Recent development in endodontie research
Leif Tronstad Division of Endodontics, Facuity of Dentistry, University of Osio, Osio, Norway
Tronstad L: Recent development in endodontie research. Scand J Denl Res 1992; -.'• 100: 52-9.
In essence, endodontics as a clinical disipline is concerned with the prevention and treatment of pulpal and periapical infection. In recent research the infective process has been investigated as well as the mechanisms by which the pulp and periodontium deal with microbial insults. With regard to the pulp, findings on the hemodynamics of pulpitis suggest that the inflammatory response in this tissue is much less inlluenced by the special anatomic environment of the tooth than was previously believed. Pulpal diseases are being underdiagnosed, mostly because of inadequate examination methods. Laser Doppler flowmetry which gives a vascular rather than a nervous response may gain importance in pulpal diagnostics in the future. It is established that apical periodontitis with bone resorption cannot develop in the absence of bacteria in the root canal system. Root canal infection is characterized by a wide variety of combinations of relatively few anaerobic bacteria, and bacterial synergism plays an important role in maintaining the infection. Microbial invasion of an apical granuloma may take place. Non-oral and environmental organisms like Pseudoinonas aeruginosa are frequently isolated from treatment-resistant cases. Success of endodontie treatment depends on the reduction or elimination of the infecting bacteria. This may predictably be obtained after a thorough chemo-mechanical instrumentation and disinfection of the root canal with calcium hydroxide. The standardized technique which entails the preparation of a cylindrical apieal box with removal of significant amounts of dentin near the root apex predictably gives a clean canal. This technique has provided excellent clinical and radiographic results in well documented follow-up studies.
In essence, endodontics as a clinical discipline is concerned with the prevention and treatment of pulpal and periapical infection. As connective tissue elsewhere in the body, the pulp and the periodontium react to infection with inflammation. Traditionally, this reaction has been studied extensively on a descriptive basis. In more recent research the infective process as such has been investigated as well as the mechanisms by which the pulp and periodontium deal with microbial insults. The results of these studies have had a major impact on our understanding of endodontie diseases and the effect of therapy, especially in nonvital teeth. The results of some of these studies will be summarized in the present paper. The pulp Pulpal inflammation
.
In the classic view of pulpal inflammation, immense importance was given to the infiuence of the anatomic environment of the pulp. Recent findings, especially regarding the hemodynamics oi pulpitis, have modified this view and greatly
Key words: bacteremia: endodontia, infection; periodontitis, apicai; puipitis Division of Endodontics, Facuity of Dentistry, University of Osio, P.O. Box 1109, N-0316 Oslo 3, Norway
contributed to our understanding of the course of the inflammatory process in the pulp (1). It is important in this regard that the pulp normally has a relatively high blood fiow which is not significantly infiuenced by vasodilator substances. Thus, only minor increases in blood flow occur during pulpal infiammation, and only locally in the inflamed area. An increase in capillary permeability, therefore, appears to be considerably more important than the increase in blood flow for the inflammatory response in the pulp. A generalized edema of the pulp during inflammation does not appear to occur in spite of the special anatomic environment, and is thought to be prevented by a localized increase in the tissue pressure in the inflamed area, by an increased lymphatic fiow, and by a net absorption into the capillaries of the uninflamed tissue adjacent to the inflamed area of the pulp (1). The cellular phase of pulpal inflammation is at first dominated by neutrophilic leukocytes; lymphocytes, macrophages and plasma cells appear later (2). The last cell types, however, dominate the histologic picture during sustained pulpal inflamma-
Endodontic research tion, giving it the character of a chronic inflammation. Immunocompetent cells are present in the pulp and both B lymphocytes and T lymphocytes are recognized in pulpal inflammation (3, 4). Mast cells are present in inflamed pulps as well (3). The immune response as such may of course inflict damage to the pulp (6). This again may result in an increased chemotactic activity and attraction of neutrophilic leukocytes. An acute inflammatory reaction may then be superimposed on the chronic inflammation. This is a rather common occurrence in inflamed pulps although in many instances an acute episode will be caused by new external irritants reaching the pulp tissue. Diagnosis of pulpal diseases
The resistance ofthe pulp to irritants and its ability to repair are considerable (7). For example, if a carious lesion is excavated and a restoration placed in the tooth, the subjacent pulpal inflammation may heal. However, in spite of this fact, and in spite ofthe fairly good understanding ofthe etiology and pathogenesis of pulpitis, diseases of the pulp are vastly underdiagnosed. Thus, during an academic year at the University of Connecticut School of Dental Medicine, 85% of the teeth that were treated endodontically had perfectly intact coronal restorations (K. LANGELAND, personal communication). In another American material comprising teeth with full crown restorations, 50% of the crowned teeth had been treated endodontically at the 2-yr follow-up examination (T. I. LEIDAL, personal communication). Similar tendencies are seen in Scandinavian follow-up studies (8, 9). Thus, there is a tremendous need for improved diagnostic methods of pulpal disease. The use of laser Doppler flowmetry is especially interesting in this regard since with this method, a vascular response (movement of blood cells in the pulpal blood vessels) rather than the nervous response given by the traditional pulp testing methods is obtained (10). Wi^th certain improvements in the hardware which are to be expected soon, this method is likely to become clinically useful. The nonvital tooth Pulp necrosis
By definition, a nonvital tooth is a tooth with a necrotic pulp. Many of the components of the necrotic pulp tissue will have a cytotoxic effect, and traditionally, such breakdown products have been regarded as the main etiologic factors for apical periodontitis (11). However, it is now established that as long as bacteria are not present in the necrotic tissue in the root canal, a periapical
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response is absent or mild, and will not lead to bone resorption and the formation of an apical granuloma (12). Infection of the root canal
The causal relationship between bacterial infection and pulpal and periapical inflammation was elegantly demonstrated in the 196O's by KAKEHASHI et al. (13). In their study it was shown that exposure of the pulp and infection from the oral cavity result in the development of pulpal necrosis and apical periodontitis in conventional rats, where germfree animals with pulp exposures fail to develop pulpal or periapical inflammation. On the contrary, in the germfree rats, formation of dentin bridges was evident at the exposure sites, suggesting a potential for hard tissue repair in the absence of infection. In humans, the relationship between infection and the development of apical periodontitis was established by SUNDQVIST (14), who found that in teeth with intact crowns and necrotic pulps, bacteria could be isolated only from teeth with apical radiolucencies. Moreover, it has been shown that bacteria which are isolated from root canals of teeth with apical periodontitis will cause an apical periodontitis when inoculated in the root canal of other teeth (15). The established infection of the root canal is heavily dominated by anaerobic bacteria (Fig. 1) (14, 16, 17). Although more than 100 different strains have been isolated from endodontic infections, usually combinations of 3-6 strains of bacteria or less are present in a root canal (14). More strains are found in teeth with large periapical lesions than in teeth with small lesions. Thus, root canal infection is characterized by a wide variety of combinations of relatively few anaerobic bacteria, and bacterial synergism appears to play a major role in maintaining the infection. Portal of entry of bacteria
The crown of the tooth is the main portal of entry for bacteria into the pulp and root canal space (18). This is readily understood in teeth with pulp exposures or carious lesions. However, apparent intact teeth usually have areas with exposed dentin, and enaniel-dentin cracks with plaque and bacteria are commonly seen (19). These cracks are almost bound to run at an angle with the dentinal tubules so that a single crack may lead to exposure of a large number of dentinal tubules (20). Another possible pathway of infection of the root canal space is the apical foramina and accessory canals through a hematogenous spreading of the bacteria. The fact that most ofthe bacteria isolated
54
Tronstad ANAEROBES BACTEROIDES FUSOBACTERIUM
EUBACTERIUM
WOLINELLA
BIFIDOBACTERIUM
SELENOMONAS
ACTINOMYCES
MITSUOKELLA VEILLONELLA
PEPTOSTREPTOCOCCUS
LACTOBACILLUS PROPIONIBACTERIUM
TREPONEMA
CZl
NEISSERIA
EIKENELLA
STREPTOCOCCUS
ACTINOMYCES
CAPNOCYTOPHAGA
STAPHYLOCOCCUS
LACTOBACILLUS
ACTINOBACILLUS
ENTEROCOCCUS
PROPIONIBACTERIUM
E. COLI
BACILLUS
ENTEROBACTER
CORYNEBACTERIUM
KLEBSIELLA SERRATIA PROTEUS PSHUDOMONAS
FACULTATIVES AND AEROBES
Fig. 1. Overview of important bacteria in endodontic infections (Diagram, courtesy of M. HAAPASALO).
from the root canal are also found in the periodontal pocket (21) has been regarded as a strong indication that hematogenous spreading to the root canal indeed occurs (22). However, exposed dentin is especially prevalent in the cervical area of the teeth adjacent to the periodontal pocket, and infection of the root canal by periodontal bacteria via a direct route through the dentinal tubules seems entirely possible (18, 23, 24). On the other hand, findings of nonoral bacteria such as Bacteroides fragilis in the root canal and apical granuloma suggest that blood-born bacteria may take part in endodontic infections (25). Infection of periapical tissues
Traditionally it has been held that the micro-organisms causing apical periodontitis are present in necrotic tissue in the root canal system and in tubules of the root dentin, whereas the periapical tissues are free of bacteria (26). The defense systems mobilized by periapical inflammation at first will eliminate the bacteria from the root canal that invade the periapical tissues. However, in longstanding infections with a more or less permanently established microfiora in the root canal, the host defenses are less effective, and microbial invasion of an apical granuloma may take place (25, 27-30) (Fig. 2). The extraradicular infections do not appear to respond to conventional root canal treatment, and
adequate systemic antibiotic treatment after identification and susceptibility tests of the infecting microorganisms, sometimes in conjunction with surgical treatment, may be necessary for repair to occur (31-34). As would be expected, the bacteria isolated from periapical tissues are many of the organisms known from studies of root canal infections (25, 27). In patients who have been subjected to inadequate treatment including inadequate antibiotic therapy and repeated openings and closings of root canals in symptomatic teeth, enteric organisms like Bacteroides fragilis, Enterobacter species, Escherichia coli, Proteus and Klebsiella species are recovered (25). In addition, environmental organisms like Pseudomonas aeruginosa are isolated (25, 27, 33), and in one study of 72 treatment-resistant teeth, this organism was recovered in 17% of the cases (25). Periapical granuloma
As the size of the apical granuloma increases, resorption of the bone (and to a lesser degree of the root end) occurs. Clearly, bacteria are the etiologic agents causing apical periodontitis, and clearly, bone resorption is an active process carried out by osteoclasts. However, the intermediate pathways linking the infection with the resorption are not fully understood at the present time. Still, there is
Endodontic research
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Fig. 2. Scanning electron tnicfographs of root surfaces of teeth with refractory apical periodontitis. A, bacterial colonies in structureless material, probably extracellular polysaccharide, outside apical foramen. B, bacterial colotiies in tissue on surface of root within apical granuloma. (From TRONSTAD L, BARNETT F, CERVONE F. Periapical bacterial plaque in teeth refractory to endodontic treatment. Endod Detit Tratttnatol 1990; 6: 73-7).
mounting evidence for the importance of various mediators derived from immune cells, termed cytokines, in the resorption process (35). These include macrophage-derived interleukin-Ia and ip (36) and tumor necrosis factor (37), and the lymphocyte product lymphotoxin (37). Of these interleukin-ip is by far the most active, and in in vitro experiments has been shown to be 15-fold more potent than interleukin-Ia, and 1000-fold more potent than lymphotoxin and tumor necrosis factor (35). The macrophages become activated to produce the cytokines by phagocytosis of bacteria during invasion of tissues, or by stimulation with bacterial components like lipopolysaccharide (35). The finding that these mediators exert similar effects in vivo and in vitro demonstrates their potential importance in the pathogenesis of apical periodontitis (35). The dominating infiammatory cells in established apical periodontitis are macrophages followed by T and B lymphocytes, plasma cells, and neutrophilic leukocytes (38). These cells can poten-
tially mediate the entire spectrum of immunologic phenomena. Of the lymphocytes, T-cells are more numerous than B-cells (39, 40), indicating an ongoing specific antibacterial reaction. T-helper and Tsuppressor cells are present in approximately equal numbers in chronic lesions (41). However, in actively developing lesions, T-helper cells outnumber the T-suppressor cells, whereas T-suppressor cells predominate when the lesion size stabilizes (41). This suggests that T-helper cells play a key role in the development of apical periodontitis whereas T-suppressor cells may dampen excessive immune reactivity, leading to cessation of lesion growth (35). Bacteremia after endodontic treatment
Invasive procedures of oral tissues may result in the translocation and release of microorganisms from the oral cavity into the bloodstream. Generally, the microorganisms are eliminated by the reticuloendothelial system within minutes, but bac-
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Tronstad
teremia is a potential hazard to certain patient groups, for instance patients with abnormal heart valves or other cardiac abnormalities predisposing them to infective endocarditis. In a recent study the incidence of bacteremia following endodontic treatment was found to be 20% compared to 70% after dental scaling and 100% after dental extractions (42). Thus, it appears that in risk patients, endodontic treatment presents a much safer treatment approach than extraction of the tooth. Treatment of apical periodontitis Antibacterial treatment
Given the importance of bacteria for the pathogenesis of apical periodontitis, it is clear that treatment success depends on their reduction and elimination. In a series of experiments BYSTROM & SUNDQVIST (43-45) and BYSTROM et al. (46, 47) have studied the effect of instrumentation, irrigation and interappointment antibacterial treatment on the root canal fiora. They conclude that predictable elimination of cultivable bacteria may be obtained only after chemomechanieal instrumentation and filling of the root canal with calcium hydroxide for 4 wk. In a later study it was shown that the use of calcium hydroxide in the root canal for 1 wk gives similar good results (48). This is in agreement with a vast body of clinical experience (18). However, from clinical experience it is also known that in some instances a long term use of calcium hydroxide, that is, for weeks and months, may be necessary to obtain a bacteria-free root canal system and periapical healing (18).
drug. Excessive or premature peaking is avoided and side effects may be reduced. An antiseptic in a controlled release delivery system that maintained its antibacterial effect for longer than 45 days in the root canal has been developed (Fig. 3) (49, 51). It is likely that such preparations may find important applications in the future (52). The idea with controlled release of therapeutic agents has also been adopted for permanent root filling materials, and especially calcium hydroxide is being incorporated in more and more commercially available products. However, in a material that is meant to give a permanent bacteria-tight seal of the root canal, even a controlled release of a component will lead to some impairment of the physical properties ofthe filling and conceivably with time cause an inferior seal of the canal (52). Instrumentation of the root canal
It has become increasingly clear that a thorough and complete chemomechanieal instrumentation of the root canal of nonvital teeth in the first visit is of the utmost importance for the course and outcome ofthe treatment (18). This will almost completely prevent interappointment complications like pain and swelling (53, 54), and together with a proper intraeanal medicament (calcium hydroxide), will ensure an asymptomatic and, with great probability, bacteria-free tooth that can be obturated in the second visit (18, 55). The standardized technique which entails the preparation of a cylindrical apical box with removal of significant
Controlled release of medicaments
The traditional endodontic antiseptics tested in the above experiments proved to be less reliable than calcium hydroxide in obtaining a bacteria-free tooth (46). Conceivably this is due to the fact that a conventional antiseptic loses its antibacterial effect after a few hours in contact with tissue and tissue fluids in the root canal (49). With calcium hydroxide on the other hand, there is a continuous and controlled release of hydroxyl and calcium ions for a long period of titne, ensuring a therapeutic effect that lasts for weeks and months (50). In medicine, controlled release delivery systems of therapeutic agents have become increasingly common. Representative medicaments may be antihistamine, antiseptics, antiinfiammatory agents, or any systemic medication that can be administered orally, rectally, transmucosally or transdermally (49). The purpose of the controlled release systems is to deliver medication over a long period of time and to maintain a reasonably constant concentration of the
Eig. 3. Antiseptic in controlled-release delivery system. Dispensers were sealed in pulp chamber of instrumented, nonvital dog teeth for 6 wk and were, after retnoval, placed on a pour plate with Streptococcus species. After incubation for 24 h, zones of inhibition of bacterial growth are seen surrounding dispensers, indicating that atitiseptic is still being released after 6 wk of contact with tissue fluids in root canal. (From TRONSTAD L, YANG Z-P, TROPE M , BARNETT F, HAMMOND BF. Controlled
release of medicaments in endodontic therapy. Endod Dent Traumatol 1985; 1:
Endodontic research amounts of dentin near the tooth apex, will in contrast to the widely used step back technique (56) give a root canal where the apical third is as clean as the coronal two-thirds of the canal (57). The standardized preparation and obturation technique has provided excellent clinical and radiographic results in well documented follow-up studies (58-60). Automated devices
The renewed understanding of the importance of a thorough instrumentation of the root canal, has led to the development of a multitude of enginedriven root canal instrumentation systems (61). There were great expectations for ultrasonically energized instruments (62), and proponents of the ultrasonic technique envisioned a "synergistic system" whereby frictional heat allegedly generated by ultrasonic movement of the root canal instrument warms up the sodium hypochiorite irrigation solution. This will increase its tissue dissolving ability as well as make it a more effective bactericidal agent (63, 64). Moreover, it is envisioned that an ultrasonic bath with cavitation and acoustic streaming develop within the root canal space during instrumentation (65), resulting not only in improved cleaning of the root canal walls (66), but also in a direct ultrasonic bactericidal effect on microorganisms (67). The results of recent research, however, suggest that these expectations were somewhat optimistic. Cavitation, that is, growth and subsequent violent collapse or implosion of submicroscopic voids in the irrigation solution, does not seem to occur at the energy levels available for clinical use (68). However, ultrasonically energized root canal files have been shown to generate a streaming field, primarily consisting of rapidly moving eddies positioned along the sides of the file (68). The clinical importance of this phenomenon is not clear since during filing, due to the physical contact with the root canal wall, a datnping of the file will occur. However, even under ideal conditions, the disruptive effect of acoustic streaming on bacteria is negligible (69), and it cannot be anticipated that a root canal is bacteria-free after ultrasonic instrumentation (70). With regard to efficacy, the ultrasonic technique is inferior to most other automated instrumentation systems (71). Thus, sonically energized instruments where the vibrations are fewer and the amplitudes larger, are more effective than the ultrasonic systems (57, 71). However, the instrument that prevails in clinical use is a mechanically driven contra angle piece where the root canal instrument moves with a combined longitudinal and rotary
57
reciprocal action (18). In controlled tests, this device is found to be suitable for the instrumentation of all canal configurations (71). Clinically, the best engine-driven systems are well suited for root canal instrumentation and they are remarkably safe (71). They may be used with ease, which is especially apparent in the instrumentation of maxillary and mandibular molars where access is difficult and the root canal may be narrow and curved. The fatigue that often accompanies the debridement procedures may be dramatically reduced with the use of a good automated instrumentation system (18).
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of root canal debridement by the endosonic ultrasonic synergistic system. Oral Surg Oral Med Oral Pathol 1976; 53:
401-6.
68. AHMAD M , PITT FORD TR, CRUM LA. Ultrasonic debride-
ment of root canals: an insight into the mechanisms involved. J Endod 1987; 13: 91-3. 69. AHMAD M . Effect of ultrasonic instrumentation on Baeteroide.i mtermedius. Endod Dent Traumatol 1989; 5; 83-6. 70. BARNETT F, TROPE M , KHOJA M , TRONSTAD L . Bacteriolog-
ic status of the root canal after sonic, ultrasonic and hand instrumentation. Endod Dent Traumatol 1985; 1: 228-34. 71. TRONSTAD L, NIEMCZYK SP. Efficacy and safety tests of six automated devices for root canal instrumentation. Endod Dent Traumatol 1986; 2: 270-5.
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Tronstad L: Recent development in endodontie research. Scand J Denl Res 1992; -.'• 100: 52-9.
In essence, endodontics as a clinical disipline is concerned with the prevention and treatment of pulpal and periapical infection. In recent research the infective process has been investigated as well as the mechanisms by which the pulp and periodontium deal with microbial insults. With regard to the pulp, findings on the hemodynamics of pulpitis suggest that the inflammatory response in this tissue is much less inlluenced by the special anatomic environment of the tooth than was previously believed. Pulpal diseases are being underdiagnosed, mostly because of inadequate examination methods. Laser Doppler flowmetry which gives a vascular rather than a nervous response may gain importance in pulpal diagnostics in the future. It is established that apical periodontitis with bone resorption cannot develop in the absence of bacteria in the root canal system. Root canal infection is characterized by a wide variety of combinations of relatively few anaerobic bacteria, and bacterial synergism plays an important role in maintaining the infection. Microbial invasion of an apical granuloma may take place. Non-oral and environmental organisms like Pseudoinonas aeruginosa are frequently isolated from treatment-resistant cases. Success of endodontie treatment depends on the reduction or elimination of the infecting bacteria. This may predictably be obtained after a thorough chemo-mechanical instrumentation and disinfection of the root canal with calcium hydroxide. The standardized technique which entails the preparation of a cylindrical apieal box with removal of significant amounts of dentin near the root apex predictably gives a clean canal. This technique has provided excellent clinical and radiographic results in well documented follow-up studies.
In essence, endodontics as a clinical discipline is concerned with the prevention and treatment of pulpal and periapical infection. As connective tissue elsewhere in the body, the pulp and the periodontium react to infection with inflammation. Traditionally, this reaction has been studied extensively on a descriptive basis. In more recent research the infective process as such has been investigated as well as the mechanisms by which the pulp and periodontium deal with microbial insults. The results of these studies have had a major impact on our understanding of endodontie diseases and the effect of therapy, especially in nonvital teeth. The results of some of these studies will be summarized in the present paper. The pulp Pulpal inflammation
.
In the classic view of pulpal inflammation, immense importance was given to the infiuence of the anatomic environment of the pulp. Recent findings, especially regarding the hemodynamics oi pulpitis, have modified this view and greatly
Key words: bacteremia: endodontia, infection; periodontitis, apicai; puipitis Division of Endodontics, Facuity of Dentistry, University of Osio, P.O. Box 1109, N-0316 Oslo 3, Norway
contributed to our understanding of the course of the inflammatory process in the pulp (1). It is important in this regard that the pulp normally has a relatively high blood fiow which is not significantly infiuenced by vasodilator substances. Thus, only minor increases in blood flow occur during pulpal infiammation, and only locally in the inflamed area. An increase in capillary permeability, therefore, appears to be considerably more important than the increase in blood flow for the inflammatory response in the pulp. A generalized edema of the pulp during inflammation does not appear to occur in spite of the special anatomic environment, and is thought to be prevented by a localized increase in the tissue pressure in the inflamed area, by an increased lymphatic fiow, and by a net absorption into the capillaries of the uninflamed tissue adjacent to the inflamed area of the pulp (1). The cellular phase of pulpal inflammation is at first dominated by neutrophilic leukocytes; lymphocytes, macrophages and plasma cells appear later (2). The last cell types, however, dominate the histologic picture during sustained pulpal inflamma-
Endodontic research tion, giving it the character of a chronic inflammation. Immunocompetent cells are present in the pulp and both B lymphocytes and T lymphocytes are recognized in pulpal inflammation (3, 4). Mast cells are present in inflamed pulps as well (3). The immune response as such may of course inflict damage to the pulp (6). This again may result in an increased chemotactic activity and attraction of neutrophilic leukocytes. An acute inflammatory reaction may then be superimposed on the chronic inflammation. This is a rather common occurrence in inflamed pulps although in many instances an acute episode will be caused by new external irritants reaching the pulp tissue. Diagnosis of pulpal diseases
The resistance ofthe pulp to irritants and its ability to repair are considerable (7). For example, if a carious lesion is excavated and a restoration placed in the tooth, the subjacent pulpal inflammation may heal. However, in spite of this fact, and in spite ofthe fairly good understanding ofthe etiology and pathogenesis of pulpitis, diseases of the pulp are vastly underdiagnosed. Thus, during an academic year at the University of Connecticut School of Dental Medicine, 85% of the teeth that were treated endodontically had perfectly intact coronal restorations (K. LANGELAND, personal communication). In another American material comprising teeth with full crown restorations, 50% of the crowned teeth had been treated endodontically at the 2-yr follow-up examination (T. I. LEIDAL, personal communication). Similar tendencies are seen in Scandinavian follow-up studies (8, 9). Thus, there is a tremendous need for improved diagnostic methods of pulpal disease. The use of laser Doppler flowmetry is especially interesting in this regard since with this method, a vascular response (movement of blood cells in the pulpal blood vessels) rather than the nervous response given by the traditional pulp testing methods is obtained (10). Wi^th certain improvements in the hardware which are to be expected soon, this method is likely to become clinically useful. The nonvital tooth Pulp necrosis
By definition, a nonvital tooth is a tooth with a necrotic pulp. Many of the components of the necrotic pulp tissue will have a cytotoxic effect, and traditionally, such breakdown products have been regarded as the main etiologic factors for apical periodontitis (11). However, it is now established that as long as bacteria are not present in the necrotic tissue in the root canal, a periapical
53
response is absent or mild, and will not lead to bone resorption and the formation of an apical granuloma (12). Infection of the root canal
The causal relationship between bacterial infection and pulpal and periapical inflammation was elegantly demonstrated in the 196O's by KAKEHASHI et al. (13). In their study it was shown that exposure of the pulp and infection from the oral cavity result in the development of pulpal necrosis and apical periodontitis in conventional rats, where germfree animals with pulp exposures fail to develop pulpal or periapical inflammation. On the contrary, in the germfree rats, formation of dentin bridges was evident at the exposure sites, suggesting a potential for hard tissue repair in the absence of infection. In humans, the relationship between infection and the development of apical periodontitis was established by SUNDQVIST (14), who found that in teeth with intact crowns and necrotic pulps, bacteria could be isolated only from teeth with apical radiolucencies. Moreover, it has been shown that bacteria which are isolated from root canals of teeth with apical periodontitis will cause an apical periodontitis when inoculated in the root canal of other teeth (15). The established infection of the root canal is heavily dominated by anaerobic bacteria (Fig. 1) (14, 16, 17). Although more than 100 different strains have been isolated from endodontic infections, usually combinations of 3-6 strains of bacteria or less are present in a root canal (14). More strains are found in teeth with large periapical lesions than in teeth with small lesions. Thus, root canal infection is characterized by a wide variety of combinations of relatively few anaerobic bacteria, and bacterial synergism appears to play a major role in maintaining the infection. Portal of entry of bacteria
The crown of the tooth is the main portal of entry for bacteria into the pulp and root canal space (18). This is readily understood in teeth with pulp exposures or carious lesions. However, apparent intact teeth usually have areas with exposed dentin, and enaniel-dentin cracks with plaque and bacteria are commonly seen (19). These cracks are almost bound to run at an angle with the dentinal tubules so that a single crack may lead to exposure of a large number of dentinal tubules (20). Another possible pathway of infection of the root canal space is the apical foramina and accessory canals through a hematogenous spreading of the bacteria. The fact that most ofthe bacteria isolated
54
Tronstad ANAEROBES BACTEROIDES FUSOBACTERIUM
EUBACTERIUM
WOLINELLA
BIFIDOBACTERIUM
SELENOMONAS
ACTINOMYCES
MITSUOKELLA VEILLONELLA
PEPTOSTREPTOCOCCUS
LACTOBACILLUS PROPIONIBACTERIUM
TREPONEMA
CZl
NEISSERIA
EIKENELLA
STREPTOCOCCUS
ACTINOMYCES
CAPNOCYTOPHAGA
STAPHYLOCOCCUS
LACTOBACILLUS
ACTINOBACILLUS
ENTEROCOCCUS
PROPIONIBACTERIUM
E. COLI
BACILLUS
ENTEROBACTER
CORYNEBACTERIUM
KLEBSIELLA SERRATIA PROTEUS PSHUDOMONAS
FACULTATIVES AND AEROBES
Fig. 1. Overview of important bacteria in endodontic infections (Diagram, courtesy of M. HAAPASALO).
from the root canal are also found in the periodontal pocket (21) has been regarded as a strong indication that hematogenous spreading to the root canal indeed occurs (22). However, exposed dentin is especially prevalent in the cervical area of the teeth adjacent to the periodontal pocket, and infection of the root canal by periodontal bacteria via a direct route through the dentinal tubules seems entirely possible (18, 23, 24). On the other hand, findings of nonoral bacteria such as Bacteroides fragilis in the root canal and apical granuloma suggest that blood-born bacteria may take part in endodontic infections (25). Infection of periapical tissues
Traditionally it has been held that the micro-organisms causing apical periodontitis are present in necrotic tissue in the root canal system and in tubules of the root dentin, whereas the periapical tissues are free of bacteria (26). The defense systems mobilized by periapical inflammation at first will eliminate the bacteria from the root canal that invade the periapical tissues. However, in longstanding infections with a more or less permanently established microfiora in the root canal, the host defenses are less effective, and microbial invasion of an apical granuloma may take place (25, 27-30) (Fig. 2). The extraradicular infections do not appear to respond to conventional root canal treatment, and
adequate systemic antibiotic treatment after identification and susceptibility tests of the infecting microorganisms, sometimes in conjunction with surgical treatment, may be necessary for repair to occur (31-34). As would be expected, the bacteria isolated from periapical tissues are many of the organisms known from studies of root canal infections (25, 27). In patients who have been subjected to inadequate treatment including inadequate antibiotic therapy and repeated openings and closings of root canals in symptomatic teeth, enteric organisms like Bacteroides fragilis, Enterobacter species, Escherichia coli, Proteus and Klebsiella species are recovered (25). In addition, environmental organisms like Pseudomonas aeruginosa are isolated (25, 27, 33), and in one study of 72 treatment-resistant teeth, this organism was recovered in 17% of the cases (25). Periapical granuloma
As the size of the apical granuloma increases, resorption of the bone (and to a lesser degree of the root end) occurs. Clearly, bacteria are the etiologic agents causing apical periodontitis, and clearly, bone resorption is an active process carried out by osteoclasts. However, the intermediate pathways linking the infection with the resorption are not fully understood at the present time. Still, there is
Endodontic research
55
Fig. 2. Scanning electron tnicfographs of root surfaces of teeth with refractory apical periodontitis. A, bacterial colonies in structureless material, probably extracellular polysaccharide, outside apical foramen. B, bacterial colotiies in tissue on surface of root within apical granuloma. (From TRONSTAD L, BARNETT F, CERVONE F. Periapical bacterial plaque in teeth refractory to endodontic treatment. Endod Detit Tratttnatol 1990; 6: 73-7).
mounting evidence for the importance of various mediators derived from immune cells, termed cytokines, in the resorption process (35). These include macrophage-derived interleukin-Ia and ip (36) and tumor necrosis factor (37), and the lymphocyte product lymphotoxin (37). Of these interleukin-ip is by far the most active, and in in vitro experiments has been shown to be 15-fold more potent than interleukin-Ia, and 1000-fold more potent than lymphotoxin and tumor necrosis factor (35). The macrophages become activated to produce the cytokines by phagocytosis of bacteria during invasion of tissues, or by stimulation with bacterial components like lipopolysaccharide (35). The finding that these mediators exert similar effects in vivo and in vitro demonstrates their potential importance in the pathogenesis of apical periodontitis (35). The dominating infiammatory cells in established apical periodontitis are macrophages followed by T and B lymphocytes, plasma cells, and neutrophilic leukocytes (38). These cells can poten-
tially mediate the entire spectrum of immunologic phenomena. Of the lymphocytes, T-cells are more numerous than B-cells (39, 40), indicating an ongoing specific antibacterial reaction. T-helper and Tsuppressor cells are present in approximately equal numbers in chronic lesions (41). However, in actively developing lesions, T-helper cells outnumber the T-suppressor cells, whereas T-suppressor cells predominate when the lesion size stabilizes (41). This suggests that T-helper cells play a key role in the development of apical periodontitis whereas T-suppressor cells may dampen excessive immune reactivity, leading to cessation of lesion growth (35). Bacteremia after endodontic treatment
Invasive procedures of oral tissues may result in the translocation and release of microorganisms from the oral cavity into the bloodstream. Generally, the microorganisms are eliminated by the reticuloendothelial system within minutes, but bac-
56
Tronstad
teremia is a potential hazard to certain patient groups, for instance patients with abnormal heart valves or other cardiac abnormalities predisposing them to infective endocarditis. In a recent study the incidence of bacteremia following endodontic treatment was found to be 20% compared to 70% after dental scaling and 100% after dental extractions (42). Thus, it appears that in risk patients, endodontic treatment presents a much safer treatment approach than extraction of the tooth. Treatment of apical periodontitis Antibacterial treatment
Given the importance of bacteria for the pathogenesis of apical periodontitis, it is clear that treatment success depends on their reduction and elimination. In a series of experiments BYSTROM & SUNDQVIST (43-45) and BYSTROM et al. (46, 47) have studied the effect of instrumentation, irrigation and interappointment antibacterial treatment on the root canal fiora. They conclude that predictable elimination of cultivable bacteria may be obtained only after chemomechanieal instrumentation and filling of the root canal with calcium hydroxide for 4 wk. In a later study it was shown that the use of calcium hydroxide in the root canal for 1 wk gives similar good results (48). This is in agreement with a vast body of clinical experience (18). However, from clinical experience it is also known that in some instances a long term use of calcium hydroxide, that is, for weeks and months, may be necessary to obtain a bacteria-free root canal system and periapical healing (18).
drug. Excessive or premature peaking is avoided and side effects may be reduced. An antiseptic in a controlled release delivery system that maintained its antibacterial effect for longer than 45 days in the root canal has been developed (Fig. 3) (49, 51). It is likely that such preparations may find important applications in the future (52). The idea with controlled release of therapeutic agents has also been adopted for permanent root filling materials, and especially calcium hydroxide is being incorporated in more and more commercially available products. However, in a material that is meant to give a permanent bacteria-tight seal of the root canal, even a controlled release of a component will lead to some impairment of the physical properties ofthe filling and conceivably with time cause an inferior seal of the canal (52). Instrumentation of the root canal
It has become increasingly clear that a thorough and complete chemomechanieal instrumentation of the root canal of nonvital teeth in the first visit is of the utmost importance for the course and outcome ofthe treatment (18). This will almost completely prevent interappointment complications like pain and swelling (53, 54), and together with a proper intraeanal medicament (calcium hydroxide), will ensure an asymptomatic and, with great probability, bacteria-free tooth that can be obturated in the second visit (18, 55). The standardized technique which entails the preparation of a cylindrical apical box with removal of significant
Controlled release of medicaments
The traditional endodontic antiseptics tested in the above experiments proved to be less reliable than calcium hydroxide in obtaining a bacteria-free tooth (46). Conceivably this is due to the fact that a conventional antiseptic loses its antibacterial effect after a few hours in contact with tissue and tissue fluids in the root canal (49). With calcium hydroxide on the other hand, there is a continuous and controlled release of hydroxyl and calcium ions for a long period of titne, ensuring a therapeutic effect that lasts for weeks and months (50). In medicine, controlled release delivery systems of therapeutic agents have become increasingly common. Representative medicaments may be antihistamine, antiseptics, antiinfiammatory agents, or any systemic medication that can be administered orally, rectally, transmucosally or transdermally (49). The purpose of the controlled release systems is to deliver medication over a long period of time and to maintain a reasonably constant concentration of the
Eig. 3. Antiseptic in controlled-release delivery system. Dispensers were sealed in pulp chamber of instrumented, nonvital dog teeth for 6 wk and were, after retnoval, placed on a pour plate with Streptococcus species. After incubation for 24 h, zones of inhibition of bacterial growth are seen surrounding dispensers, indicating that atitiseptic is still being released after 6 wk of contact with tissue fluids in root canal. (From TRONSTAD L, YANG Z-P, TROPE M , BARNETT F, HAMMOND BF. Controlled
release of medicaments in endodontic therapy. Endod Dent Traumatol 1985; 1:
Endodontic research amounts of dentin near the tooth apex, will in contrast to the widely used step back technique (56) give a root canal where the apical third is as clean as the coronal two-thirds of the canal (57). The standardized preparation and obturation technique has provided excellent clinical and radiographic results in well documented follow-up studies (58-60). Automated devices
The renewed understanding of the importance of a thorough instrumentation of the root canal, has led to the development of a multitude of enginedriven root canal instrumentation systems (61). There were great expectations for ultrasonically energized instruments (62), and proponents of the ultrasonic technique envisioned a "synergistic system" whereby frictional heat allegedly generated by ultrasonic movement of the root canal instrument warms up the sodium hypochiorite irrigation solution. This will increase its tissue dissolving ability as well as make it a more effective bactericidal agent (63, 64). Moreover, it is envisioned that an ultrasonic bath with cavitation and acoustic streaming develop within the root canal space during instrumentation (65), resulting not only in improved cleaning of the root canal walls (66), but also in a direct ultrasonic bactericidal effect on microorganisms (67). The results of recent research, however, suggest that these expectations were somewhat optimistic. Cavitation, that is, growth and subsequent violent collapse or implosion of submicroscopic voids in the irrigation solution, does not seem to occur at the energy levels available for clinical use (68). However, ultrasonically energized root canal files have been shown to generate a streaming field, primarily consisting of rapidly moving eddies positioned along the sides of the file (68). The clinical importance of this phenomenon is not clear since during filing, due to the physical contact with the root canal wall, a datnping of the file will occur. However, even under ideal conditions, the disruptive effect of acoustic streaming on bacteria is negligible (69), and it cannot be anticipated that a root canal is bacteria-free after ultrasonic instrumentation (70). With regard to efficacy, the ultrasonic technique is inferior to most other automated instrumentation systems (71). Thus, sonically energized instruments where the vibrations are fewer and the amplitudes larger, are more effective than the ultrasonic systems (57, 71). However, the instrument that prevails in clinical use is a mechanically driven contra angle piece where the root canal instrument moves with a combined longitudinal and rotary
57
reciprocal action (18). In controlled tests, this device is found to be suitable for the instrumentation of all canal configurations (71). Clinically, the best engine-driven systems are well suited for root canal instrumentation and they are remarkably safe (71). They may be used with ease, which is especially apparent in the instrumentation of maxillary and mandibular molars where access is difficult and the root canal may be narrow and curved. The fatigue that often accompanies the debridement procedures may be dramatically reduced with the use of a good automated instrumentation system (18).
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following endodontic treatment. J Etidod 1989; 15; 214. 54. TROPE M . Relationship of intraeanal medicaments to endodontic flare-ups. Ettdod Dent Tratttnatol 1990; 6; 226-9. ' 55. ORSTAVIK D , KEREKES K , MOLVEN O. Effects of extensive
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56. McCoMB D, SMITH DC, BEAGRIE GS. The results of in
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JM. Synergistic interactions between interleukin 1, tumor necrosis factor, and lymphotoxin in botie resorption. / fmtnwwl 1987; 138; 1464-8.
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characterization of mononuclear cells in human dental periapical inflammatory lesions using monoclonal antibodies. Oral Surg Oral Med Oral Pathol 1984; 58; 160-5.
ence with the use of dentine chips in pulpectomies. Int J Endod 1982; 15; 161-7. periodontitis after endodontic treatment using three different root canal sealers. Etidod Dent Trautnatol 1988; 4: 114-7. ] 61. TRONSTAD L. Maskindrevne instrumenter til preparering av' rotkanaler. In; HJORTING-HANSEN E , ed. Odontologi '91. Copenhagen; Munksgaard, 1991. :
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