bacterial association of the smear layer/ rotary endodontic courses by indian dental academy


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bacterial association of the smear layer/ rotary endodontic courses by indian dental academy

  1. 1. Bacterial Association of Smear Layer The pathological consequences of the smear layer and whether it should be present or absent under restorations are rather complicated questions. To a great extent, they seem to be related to the presence of bacteria under restoration. Brannstrom and Nyborg (1971) first reported the growth of bacteria under silicate and composite resin restorations. One important question was: Is it possible that bacteria entrapped in the smear layer survive and multiply under these restorations? Similar concern exists regarding the Endodontic smear layer. The bacteria present in infected root canals are predominantly gram-negative anaerobes. Davis et al (1972) have shown that the morphology of root canals is very complex and that mechanically prepared canals contain areas not accessible by currently used endodontic instruments. Bacteria can be found in all areas of the root canals system and in the dentinal tubules. DENTINAL TUBULES In Restorative Dentistry: Dentinal tubules originating from a cavity do not only lead to the pulp. Tubules on the side walls of the cavity may also lead outward toward the enamel or to the root cementum. These tubules are filled with fluid and viable bacteria may sometimes enter these tubules from a liquid-filled gap under a restoration. A grinding debris plug in the tubule apertures does not guarantee a permanent barrier against bacterial invasion. This plug can be removed by microorganisms. These are the contributing factors towards secondary caries. This implies that even the side wall of the cavity ought to be correctly pretreated and lined. The tubules which lead to the pulp are the ones which are the transportation channels for irritants such as zinc oxide eugenol, bacterial toxins etc. The more tubules per square millimeter leading to the pulp, the more permeable the dentin, and the greater the danger to the pulp. Garberoglio and Brannstrom (1976) examined under SEM, occlusal dentin with cross fractured dentinal tubules at various distances from the pulp (refer table 36
  2. 2. Bacterial Association of Smear Layer 2). However, the number of dentinal tubules reaching the pulp varies considerably on the floor, axial and pulpal walls of buccal/lingual/approximal cavities depending on the shape and depth of these cavities. For instance, on the floor (axial/pulpal) of a proximal cavity there may be only 2 tubules/mm2 , whereas in the cervical wall there may be 20/mm2 . The number of cross-cut dentinal tubules increases towards the inner half of the cervical wall. The floor of the cavity, on the other hand, may sometimes contain a majority of tubules which are obliquely cut or cut in a parallel direction. Since a local anaesthetic is usually administered prior to cavity preparation, it is difficult to determine when cross-cut tubules are open to the pulp. Therefore, all surface should be pretreated in the same manner. Fig. 15 Axial (pulpal) wall in an approximal cavity, acid etched for removal of smear layer. tubules are cut obliquely in a parallel manner. The tubule apertures in this area number 2.000/mm2 37
  3. 3. Bacterial Association of Smear Layer Fig. 16 Cervical wall, about half the way to the outer margin in the same cavity as seen in fig. 15. cross cut tubules numbering about 20.000/ mm2 Fig. 17 Cervical wall of buccal cavity. The dentin nearest the enamel (above) has tubules running parallel to surface. Below, 1/5 mm from enamel surface, the tubules are cross cut 38
  4. 4. Bacterial Association of Smear Layer In Endodontics: In the root, dentinal tubules extend from the pulp-predentin junction to the intermediate dentin just inside the cementum-dentin junction. Dentinal tubules in the root run a relatively straight course between the pulp and the periphery in contrast to the typical S-shaped contours of the tubules in the crown. They range in size from approximately 1-3 µm in diameter. The density of dentinal tubules per square millimeter varies from 4900 to 90,000. This density increases in an apico-coronal direction and similarly in an external to internal direction from the root surface. At the cementoenamel junction, the number of dentinal tubules has been estimated to be approximately 15,000/ mm2 . BACTERIA IN THE SMEAR LAYER UNDER RESTORATIONS: Brannstrom and Nyborg in 1973 prepared facial cavities in 20 contralateral pairs of human premolars. One cavity, randomly selected after preparation, was cleaned with water spray, while the other was cleaned with an antiseptic detergent. Both the cavities were then filled with composite and allowed to set. In both the teeth, the outer part of the filling was removed and replaced with zinc oxide eugenol or Cavit cement. In this way, they prevented the growth of bacteria into the contraction gap between the resin and the cavity walls. The teeth were extracted after 3-6 weeks. They were coded and histologic evaluation was made. The histological evaluation revealed that in 17 of the water-cleaned cavities, with the smear layer remaining numerous bacteria were present; in the antiseptically cleaned cavities, bacteria were absent. These results were highly significant and showed that a few bacteria entrapped in the smear layer may survive and multiply. There was also pulpal inflammation under these cavities. The fact that bacteria may multiply on cavity walls if there was no appreciable communication to the oral cavity seems to indicate that certain microorganisms get sufficient nourishment from the smear layer and dentinal fluid. This view was also supported by the results from the experiments with inlays cemented with phosphate cements without any protective lining of the 39
  5. 5. Bacterial Association of Smear Layer cavity walls (Brannstrom and Nyborg I960, 1974, 1977).They used inlays made of lead because it was soft and more easily adapted to the margins of the cavity. In this way, they got a good seal and minimal communication to the oral cavity. In the 59 inlays they had cemented in antiseptically cleaned cavities, almost all the teeth demonstrated no bacteria on cavity walls and no inflammation in the corresponding pulp, not even when there was a pulpal exposure. On the other hand, when the cavities had been cleaned only with water before cementation, a high frequency of inflammation was found in 22 of 25 teeth and in 10 teeth the inflammation was moderate to severe. There were also indications that in these teeth, bacteria were present. Fig. 18 Smear layer with a few microorganisms These considerations favor the opinion that most of the smear layer should be removed and any smear layer remaining for instance at the tubule apertures, should be antiseptically treated before the application of a lining or luting cement. The presence of a smear layer may also affect the retention of a lining or luting cement. Their retention was obtained mainly by mechanical interlocking in the micro undercuts present in the dentin (Oilo, 1978). It is possible that the presence of a superficial smear layer will weaken mechanical retention between the lining and the surface of the cut dentin. 40
  6. 6. Bacterial Association of Smear Layer It has been suggested that bacteria are not present in freshly prepared smear layers (Mjor, 1974). This suggestion was based on stained sections of freshly cut intact teeth It seems clear that histologic techniques cannot reveal a few bacteria entrapped within a smear layer They must multiply for sometime, form a thicker layer, replace the smear layer, and become attached to the cut dentin if we are to find them with certainity on the stained sections, because, during the demineralization of freshly cut and unprotected dentin in preparation for cutting sections, not only enamel, but also the smear layer disappears At the same time, microbes entrapped within the smear layer disappear as well. It is true that a smear layer without bacteria can be produced when intact teeth are cut experimentally. On the other hand, in normal clinical procedures, especially when operating on carious teeth, usually with low-speed or hand instruments in the final preparation, we must consider the great risk of bacteria surviving in the smear layer. Bacteria may even be left in the narrow gap between the enamel and dentin at the lateral walls as well in single tubules in mineralized dentin underneath. There was no evidence that common permanent restorative materials are sufficiently antibacterial to kill bacteria entrapped within the smear layer, especially when a fluid filled contraction gap 5-20 µm wide, separates the restoration from the smear layer. It has been found that bacteria may also enter from the tooth surface into the fluid-filled contraction gap around composite restorations. Bergenholtz & others (1982) found that microbial invasion occurred frequently around amalgam restorations. Thus all cavity walls should not only be cleaned and antiseptically treated but also protected with a thin lining. This lining, applied to all cavity walls, should not be placed over a superficial smear layer, as a thin lining may be insufficiently antibacterial (Brannstrom, 1982, 1984; Brannstrom, Nordenvall &Glantz, 1983). Moreover, for adequate retention of the lining to the cut enamel and dentin, a superficial smear layer must not be present. However, Jodaikin et al (1986) showed that more pulpal inflammation was seen beneath amalgam 41
  7. 7. Bacterial Association of Smear Layer restorations wherein smear layer had been removed prior to placement of the restoration. Fig. 19 & Fig. 20 LINER ON THE SURFACE WITH AND WITHOUT SMEAR LAYER Smear layer left – Bacteria enclosed in smear: Antibacterial effects from liner or filling may not reach bacteria enclosed deep in smear in which they may multiply. Smear layer removed – A few bacteria contaminating the surface. Antibacterial effects from liner may eliminate bacteria still present or contaminating after cleaning. 42
  8. 8. Bacterial Association of Smear Layer Bases of zinc oxide and eugenol and calcium hydroxide may have good antiseptic effects but, unfortunately, under permanent restorations these bases cannot be placed on all cavity walls. Also, bases of calcium hydroxide, such as Dycal, may disappear when leakage occurs, leaving a fluid space for bacteria to enter. Bases of fast setting calcium hydroxide may attach poorly to the cut surface and there was the risk that a fluid filled gap may develop on both sides of the lining. Pure calcium hydroxide is an excellent antibacterial temporary dressing and should be applied under temporary fillings. This has been confirmed in many studies of pulp capping. It is also possible-but not proved-that calcium hydroxide may reinforce the remaining smear plugs in the outer apertures of the dentinal tubules. To summarize, the cut dentin surface with its smear layer should be regarded as an infected wound. Non-irritating antibacterial detergents should remove the main part of the smear layer thereby reducing or eliminating the infectious material at the cut surface. The reduced dentin permeability created by the smear layer should then be retained by the residual smear plugs in the dentinal tubule apertures. SMEAR LAYER ON DENTIN EXPOSED TO THE ORAL CAVITY: Another question concerns what may happen to the smear layer on surfaces exposed to the oral cavity and left unrestored, for example in root planing after superficial grinding, or under poorly fitting temporary crowns. It was found that when a smear layer is produced experimentally on the human dentin and left exposed it disappears after a couple of days and was replaced by bacteria and after a week almost all the tubules are opened and some even widened (Brannstrom, 1982). There may be 10,000-20,000 tubules per square millimeter exposed on a superficial hypersensitive exposure. The consequence is the invasion of bacteria. Dentinal smear layers are very acid labile, and it is possible that acids present in the diet may have caused dissolution of the smear layer and invasion of bacteria. Cariogenic plaque may also cause dissolution of the smear layer. In single tubules, bacteria can be found to have penetrated rather deeply (Olgart et al, 1974). Vojinovic et al (1973) reported that dentinal smear layer beneath restorations significantly prevented bacterial penetration into dentinal tubules by occluding the 43
  9. 9. Bacterial Association of Smear Layer superficial portion of the tubule. Bacteria may also plug the tubular apertures. However after 2 weeks, occasionally a mineralized pellicle was seen blocking the aperture of the tubules (Brannstrom, 1982). FATE OF SMEAR LAYER UNDER RESTORATIONS: We cannot expect a mineralized pellicle to develop under a restoration where saliva does not circulate. However, we know that the outward flow of fluid in dentinal tubules and around the fillings may be reduced with time. The pulpal ends of the tubules may be partly blocked by irregular dentin. As reported by Pashley (1984), accumulation of solids in tubules and at their outer apertures may contribute to a reduced flow of fluid. Under favorable conditions, a mineralized pellicle may develop at the outer aperture of the contraction gap. The same has been observed in the aperture of tubules of cut dentin left unprotected. Little research is available to indicate what happens to the smear layer left under a restoration. The smear layer may be detached and follow the outward flow of fluid in the contraction gap. In a vital tooth, this flow is directed outward due to the pressure gradient - a higher pressure of fluid in the pulp. The size of the gap around the restoration may vary from 5-20 µm. Johnson & Brannstrom (1971) noticed that parts of the smear layer had been removed from the floor of a cavity containing a poorly fitting temporary restoration of gutta percha for 3 days. Certain bacteria may remove atleast parts of the smear layer. Histologic sections reveal that the bacterial layer is closely oriented to the surface of cut dentin; the bacteria have, in other words, occupied the smear layer. Before sectioning of a tooth in the laboratory, a composite or amalgam restoration is removed. Under the scanning electron microscope, we can see the bacterial layer attached also to the inner surface of the restoration. Sometimes, the whole bacterial layer is detached from the cavity and no bacteria are seen in the dentinal tubules because of the presence of smear plugs in the tubular apertures. This is one reason why we may not always find a correlation between pulpal inflammation and the presence of bacteria on the cavity walls. Inflammation may be present in the pulp, but a bacterial layer may not appear on 44
  10. 10. Bacterial Association of Smear Layer the actual sections because it has been detached. Another reason for this failure is that usually the sections examined in the microscope cover only a small part of the total area of cavity walls. Bacteria might multiply on a lateral wall and the concentration of toxins may increase in the fluid filled gap, but in the area sectioned, or microbiologically sampled, the bacteria may not be attached to the dentin. Conversely, bacteria may be present on the sections but no inflammation seen in the corresponding pulp because of the presence of atubular, irregular dentin blocking the pulpal ends of the tubules. This "reparative" dentin may develop after two weeks in monkeys and dogs, animals often used in experimental studies. In humans, usually, 2-3 months are needed for developing this barrier. This fact makes it difficult to interpret results from such animal experiments and correlate them with the clinical situation in humans (Brannstrom 1982). PRESENCE OF BACTERIA IN ENDODONTIC SMEAR LAYER: It is generally accepted that one of the main causes of periapical disease is bacterial infection of the root canal system (Yawata, 1973; Bystrom, 1987). Thus eradication of bacteria form the root canal system is important for a successful outcome. The bacteria that are most frequently found inside the root canals of infected teeth are: Obligate anaerobes: • Fusobacterium nucleatum • Porphyromonas gingivalis • Prevotella melaninogenica • Actinomyces odontolyticus Facultative anaerobes: • Enterococcus faecalis • Escherechia coli • Pseudomonas aeruginosa • Streptococcus mitis 45
  11. 11. Bacterial Association of Smear Layer • Streptococcus mutans • Streptococcus sanguis • Streptococcus salivarius Microaerophiles: • Actinobacillus actinomycetemcomitans These bacteria may also be incorporated in smear layers during preparation or enlarging of root canals with files and burs because it consists mainly of debris of dentin and pulp tissue (McComb et al, 1975; Norman et al, 1980; Mader et al, 1984; Garberoglio & Becce, 1994; Sen et al, 1995). Baker et al (1975) and Yamada et al (1983) observed that bacteria could remain in the smear layer and in the dentinal tubules despite instrumentation of the root canal and thus they may survive and multiply (Brannstrom and Nyborg, 1973). Fig. 21 ROOT CANAL SURFACE WITH AND WITHOUT SMEAR LAYER Persistence of this smear layer with viable bacteria surviving in it may result in bacterial penetration into the dentinal tubules of the root canal which in turn depends upon several factors that act by increasing or decreasing the depth of penetration. Michelich et al (1980) and Diamond & Carell (1984) stated that bacteria could not penetrate into dentin in the presence of smear layer. It has been 46
  12. 12. Bacterial Association of Smear Layer shown that removal of smear layer facilitated passive penetration of bacteria (Olgart et al, 1974; Michelich et al, 1980; Haapasalo & Orstavik, 1987; Safavi et al, 1989; Orstavik & Haapasalo, 1990). This layer though is not a strict barrier to bacteria. 1. Type of microorganism: The existence of bacteria in the dentinal tubules can cause a possible pathology to the pulp and/or periapex. It is therefore of extreme importance to eliminate these microorganisms during the accomplishment of the endodontic treatment. It has been demonstrated in studies that bacteria are able to colonize and survive inside the dentinal tubules of root canals and sometimes does not obtain it elimination with instrumentation. Studies have been done with different microorganisms under different circumstances to determine the degree of depth of bacterial invasion inside the tubules. The extent of bacterial invasion is dependant on the type of bacterial species and on time (Akpata & Blechman, 1982; Meryon & Brook, 1990; Orstavik & Haapasalo, 1990). Type of bacteria: Williams & Goldman (1985) showed that smear layer delayed the penetration of Proteus vulgaris, but was not a complete barrier to these bacteria. Meryon et al (1986) also found that Pseudomonas aeruginosa penetrated even thicker dentin slices, by removing the smear layer itself and by opening the orifices of dentinal tubules after possible collagenase production. Meryon & Brook (1990) observed that Actinomyces viscosus, Corynebacterium species and Streptococcus sanguis digested the smear layer and facilitated their penetration. After degradation of the smear layer by proteolytic enzymes released by certain bacteria (Uitto, 1988) a gap will develop between the filling material and the canal wall, permitting the leakage of other bacterial species and their byproducts along the canal walls into dentinal tubules and the periradicular tissues. Depth of penetration: Armitage et al (1983), Ando & Hoshino (1990) have reported the presence of bacteria in the dentinal tubules of infected teeth at 47
  13. 13. Bacterial Association of Smear Layer approximately half the distance between the root canal walls and the cementodentinal junction. Sen et al (1995) reported bacterial penetration into the tubules upto 150 µm in the apical 2/3rd of the roots of teeth with necrotic pulps. Horiba et al (1990) found endotoxin within dentinal walls of infected root canals. Siqueira et al (1996) removed the smear layer and inoculated with 5 species of bacteria and showed that all the test bacteria were able to penetrate into dentinal tubules to varying depths. Perez et al (1993) found a mean penetration depth of 479 µm for Streptococcus sanguis after 28 days of incubation, with maximum penetration of 737 µm. Peters et al (2001) reported the presence of bacteria in more than half their samples (teeth with periapical lesions) close to the cementum. Drake et al (1994) showed that removal of smear layer opened the tubules, allowing bacteria to colonize in the tubules to a much higher degree (10-fold) compared with roots with an intact smear layer. This indicated that smear layer may inhibit bacterial colonization of root canals. Love et al (1996) showed that Streptococcus gordoniii penetrated all non-smeared samples while 9 out of 10 smeared samples showed no bacterial penetration. This suggests that dentinal smear layer is an effective barrier to dentinal tubule invasion by S. gordonii. Thus factors such as the number and type of bacteria in addition to the length of exposure and the presence or absence of smear layer, could influence the depth of penetration of bacteria into the dentinal tubules. Adherence of bacteria: Love (1996) investigated the adherence of S.gordonii to smeared and non-smeared dentin and assessed the influence of patent dentinal tubules on bacterial retention. He found that smear layers do not impede bacterial adherence to dentin matrix and that surfaces with patent dentinal tubules retain more bacteria than a smeared surface. Bilge Hakan Sen et al (2001) demonstrated that the number of adherent Candida albicans cells to dentin decreased after removal of the smear layer. This may be because C. albicans retains poorly to clean dentinal surfaces and always requires a pellicle of proteins. Here the smear layer acted as the pellicle of proteins. Yang & Bae et al evaluated the effect of presence or absence of smear layer on the adhesion of Prevotella nigrescens (a black-pigmented gram negative anaerobic bacteria considered to be 48
  14. 14. Bacterial Association of Smear Layer the most virulent bacterial strains of the root canal system) to the dentinal walls and concluded that removal of smear layer inhibited bacterial adherence. They applied the same methodology as this study except that they used a different bacterial strain, Staphylococcus aureus and showed the opposite result. Teeth with smear layer contained significantly fewer bacteria than those in which the smear layer has been removed. They cncluded that different results have been obtained due to different growth rates, physiological characteristics and motility status of the test organisms. 2. Vitality of the teeth: Although some authors defended that the bacterial invasion is greater in vital teeth than in non-vital ones by the contribution of nutrients, it has been demonstrated that the depth, extension of invasion and bacterial proliferation were greater in non-vital teeth, since odontoblastic processes act like defensive barrier in vital teeth. 3. Age of the teeth: In mature teeth, the depth of invasion is smaller since the number and diameter of tubules diminish with age. 4. Dentinal permeability: According to Pashley & colleagues, a greater bacterial invasion exists with a higher permeability. For example, in a non-vital tooth, where the diameter of the tubules remains constant and does not diminish, maintaining the permeability, the invasion is much greater. 49