow mutated into a more dangerous form. The new mutated bacteria and /or the toxic poisons they produced would travel through the blood stream and lymphatic system to remote body parts and cause disease elsewhere. Price went on to show that even when root canal treatment was done according to what at the time was accepted modern principles and standards, and even when follow-up radiographs showed  evidence of adequate healing, such treatment did not prevent or preclude the presence and subsequent spread of infection in laboratory animals.

In addition, Price also proved that infection in the area of a treated tooth can spread contiguously to infect adjacent bone in that biopsy specimens of bone adjacent to RCT-treated teeth revealed bacteria within the first millimeter or two from the apical surface.(10) Clearly, there is abundant evidence from Price’s work alone that even clinically adequate, root-canal-treated teeth can and do harbor residual bacteria that, at least potentially, can cause problems for implant dentists when subsequently placing dental implants in bone adjacent to root-canal-treated teeth.

Research done much later adds additional evidence in support of Price’s earlier conclusions. In his classic 1967 study, Brynolf (11), used cadavers as source material to study root canal treated teeth. These cadaver teeth, all previously treated by RCT, were radiographed and evaluated for evidence of apical radiolucent lesions and subsequently divided into those with and without periapical lucenceis. The teeth and surrounding bone were then cut from the jaws in block sections and later treated, prepared and sectioned for microscopic examination. As a result of his investigation, Brynolf’s concluded that the lack of radiographic evidence of pathologic change at the base of a root canal–treated tooth did not preclude the presence of small foci of inflammation or infection at the apex of the tooth in question. He went onto say that 93 percent of root canal–treated teeth examined in his cadaver study had microscopic signs of inflammation (infection), presumably caused by bacteria in the area. Later,  Green et al (12) performed additional cadaver studies and characterized Brynolf’s previous results as somewhat questionable due primarily to differences both in treatment techniques and methods of radiographic and histological analysis that were being used at the time. Green reported that out of the 29 teeth examined, 15, (52 percent of his cases) exhibited histologic evidence of inflammation, presumably due to causative infective bacteria that remained in the periapical area after root canal treatment was performed.

 

The question as to which specific bacteria are involved in apparent residual low-grade periapical infection (related to prior root-canal-treated teeth) has not been addressed until relatively recently when  techniques became available that enabled identification of small amounts of DNA material unique to a specific bacterial genus or species. With specific regard to the oral spirochetes, Ôças (13) and his group used a nested PCR assay in an effort to determine the presence or absence of four distinct Treponema species associated with primary root canal infections. Samples from 32 cases of infected root canals were obtained, twenty-two of which exhibited chronic, asymptomatic peri-radicular lesions whereas 10 were symptomatic cases diagnosed as acute apical periodontitis. Small traces of DNA extracted from all samples were amplified using universal 16S rDNA primers to detect a specific fragment of the 16S rDNA from each of the following Treponema species: Treponema denticola, T. socranskii, T. vincentii and T. pectinovorum. Results showed that in asymptomatic cases, T. denticola, the most common oral spirochete, was detected in 77.3% of the samples; T. socranskii was seen in 40.9%, T. vincentii in 18.2% and T. pectinovorum in 13.6%. whereas in the  acute apical periodontitis cases, T. denticola was detected in 80%, whilst T. socranskii and T. vincentii were detected in 40% and 10% of cases, respectively. Based on these data, it is clear that, in addition to a number of other bacteria (tests for such were not run), the various oral spirochetes must be considered as potential infectious microbial sources with regard to their likely role as putative pathogens for endodontically-related periapical disease as well as for other oral infections.

 

In a later investigation involving spirochetes, Montagner (14) designed a study to detect the presence of Treponema species in infected root canals (RCs) and exudates related to acute apical abscesses (AAAs) as well as to determine positive association between targeted species and clinical signs/symptoms. Paired samples of infected RCs and AAAs were collected from 20 subjects. Nested polymerase chain reaction assay with species-specific primers for 16S rDNA and downstream intergenic spacer region was used for microbial detection. The frequency of species and statistical associations between species and signs/symptoms of endodontic origin as well as their simultaneous detection in both milieus were probed.

 

The most frequently detected species were T. socranskii (RC, 17/20; AAA, 15/20), T. denticola (RC, 8/20; AAA, 11/20); T. medium (RC, 6/20; AAA, 9/20); and T. amylovorum (RC, 5/20; AAA, 9/20). Positive correlation was found for simultaneous presence of T. denticola in both RCs and AAAs (p = 0.01). Positive association was observed between T. medium and T. vincentii (p = .037). No positive statistical association was observed between the targeted species and signs/symptoms. The high prevalence of Treponema species in RC and AAA samples from the same tooth indicated that these organisms are important pathogens in acute endodontic infections.

 

Other more recent research perhaps gives us more cause to be concerned about potential dangers of oral spirochetes. In his excellent article published in the Journal of Dental Research, Foschi (15) showed that Treponema denticola, the most commonly implicated oral spirochete associated with periodontal disease can disseminate into a variety of distant body tissues subsequent to being artificially introduced into the pulp chambers of healthy mouse teeth by surgical means. Within a short period of time following surgical implantation, spirochetes produced abscesses that drained through the “gums” adjacent to the roots of the infected teeth. He later sacrificed the mice and studied a variety of tissues to determine the anatomic location where the spirochetes were able to migrate and later infect. He found that the spirochetes were able to spread to virtually all vital tissues of the mice including the brain. Although spirochetes may have been present in far greater numbers in Foschi’s experiment than in actual human periapical disease, this is nonetheless powerful evidence that implicates spirochetes as possible, if not likely, candidates for causing or initiating chronic inflammatory diseases in remote tissues distant from their site of origin.

 

Nordquist (16 – 20) has discussed the potential role of infected teeth (including root canal treated teeth) in the complex labyrinth of systemic chronic inflammatory diseases. He showed that undiagnosed, clinically silent, infected teeth adjacent to a subsequently placed dental implant can be the source of the infection that ultimately causes the adjacent implant to fail.

 

Reports of a disproportionate number of dental implant failures (when the latter are placed adjacent to RCT-treated teeth) along with the large percentage of periapical infections associated with root canal teeth in cadavers gives both the dental and medical professions real cause for concern. How do we know with certainty which root canal teeth, if any, will later surface as problematic sources of infection prior to the time that implants are placed? Can dentists afford to ignore adjacent root-canal-treated teeth when contemplating the placement of an implant? The risks to patients regarding local contiguous spread of infection to adjacent bone and implant failure are obvious. However, there would seem to be a much more serious potential risk to those involved in various fields of dental practice, and these involve potential liability issues that may arise for dental clinicians. That is, if a causative link between dental infection and systemic disease becomes more firmly established, dentists could potentially be held liable for failing to deal with asymptomatic periapical infection should that infection lead to more serious consequences down the road. Clearly, an acceptable therapeutic alternative to RCT that diminishes such risks both to the patient and the dentist would not only be beneficial but also desirable. With this report, we wish to state that such a procedure, henceforth called, “Actual Tooth Replacement” (ATR for short) is, in fact, now available as an alternative to conventional root canal therapy.

 

Basically, the recently developed ATR technique offers dental clinicians  a novel, alternative  method for replacing decayed or abscessed teeth in lieu of performing root canal therapy. The basics of the technique are as follows:

  1. Once a tooth is deemed necrotic or a potential problem for the anticipated placement of a dental implant, it is carefully extracted, and immediately sent to a laboratory such that a replacement tooth can be quickly manufactured that simulates the identical morphologic structure, measurements and form of the tooth as closely as possible.
  2. Once the “Actual Tooth” is replicated in ceramic with the aid of computer imaging, it is then treated by applying a thin layer of durable, biocompatible material to the root surface and then returned to the operatory for placement back into the extraction socket as a form of dental implant.
  3. The tooth is then stabilized such that the replacement tooth can be fixed in place and removed as much as possible from oral trauma during the phase of osseous attachment.

As such, this technique is thought to represent an excellent alternative to conventional root canal therapy which, under situations previously described, could serve as a significant source of infection to other tissues, both local and distant.


4 Sussman H.  Periapical implant pathology.  J Oral Implantol 1998;24(3):133-38.

5 Sussman H.  Cortical bone resorption secondary to endodontic-implant pathology. A case report.  N Y State J 1997 Nov;63(9):38-40.

6 Sussman H, Moss S. Localized osteomyelitis secondary to endodontic-implant pathosis. A case report.  J Periodontol 1993;64(4):306-10.

7 Price WA. Dental Infections and the Degenerative Diseases. Volume II. Part II. Price-Pottenger Nutrition Foundation La Mesa California 2008

8 Price: Ibid:155-171.

9 Price WA. Ibid;407.

10 Meinig GE. Ibid. Pg.31.

11 Brynolf I. A histological and roentgenological study of the periapical region of upper incisors. Odont Revy. 1967;(11):1-97.

12 Green T, Walton R, Merrell P. Radiographic and histologic periapical findings of root canal treated teeth in cadaver. Oral surg Oral Med Oral Pathol Radiol Endol 1997;83:707-11.

13 IN ôças, JF Siqueira, AF Andrade, M Uzeda. Oral treponemes in primary root canal infections as detected by nested PCR. Int Endod J 2003;36:20-6.

14 Montagner F, Jacinto RC, Signoretti FG, Gomes BP. Treponema species detected in infected root canals and acute apical abscess exudates. J Endod. 2010 Nov; 36 (11):1796-9.

15 Foschi F. Treponema denticola in disseminating endodontic infections. J Dent Res 2006; 85(8):761-765.

16 Nordquist W. Ibid. 2009.

17 Nordquist W. Oral spirochetosis associated with dental implants: Important clues to systemic disease. Int’n J of Clin Impl Dent 2009 Jan-Apr;1(1):32-39.

18 Kimoto K et al. Part I: Crystalline fluorapatite-coated hydroxyapatite, physical properties. 2011 JOI;XXXVII(1):27-33.

19 Nordquist WD et al. Part II: Crystalline fluorapatite-coated hydroxyapatite implant [xix]Material: A dog study with histologic comparison of osteogenesis seem with FA-coated HA grafting material versus HA controls: Potential bacteriostatic effect of fluorated HA. 2011 JOI;XXXVII(1):35-42.

20 Nordquist WD and Krutchkoff DJ. Part III: Crystalline fluorapatite-coated hydroxyapatite; Potential use as a bacteriostatic agent for both pre-implant cases and retreatment of infected implant sites: A report of 4 cases. 2011 JOI;XXXVII(1):44-51.

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