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The cause of postrestorative sensitivity and its prevention
0099-2399/86/1210-0475/$02 00/0 JOURNALOF ENDODONTICS COpyright 9 1986 by The American AssocJatK:)nof ErEkxIontlsts
Printed In U.S A
VOL 12, NO 10, OCTOBER1986
The Cause of Postrestorative Sensitivity and Its Prevention Martin Brannstrbm, DDS,
Dr, Odont.
As far as restorations are concerned, infection beneath the filling material itself is the greatest threat to the pulp. Thus, the main biological problem we face in restorative dentistry concems the favorable environment for microbial growth under restorations. Bacterial activity may result in increased pulp sensitivity, pulpal inflammation, and secondary caries. We need more biological testing of materials that is not complicated by the presence of bacteria in the space between the filling material and the walls of the cavity.
(d) ZOE does not provide a hermetic seal. Thus, we may have some drainage of fluid outward and this drainage may have a beneficial effect if the pulp is inflamed. When a permanent filling is replaced with ZOE because of postrestorative sensitivity due to pulpitis, the sensitivity may disappear because the bacteriafilled contraction gap is eliminated, drainage is established, and nerve excitability has been reduced. Fifteen years ago we first reported finding bacteria under fillings, and this observation has been confirmed by numerous studies conducted by our group and others. Therefore, I am convinced that as far as restorations are concerned, infection beneath the filling material itself is the greatest threat to the pulp. Thus, the main biological problem we face in restorative dentistry concerns the favorable environment for microbial growth under restorations. Bacterial activity may result in increased pulp sensitivity, pulpal inflammation, and secondary caries. Amalgamfillings may lead to sensitivity to cold during the first 1 to 2 wk. We know from recent experiments that when infection is avoided, amalgam can be placed on the exposed pulp without causing any harm to the pulp (M. Cvek and C. Cox, personal communications). In one series of experiments (3) we produced local inflammation in the pulp under cavities cut in human teeth. Control cavities were prepared in contralateral teeth with intact pulps. Both experimental and control cavities were lined with a very thin resin film and filled with amalgam. It was found that all teeth with inflamed pulps were more sensitive to cold. Bacteria have been found under amalgam fillings, even under copper amalgam (4, 5). The presence of microbes in the fluid gap under an amalgam filling results in a situation analogous to that of the dentinal crack syndrome, i.e. increased exitability of the nerves due to inflammation evoked by bacterial products and the presence of a fluid gap which favors hypersensitivity. Contraction of the fluid within the gap occurs when cold is applied to the tooth. This causes a rapid outward movement of fluid in the tubules, thus stimulating nerve fibers in the underlying pulp. However, within a few weeks the sensitivity to cold often disappears. This is because the contraction gap may be partly occluded
Let us first discuss the way in which our filling materials may contribute to postoperative sensitivity. The first question is: are filling materials irritating to the pulp and will their toxicity cause the pulp to become sensitive? The answer is no. This is true for the materials we have tested in human experiments (1), such as amalgam, silicate, various cements and composites, and those that have been studied by Cox et al. (2)in monkeys. However, we cannot be certain about materials we have not tested or those that are not yet on the market. For the future, we need biological testing of materials that is not complicated by the presence of bacteria in the space between the filling material and the walls of the cavity. In numerous studies we have found that when bacteria are not allowed to enter this space that only zinc oxide-eugenol (ZOE) cement, even in a thick mix, evokes a slight cellular necrosis and inflammation when placed in deep cavities. In spite of the fact that it elicits a mild inflammatory reaction, ZOE is a good temporary dressing for the following reasons: (a) Soon after ZOE is inserted, free eugenol leaches out, and after a few weeks the pulp usually returns to normal. (b) ZOE does not contract, and so it does not permit bacterial growth on cavity walls. This explains why other filling materials that contract and allow fluid and bacteria to multiply within the gap between the restoration and the cavity walls are irritating to the pulp for a longer period of time than ZOE. (c) Free eugenol may diffuse to the pulp and block the transmission of impulses by sensory nerve fibers located beneath the cavity. 475
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by expansion of the amalgam and corrosion products that form within the gap. Furthermore, the slow outward flow of fluid in the dentinal tubules due to the higher fluid pressure in the pulp may lead to accumulation of plasma proteins and cell remnants in the dentinal tubules. In this way the resistance to fluid flow across dentin is increased (6). In addition, the gap may be sealed at the outer margin by the formation of a calcified pellicle, and after 2 to 3 months the formation of irregular dentin may seal the pulpal ends of the tubules. There is no evidence that "thermal shock" is a cause of damage to the pulp when it occurs under normal conditions. Dentin is an excellent thermal insulator and therefore there is no reason to place a thick base under an amalgam restoration. It is a mistake to assume that a thick base of calcium hydroxide or a cement will solve the problem of sensitivity to heat or cold. A thick base cannot be placed on the outer margin of the cervical wall or on the lateral wall of cavities. In the clinic it has been observed that such linings may not prevent sensitivity to cold even in teeth with composite resin fillings, nor can they prevent the development of secondary caries. When a fluid-filled space develops at the cervical and lateral walls, a calcium hydroxide base wilt wash out and the remaining gap will be invaded by bacteria (7, 8). A calcium hydroxide base such as Dycal or Life has several disadvantages, but the tendency to wash out is the most serious one. How can we reduce the risk of postrestorative sensitivity? First, in cavities that are to be filled with amalgam, composites, or glass ionomer cements, removal of the infected superficial smear layer is essential. Microbes entrapped within the smear layer are able to multiply and after a few weeks they can almost completely replace it. This may occur even if there is not much microleakage (9). In this context it should be stressed that invasion of microbes from the oral cavity into the gap is not the only route of infection. In addition to the smear layer, bacteria may remain in the dentinal tubules or in a fluid gap between enamel and dentin at the lateral walls (1). These bacteria, usually cariogenic, are easily left behind after cavity preparation, and they may multiply and fill a fluid space along the cavity walls (Fig. 1). Smear plugs in the tubule apertures should not be removed, as they reduce permeability and facilitate desiccation of the cavity with an air jet. Cavity walls should be disinfected, as we should treat infected dentin as we treat wounds in other tissues. Smear plugs in tubule apertures should also be reinforced with fluoride (1). A thin varnish or liner should then be applied to all cavity walls in order to block communication between dentinal tubules and the fluid gap which develops during contraction of the filling material. This gap will be in communication with the oral cavity but should not be in communication with the pulp via the dentinal tubules (1). A thin antibacterial lining should
Joumal of Endodontics
FtG 1. Scanning electron micrograph of dentin facing a gap at the DEJ some distance from a cawty. Bactena of coccal type tnvading the dentin. (From Brannstrom et al., Archives Oral Biology 22:571578, 1977.)
also be applied to the cavity walls to prevent bacteria from contaminating the dentinal surface and prevent invasion from a gap that may exist at the dentinoenamel junction (DE J) along the lateral walls of the cavity. The same treatment procedure should be utilized prior to inserting any type of filling material. In the case of composites, after the material has polymerized and contraction is nearly complete, the cervical gap should be impregnated with Enamel Bond resin (3M Co.). As seen in Fig. 2, capillary forces will cause the resin to flow into the air-filled gap. This will better preserve any lining that is used and, hopefully, eliminate postoperative sensitivity and reduce the risk of pulpal injury and development of secondary caries. This technique has been described in a recent publication (10). Concerning the risk of postrestorative sensitivity, we may have the greatest problem with cervical walls, because they cannot be etched. This is especially true for some of the newer materials such as P10, P30, Occlusin, and Command II, which are associated with little or no hygroscopic expansion (unpublished data). As seen in Fig. 2, gaps about 15 to 25 #m in width may persist at the cervical wall. From a biological point of view, this type of filling can be even more dangerous than amalgam. With the use of the same technique as demonstrated in Fig. 3, we have also observed gaps associated with glass ionomer restorations but to a lesser extent than with the above materials. Bacteria
Vol. 12, No. 10, October 1986
FIG 2. Cervical wall of proximal restoration (Enamel Bond Concise). Cavity walls had been I~nedwith the Tubulitec lining system (L). The contraction gap was impregnated from the margin with fluorescent Enamel Bond resin about 12 rain after the restoration was placed. Bar = 20 ~m. D, dentin. (From M. Brannstrom, Composite restn restorations' biological considerations with spe~al reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Restorative Materials. St. Paul, MN: 3M Co., 1985:71-81 .)
/
i~
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FtG 4. The inner surface of a composite restoration corresponding to the axial wall. Cocci as well as fdaments are present. (From M. Brannstr0m, Composite resin restorations: biological considerations with special reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Restorative Materials. St. Paul, MN: 3M Co., 1985:71-81 .)
:
FOG3. A ground section of tooth with proximal restorations photographed wtth UV light. Left, Occlusin (R1). Right, Scotchbond and P30 (R2). P, pulp. Fluorescent Enamel Bond resin apphed to the cervical margin has penetrated the contraction gap at the cervical wall and also parts of the axial wall. (From M. Brannstr0m, Composite resin restorations" btological considerations with special reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Resotrative Materials. St. Paul, MN: 3M Co., 1985: 71-81 .)
were found beneath many of these restorations (11, 12), although not as frequently as under composites. Therefore, the same pretreatment procedures should be applied when using glass ionomer cements (12). In summary, in order to reduce the risk of sensitivity and other postrestorative complications, we must provide a good marginal seal and avoid infected fluid gaps from developing between cavity walls and filling materials. When bacteria become established on cavity walls (Figs. 4 and 5) and there is fluid communication between the oral cavity and the pulp, it is not surprising that postoperative sensitivity develops.
1. FIG 5. Axial wall of buccal cavtty filled with silicate for 4 wk. A bacterial layer is seen closely attached to the cut dentin with bacteria present ~nsome tubules. (From M. Brannstrom, Composite resin restorations: biological considerations with special reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Restorative Materials. St. Paul, MN: 3M Co., 1985:71-81 .)
I would like to say a few words about cementation and failures in crown and bridge construction that lead to pulpitis and postoperative sensitivity. First, problems may develop when we fail to properly diagnose the condition of the pulp before and during crown preparation. We should be concerned about old fillings, leaky fillings, and secondary caries. Bacteria may already be present deep in the dentin, perhaps even in a local necrotic area of the pulp, There may be no symptoms because fairly good drainage of inflammatory exudate
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has been established through the thousands of tubules that open into fluid gaps and carious lesions. During the period that a crown is temporarily cemented, there will still be good drainage, so there will be no discomfort. However, when the crown is permanently cemented, the tooth may become symptomatic, probably because outward drainage has been blocked, resulting in an accumulation of noxious substances in the pulp. On the other hand, the infected pulp may gradually undergo necrosis in the absence of pain. What should we do in order to reduce the risk of pulp disease? First, we should remove all old fillings and secondary caries and treat the dentin as though we were going to insert a permanent restoration. Before administering a local anesthetic, the sensitivity of the dentin under old fillings and caries should be tested. Unless the pulp lumen is almost obliterated for unknown reasons, the dentin under old fillings and soft caries should be insensitive, indicating the presence of irregular dentin. Sensitive dentin under lesions may indicate that the pulp is not healthy, in which case the prognosis is poor. Dentin should be sensitive only in areas where it is intact. The second cause of failure is the operative procedure. Crown preparation must be performed with care and with abundant cooling. Heat will cause expansion of fluid in the dentin. The pulpal blood flow should compensate for the increase in tissue pressure, but it may fail if blood flow has been drastically reduced by the administration of a vasoconstrictor-containing local anesthetic (L. Olgart, personal ocmmunication). In addition, heat may reach the pulp and cause hemorrhage and perhaps local necrosis as well. It may be difficult for an old pulp to withstand the trauma of crown preparation. In addition, some tubules may already harbor bacteria or bacteria may arrive via the bloodstream and settle in a localized area of pulpal necrosis. By using an anesthetic solution which does not reduce blood flow, adequate cooling during grinding, and care in preparation, the risk of failure can be minimized. The third cause of failure involves the placement of a temporary crown. We found that under shallow guttapercha fillings bacteria reached the pulp within 3 wk (1). Occasionally, bacteria can be present deep in some dentinal tubules under a white spot carious lesion (1, 13). In experiments in which dentin was superficially exposed and left uncovered for 1 wk, bacteria were observed deep in the tubules (1). After a few weeks we found that in a few tubules bacteria had nearly reached the pulp. Poor placement of a temporary crown may leave cervical dentin unprotected. Thus, as many as 10,000 to 20,000 exposed tubules may become open and be invaded by microbes within 1 wk. Under the crown there may be an infected smear layer, but it may be replaced by bacteria as they proliferate. A flexible, elastic temporary cement may cause the crown to become dislodged and this opens up spaces for fluid to accumulate.
Journal of Endodontics
We may have an ill-fitting temporary crown in place for 2 to 3 wk, and during this period smear plugs in the tubule orifices disappear and bacteria enter the tubules. Perhaps you have seen how quickly dentin is softened when a crown in a large bridge has become loose. This is mainly due to bacteda invading the dentin. It is not unusual to find very sensitive dentin when a temporary crown is removed. You must not be surprised if permanent cementation that provides a good seal and blocks drainage is followed by pulpitis and toothache, as bacteria have been introduced into the dentin. In order to avoid these problems the following precautions should be observed: (a) Shorten the period that the temporary crown is in place to a few days. (b) Before temporary cementation, clean the dentin and remove the superficial smear layer with an antibacterial detergent. Then desiccate the dentin meticulously and apply a thin lining in the same way as you would for a permanent filling. Before permanent cementation, check the occlusion, as cuspal interference may possibly contribute to hypersensitivity. Remove the liner using a rubber cup in a slow-speed handpiece, then apply a cleanser mixed with pumice. After rinsing, desiccate the crown preparation for at least 10 s with the air stream directed from various positions parallel with the dentin. This will produce pain, but it is an important step before applying the cement to the dentin and the inside of the crown with a brush. If dentin is not properly desiccated, dentinal fluid may seep out onto the surface prior to or during setting of the cement. This will prevent good contact between the cement and dentin, thus preventing mechanical interlocking. The presence of fluid is thought to be particularly hazardous in the case of glass ionomer cements. As a result of several experiments I conducted, I have concluded that air jet desiccation does not injure the pulp and that the cements we use are not irritating, even if they are placed on an exposed pulp (1).
DENTIN EXPOSURES, DENTINAL PAIN In the clinic, fluid communication between the oral cavity and the pulp becomes obvious when dentin has been exposed. This may occur as a result of caries, abrasion, consumption of acidic foods, or because the dentist has failed to protect exposed dentin. Fluid communication may result in pain due to touch, sugar, and cold. These warning signals should be heeded. Pain of this nature is a positive reaction, as dentin hypersensitivity implies that the pulp may be in danger and it may bring the patient to the dentist in time to save the pulp. Dentinal tubules are highways along which stimuli can reach the pulp. In the clinic, it is important to realize that whenever we have exposed dentin, the underlying tubules are accessible not only to pain-producing stimuli but also to toxic products elaborated by bacteria. These products can easily diffuse inward and evoke an inflam-
Vol. 12, No. 10, October 1986
matory reaction in the pulp. This will result in sensitivity to the slightest fluid movement, because inflammation has the ability to increase the excitability of the A-fibers located along the pupal wall. In our experiments on human premolars, we exposed dentin by grinding oft the cuspal enamel. The smear plugs disappeared within a couple of days and after 1 wk all of the tubules were open and many were widened due to the removal of peritubular dentin. Many of the tubules had been invaded by bacteria and there were plugs of bacteria in their apertures (Fig. 6) (14-17). The pulps were slightly to moderately inflamed, and there was a loss of odontoblasts and usually a reduction in the width of the predentin. Two weeks following superficial exposure of cuspal dentin, we observed localized pulpal necrosis in 2 of 40 specimens. The pulp horns of these teeth were packed with neutrophilic leukocytes (14). DEFENSE MECHANISMS
Now that you are aware of the high incidence of infection associated with sensitive exposed dentin and beneath restorations, you may wonder how dentin becomes insensitive and how so many pulps have managed to survive. Thanks to the natural defenses of the tooth, the pulp is usually able to survive and the dentin can become insensitive. The term defense is used here in the broadest sense in that it refers to any active or passive change occurring in the tooth which results in the obstruction of dentinal tubules so that the enemy, i.e. bacteria and their toxic products, does not gain access to the pulp, or if it does, it is quickly eliminated.
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Together with dentinal pain providing a warning signal, pulpal inflammation is the first defense reaction we can expect. Slight to moderate inflammation is a positive reaction. However, if the inflammatory reaction is too strong, it may have a negative effect, as has been shown by Bergenholtz and co-workers (18-20). Thus, in the narrow pulp lumen severe inflammation may lead to localized necrosis. On the other hand, a weak immunological response may also have a negative effect and if pulp necrosis develops, bacteria may invade and colonize the pulp. Consequently, when dentin is exposed and left unprotected, the orifices of the dentinal tubules must be sealed as soon as possible in order to reduce the risk of pulpal infection. In our experiments dealing with exposed dentin in human teeth, we found that in some exposed cusps, even after 2 wks, the dentin was covered by a thin, granulated pellicle that had become mineralized (1). In this way the dentin can become less sensitive, and the grateful patient will be willing to keep the surface of the dentin clean. As a result, fewer toxic products will reach the pulp and the pulp will respond favorably. Inflammation will subside and the leukocytes that have accumulated along the pulpal wall will disappear. Subsequently, cells in the cell-rich zone of the pulp will, if they are still viable, divide, differentiate, and produce irregular dentin in order to block the pulpal ends of the tubules. In this way both ends of the tubules will be obstructed, and bacteria within the tubules will have less opportunity to survive. In addition, deposition of mineral salts within the tubules close to the exposed surface will gradually increase. This obstruction of tubules by calcium phosphate crystals is termed dentinal sclerosis (Fig. 7), and
J
FIG 6. Profile view of base (left) of acid-treated cavity exposed for 1 wk, photographed w~th scanning electron microscope. Microorganisms of varying form in longitudinally fractured, w~dened dentinal tubules. (From Olgart et al., Acta Odontologica Scandinavica 32:6170, 1974.)
FiG 7. Cross-fractured section through the center of the dentin located between the attnted surface and the pulpal lumen. Various degrees of closure of the tubule lumen are observed.
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it seems to develop following the formation dentin. Presumably, sclerosis develops as the ingress of mineral salts, derived from dentinal fluid, that precipitate in the tubules
Journal of Endodontics
of irregular a result of salvia and (21).
TREATMENT OF SENSITIVE EXPOSURES
There are some patients who need our help, as they experience a great deal of pain because dentin has become exposed. In such cases the natural defense mechanisms appear not to be adequate. Too dense an accumulation of inflammatory cells at the pulpal wall may interfere with the formation of irregular dentin, or the salivary "healing effect" (dentinal sclerosis) is not sufficient. Other factors that may contribute to excessive sensitivity include consumption of an excessive amount of acidic foods, mechanical removal of hard tissue due to bruxism, and frequent, energetic use of abrasive toothpastes that expose a large number of tubules each time the affected tooth is brushed. Undoubtedly, a combination of one or more of these factors plus formation of bacterial plaque on the exposed dentin will not allow the pellicle to calcify and, in addition, more tubules will be exposed. Diffusion of irritants from the plaque to the pulp will prevent the pulp from forming a complete barrier of irregular dentin. In addition, when cuspal dentin is exposed, fluid gaps may easily develop at the DEJ, and these gaps will become packed with microbes in the same way and for the same reason that I have described in the case of early enamel caries. Patients suffering from anorexia nervosa may have severe problems with hypersensitive dentin. The teeth of many patients with this disease are exposed to large amounts of acid because of repeated regurgitation of the stomach contents. These patients, usually young girls but occasionally adults with similar problems, need our help. First, we should prescribe proper dental hygiene. The patient should use only nonabrasive, fluoride-active toothpastes which have an efficient cleansing effect. Second, the patient should reduce the consumption of acidic foods and beverages, and if bruxating, a splint should be fabricated. Third, daily rinsing with 0.05% sodium fluoride solution should be strongly recommended. The above measures will often be sufficient to eliminate or greatly reduce dentinal sensitivity and this will allow the patient to better clean the tooth surfaces and remove plaque, thus reducing the risk of acid attack on the exposed dentin. In addition, we may treat sensitive occtusat exposures by impregnating the tubules and gaps at the DEJ with a resin. The rationale and technique for this treatment has been described elsewhere (1,22, 23). When tubules are open and desiccated with a blast of air that is directed parallel to the surface of the dentin and at a right angle to the long axis of the tubules, there will be a rapid outward movement of fluid
in the tubules that will evoke pain. After desiccation for 0.5 to 1 rain, the pain usually subsides. The reason for this is that when the tubules are opened, the outward flow of fluid stops some distance short of the surface. Thus, the outer part of the tubule becomes filled with air. When a resin such as Enamel Bond (3M Co.)is applied to the surface of the dentin, it will quickly flow into the tubules because of capillary attraction. With the same pretreatment procedure, i.e. by producing open, air-filled tubules via desiccation, we can treat sensitive tooth necks by impregnation with 2% sodium fluoride. We may be able to obtain just as high a fluoride concentration within the tubules with this method as with iontophoresis. A fluoride-containing resin, or even better a calcium hydroxide dressing, may then be applied to the surface for a couple of hours. The calcium hydroxide paste should be kept in place with a surgical pack. This actually combines two different techniques which have each been highly recommended. These two components, i.e. fluoride in high concentration and calcium hydroxide, both have antibacterial properties. In addition, precipitation of calcium fluoride should block the tubules. Some fluoride may be released at the surface of the dentin and promote the development of a calcified pellicle. Some will be incorporated into fluorapatite crystals. An alternative to fluoride is potassium oxalate treatment, as suggested by Pashley (see Pashley's article "Dentin Permeability, Dentin Sensitivity, and Treatment Through Dentin Tubule Occlusion" in this issue). I have tested both solutions clinically and found them to be equally efficacious. The disadvantage with the impregnation technique, using either resin or salts, is that it is painful during desiccation and may require local anesthesia. On the other hand, a 1- or 2-min application of agents such as fluoride or oxalate to moistened dentin may result in only limited diffusion of the active ingredients into the tubules. Such a treatment is not likely to produce the desired results. Since the surface layer of dentin is easily removed by attrition, the agents would have to be applied repeatedly over a considerable period of time. Any treatment is likely to be successful if the patient is cooperative and agress to use only a nonabrasive fluoride toothpaste and curtail his or her consumption of acidic foods and beverages. By blocking the tubules as soon as possible, sensitivity of the dentin to touch will be decreased and the patient can then keep the tooth surface clean. By controlling plaque formation and thus limiting the diffusion of irritants to the pulp, pulpal inflammation should gradually subside. However, the tooth may remain sensitive to cold until the pulp is no longer inflamed and can deposit a layer of irregular dentin over the pulpal ends of the tubules. Presented at the F~rst Wodd Co~ference on Dental and Pulpal Pare, New York, NY, October 25-27, 1985
Vol. 12, No. 10, October 1986 Dr Brannstrom is affiliated with the Department of Oral Pathology, Karolinska Institute, Hudd~nge, Sweden
References 1 Brannstrom M Dentin and pulp m restorative dent~sty. London: Wolfe Medical Publ~cat~ens Ltd, 1982. 2 Cox CF, Heall CL, Keall HJ, Ostro E. Biocompatib~lJty of various dental matenals against exposed monkey pulps J Prosthet Dent (in press). 3 Johnson G, Brannstrom M. Pain reaction to cold stimulus m teeth wtth expenmental fillings. Acta Odontol Scand 1971 ;29:639-47. 4 Tobias RS, Plant CG, Browne RM. A comparative pulpal study of two dental amalgam alloys [Abstract 93}. J Dent Res 1985;64(special issue):673. 5. Bergenholtz G, Cox CF, Loesche W J, Syed SA Bactanal leakage around dental restorations, ~ts effect on the dental pulp J Oral Pathol 1982;11:43950. 6 Pashley DH, Nelson R, Kepler EE The effects of plasma salivary constituents on dent~n permeability J Dent Res 1982;61:978-81. 7. Grajower R, B~elak S, E~delman E Caloum hydroxtde I~n~js in retrieved dec~ous teeth [Abstract 40}. J Dent Res 1984;63:550. 8. Cox C, Bergenholtz G, Heys DR, Syed SA, Fttzgerald M, Heys RJ. Pulp cap~ng of dental pulp mechancally exposed to oral mtcroflora' a 1-2 year observation of wound healing ~n the monkey. J Oral Patho11985;14:156-68 9 Brannstrom M, Nyborg H. Cawty treatment with a microblcidal fluonde solution, growth of bactena and effect on the pulp. J Prosthet Dent 1973;30:303-10 10. Torstenson B, Brannstrom M, Mattsson B. A new method for seahng composite resin contraction gaps tn lined ca~ties. J Dent Res 1985,64:450-3.
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11. Nordenvafl KJ, Brannstrorn M, Torstenson B. Pulp reactions and m~croorgantsms under ASPA and Con~se compostte fillings. J Dent Chdd 1979;46.449-53. 12. Watts A, Paterson RC, Gtllespie J, Kelly J. Pulp response to a glass tonomer cement IAbstract 192]. J Dent Res 1984,63:511. 13. Mej~re I, Brannstrom M. Deep bacterial penetration of early proximal canes les~ons m young human premolars. J Dent Child 1985;52:103-7 14 Nordenvall KJ, Malmgren B, Brannstrom M. Desensttizatlon of dentin by resin impregnation: a clin~al and IEjht-microscopic investigation. J Dent Chdd 1984;51 274-6. 15. Lundy T, Stanley HR. Correlation of pulpal htstopatholegy and clinical symptoms on human teeth subjected to experimental ~mtation. Oral Surg 1969; 27187-201. 16 Tronstad L, Langeland K. Effect of attrition on subjacent dentin and pulp. J Dent Res 1971 ;50:17-30 17. Olgart L, Brannstrom M, Johnson G. Invasion of bacteria into dent~nal tubules. Experiments ~n vivo and vttro. Acta Odontol and Scand 1974;32:6170. 18. Bergenholtz G. Effect of bacterial products on inflammatory reactions in the dental pulp. Scand J Dent Res 1977;85:122-9. 19. Bergenholtz G, Ahlstedt S, IJndhe J. Expenmental pulpttis in immunmzed monkeys. Scand J Dent Res 1977;85:396-406 20. Bergenholtz G. Inflammatory response of the dental pulp to bacterial trdtation. J Endodon 1981 ;7.100-4. 21. Brannstrorn M, Garberogllo R. Occulston of dantrnal tubules under superficial attrited dentine. Swed Dent J 1980;4.87-91. 22. Nordenvall KJ, Brannstrom M. In vtvo impregnation of dentinal tubules. J Prosthet Dent 1980;44:630-7. 23. Nordenvall KJ, Brannstr0m M. In wvo resm ~mpregnation of dentin fractures Swed Dent J 1980;4.177-82
Printed In U.S A
VOL 12, NO 10, OCTOBER1986
The Cause of Postrestorative Sensitivity and Its Prevention Martin Brannstrbm, DDS,
Dr, Odont.
As far as restorations are concerned, infection beneath the filling material itself is the greatest threat to the pulp. Thus, the main biological problem we face in restorative dentistry concems the favorable environment for microbial growth under restorations. Bacterial activity may result in increased pulp sensitivity, pulpal inflammation, and secondary caries. We need more biological testing of materials that is not complicated by the presence of bacteria in the space between the filling material and the walls of the cavity.
(d) ZOE does not provide a hermetic seal. Thus, we may have some drainage of fluid outward and this drainage may have a beneficial effect if the pulp is inflamed. When a permanent filling is replaced with ZOE because of postrestorative sensitivity due to pulpitis, the sensitivity may disappear because the bacteriafilled contraction gap is eliminated, drainage is established, and nerve excitability has been reduced. Fifteen years ago we first reported finding bacteria under fillings, and this observation has been confirmed by numerous studies conducted by our group and others. Therefore, I am convinced that as far as restorations are concerned, infection beneath the filling material itself is the greatest threat to the pulp. Thus, the main biological problem we face in restorative dentistry concerns the favorable environment for microbial growth under restorations. Bacterial activity may result in increased pulp sensitivity, pulpal inflammation, and secondary caries. Amalgamfillings may lead to sensitivity to cold during the first 1 to 2 wk. We know from recent experiments that when infection is avoided, amalgam can be placed on the exposed pulp without causing any harm to the pulp (M. Cvek and C. Cox, personal communications). In one series of experiments (3) we produced local inflammation in the pulp under cavities cut in human teeth. Control cavities were prepared in contralateral teeth with intact pulps. Both experimental and control cavities were lined with a very thin resin film and filled with amalgam. It was found that all teeth with inflamed pulps were more sensitive to cold. Bacteria have been found under amalgam fillings, even under copper amalgam (4, 5). The presence of microbes in the fluid gap under an amalgam filling results in a situation analogous to that of the dentinal crack syndrome, i.e. increased exitability of the nerves due to inflammation evoked by bacterial products and the presence of a fluid gap which favors hypersensitivity. Contraction of the fluid within the gap occurs when cold is applied to the tooth. This causes a rapid outward movement of fluid in the tubules, thus stimulating nerve fibers in the underlying pulp. However, within a few weeks the sensitivity to cold often disappears. This is because the contraction gap may be partly occluded
Let us first discuss the way in which our filling materials may contribute to postoperative sensitivity. The first question is: are filling materials irritating to the pulp and will their toxicity cause the pulp to become sensitive? The answer is no. This is true for the materials we have tested in human experiments (1), such as amalgam, silicate, various cements and composites, and those that have been studied by Cox et al. (2)in monkeys. However, we cannot be certain about materials we have not tested or those that are not yet on the market. For the future, we need biological testing of materials that is not complicated by the presence of bacteria in the space between the filling material and the walls of the cavity. In numerous studies we have found that when bacteria are not allowed to enter this space that only zinc oxide-eugenol (ZOE) cement, even in a thick mix, evokes a slight cellular necrosis and inflammation when placed in deep cavities. In spite of the fact that it elicits a mild inflammatory reaction, ZOE is a good temporary dressing for the following reasons: (a) Soon after ZOE is inserted, free eugenol leaches out, and after a few weeks the pulp usually returns to normal. (b) ZOE does not contract, and so it does not permit bacterial growth on cavity walls. This explains why other filling materials that contract and allow fluid and bacteria to multiply within the gap between the restoration and the cavity walls are irritating to the pulp for a longer period of time than ZOE. (c) Free eugenol may diffuse to the pulp and block the transmission of impulses by sensory nerve fibers located beneath the cavity. 475
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by expansion of the amalgam and corrosion products that form within the gap. Furthermore, the slow outward flow of fluid in the dentinal tubules due to the higher fluid pressure in the pulp may lead to accumulation of plasma proteins and cell remnants in the dentinal tubules. In this way the resistance to fluid flow across dentin is increased (6). In addition, the gap may be sealed at the outer margin by the formation of a calcified pellicle, and after 2 to 3 months the formation of irregular dentin may seal the pulpal ends of the tubules. There is no evidence that "thermal shock" is a cause of damage to the pulp when it occurs under normal conditions. Dentin is an excellent thermal insulator and therefore there is no reason to place a thick base under an amalgam restoration. It is a mistake to assume that a thick base of calcium hydroxide or a cement will solve the problem of sensitivity to heat or cold. A thick base cannot be placed on the outer margin of the cervical wall or on the lateral wall of cavities. In the clinic it has been observed that such linings may not prevent sensitivity to cold even in teeth with composite resin fillings, nor can they prevent the development of secondary caries. When a fluid-filled space develops at the cervical and lateral walls, a calcium hydroxide base wilt wash out and the remaining gap will be invaded by bacteria (7, 8). A calcium hydroxide base such as Dycal or Life has several disadvantages, but the tendency to wash out is the most serious one. How can we reduce the risk of postrestorative sensitivity? First, in cavities that are to be filled with amalgam, composites, or glass ionomer cements, removal of the infected superficial smear layer is essential. Microbes entrapped within the smear layer are able to multiply and after a few weeks they can almost completely replace it. This may occur even if there is not much microleakage (9). In this context it should be stressed that invasion of microbes from the oral cavity into the gap is not the only route of infection. In addition to the smear layer, bacteria may remain in the dentinal tubules or in a fluid gap between enamel and dentin at the lateral walls (1). These bacteria, usually cariogenic, are easily left behind after cavity preparation, and they may multiply and fill a fluid space along the cavity walls (Fig. 1). Smear plugs in the tubule apertures should not be removed, as they reduce permeability and facilitate desiccation of the cavity with an air jet. Cavity walls should be disinfected, as we should treat infected dentin as we treat wounds in other tissues. Smear plugs in tubule apertures should also be reinforced with fluoride (1). A thin varnish or liner should then be applied to all cavity walls in order to block communication between dentinal tubules and the fluid gap which develops during contraction of the filling material. This gap will be in communication with the oral cavity but should not be in communication with the pulp via the dentinal tubules (1). A thin antibacterial lining should
Joumal of Endodontics
FtG 1. Scanning electron micrograph of dentin facing a gap at the DEJ some distance from a cawty. Bactena of coccal type tnvading the dentin. (From Brannstrom et al., Archives Oral Biology 22:571578, 1977.)
also be applied to the cavity walls to prevent bacteria from contaminating the dentinal surface and prevent invasion from a gap that may exist at the dentinoenamel junction (DE J) along the lateral walls of the cavity. The same treatment procedure should be utilized prior to inserting any type of filling material. In the case of composites, after the material has polymerized and contraction is nearly complete, the cervical gap should be impregnated with Enamel Bond resin (3M Co.). As seen in Fig. 2, capillary forces will cause the resin to flow into the air-filled gap. This will better preserve any lining that is used and, hopefully, eliminate postoperative sensitivity and reduce the risk of pulpal injury and development of secondary caries. This technique has been described in a recent publication (10). Concerning the risk of postrestorative sensitivity, we may have the greatest problem with cervical walls, because they cannot be etched. This is especially true for some of the newer materials such as P10, P30, Occlusin, and Command II, which are associated with little or no hygroscopic expansion (unpublished data). As seen in Fig. 2, gaps about 15 to 25 #m in width may persist at the cervical wall. From a biological point of view, this type of filling can be even more dangerous than amalgam. With the use of the same technique as demonstrated in Fig. 3, we have also observed gaps associated with glass ionomer restorations but to a lesser extent than with the above materials. Bacteria
Vol. 12, No. 10, October 1986
FIG 2. Cervical wall of proximal restoration (Enamel Bond Concise). Cavity walls had been I~nedwith the Tubulitec lining system (L). The contraction gap was impregnated from the margin with fluorescent Enamel Bond resin about 12 rain after the restoration was placed. Bar = 20 ~m. D, dentin. (From M. Brannstrom, Composite restn restorations' biological considerations with spe~al reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Restorative Materials. St. Paul, MN: 3M Co., 1985:71-81 .)
/
i~
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FtG 4. The inner surface of a composite restoration corresponding to the axial wall. Cocci as well as fdaments are present. (From M. Brannstr0m, Composite resin restorations: biological considerations with special reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Restorative Materials. St. Paul, MN: 3M Co., 1985:71-81 .)
:
FOG3. A ground section of tooth with proximal restorations photographed wtth UV light. Left, Occlusin (R1). Right, Scotchbond and P30 (R2). P, pulp. Fluorescent Enamel Bond resin apphed to the cervical margin has penetrated the contraction gap at the cervical wall and also parts of the axial wall. (From M. Brannstr0m, Composite resin restorations" btological considerations with special reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Resotrative Materials. St. Paul, MN: 3M Co., 1985: 71-81 .)
were found beneath many of these restorations (11, 12), although not as frequently as under composites. Therefore, the same pretreatment procedures should be applied when using glass ionomer cements (12). In summary, in order to reduce the risk of sensitivity and other postrestorative complications, we must provide a good marginal seal and avoid infected fluid gaps from developing between cavity walls and filling materials. When bacteria become established on cavity walls (Figs. 4 and 5) and there is fluid communication between the oral cavity and the pulp, it is not surprising that postoperative sensitivity develops.
1. FIG 5. Axial wall of buccal cavtty filled with silicate for 4 wk. A bacterial layer is seen closely attached to the cut dentin with bacteria present ~nsome tubules. (From M. Brannstrom, Composite resin restorations: biological considerations with special reference to dentin and pulp. In: Vanherle G, Smith DC, eds. Posterior Composite Resin Dental Restorative Materials. St. Paul, MN: 3M Co., 1985:71-81 .)
I would like to say a few words about cementation and failures in crown and bridge construction that lead to pulpitis and postoperative sensitivity. First, problems may develop when we fail to properly diagnose the condition of the pulp before and during crown preparation. We should be concerned about old fillings, leaky fillings, and secondary caries. Bacteria may already be present deep in the dentin, perhaps even in a local necrotic area of the pulp, There may be no symptoms because fairly good drainage of inflammatory exudate
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has been established through the thousands of tubules that open into fluid gaps and carious lesions. During the period that a crown is temporarily cemented, there will still be good drainage, so there will be no discomfort. However, when the crown is permanently cemented, the tooth may become symptomatic, probably because outward drainage has been blocked, resulting in an accumulation of noxious substances in the pulp. On the other hand, the infected pulp may gradually undergo necrosis in the absence of pain. What should we do in order to reduce the risk of pulp disease? First, we should remove all old fillings and secondary caries and treat the dentin as though we were going to insert a permanent restoration. Before administering a local anesthetic, the sensitivity of the dentin under old fillings and caries should be tested. Unless the pulp lumen is almost obliterated for unknown reasons, the dentin under old fillings and soft caries should be insensitive, indicating the presence of irregular dentin. Sensitive dentin under lesions may indicate that the pulp is not healthy, in which case the prognosis is poor. Dentin should be sensitive only in areas where it is intact. The second cause of failure is the operative procedure. Crown preparation must be performed with care and with abundant cooling. Heat will cause expansion of fluid in the dentin. The pulpal blood flow should compensate for the increase in tissue pressure, but it may fail if blood flow has been drastically reduced by the administration of a vasoconstrictor-containing local anesthetic (L. Olgart, personal ocmmunication). In addition, heat may reach the pulp and cause hemorrhage and perhaps local necrosis as well. It may be difficult for an old pulp to withstand the trauma of crown preparation. In addition, some tubules may already harbor bacteria or bacteria may arrive via the bloodstream and settle in a localized area of pulpal necrosis. By using an anesthetic solution which does not reduce blood flow, adequate cooling during grinding, and care in preparation, the risk of failure can be minimized. The third cause of failure involves the placement of a temporary crown. We found that under shallow guttapercha fillings bacteria reached the pulp within 3 wk (1). Occasionally, bacteria can be present deep in some dentinal tubules under a white spot carious lesion (1, 13). In experiments in which dentin was superficially exposed and left uncovered for 1 wk, bacteria were observed deep in the tubules (1). After a few weeks we found that in a few tubules bacteria had nearly reached the pulp. Poor placement of a temporary crown may leave cervical dentin unprotected. Thus, as many as 10,000 to 20,000 exposed tubules may become open and be invaded by microbes within 1 wk. Under the crown there may be an infected smear layer, but it may be replaced by bacteria as they proliferate. A flexible, elastic temporary cement may cause the crown to become dislodged and this opens up spaces for fluid to accumulate.
Journal of Endodontics
We may have an ill-fitting temporary crown in place for 2 to 3 wk, and during this period smear plugs in the tubule orifices disappear and bacteria enter the tubules. Perhaps you have seen how quickly dentin is softened when a crown in a large bridge has become loose. This is mainly due to bacteda invading the dentin. It is not unusual to find very sensitive dentin when a temporary crown is removed. You must not be surprised if permanent cementation that provides a good seal and blocks drainage is followed by pulpitis and toothache, as bacteria have been introduced into the dentin. In order to avoid these problems the following precautions should be observed: (a) Shorten the period that the temporary crown is in place to a few days. (b) Before temporary cementation, clean the dentin and remove the superficial smear layer with an antibacterial detergent. Then desiccate the dentin meticulously and apply a thin lining in the same way as you would for a permanent filling. Before permanent cementation, check the occlusion, as cuspal interference may possibly contribute to hypersensitivity. Remove the liner using a rubber cup in a slow-speed handpiece, then apply a cleanser mixed with pumice. After rinsing, desiccate the crown preparation for at least 10 s with the air stream directed from various positions parallel with the dentin. This will produce pain, but it is an important step before applying the cement to the dentin and the inside of the crown with a brush. If dentin is not properly desiccated, dentinal fluid may seep out onto the surface prior to or during setting of the cement. This will prevent good contact between the cement and dentin, thus preventing mechanical interlocking. The presence of fluid is thought to be particularly hazardous in the case of glass ionomer cements. As a result of several experiments I conducted, I have concluded that air jet desiccation does not injure the pulp and that the cements we use are not irritating, even if they are placed on an exposed pulp (1).
DENTIN EXPOSURES, DENTINAL PAIN In the clinic, fluid communication between the oral cavity and the pulp becomes obvious when dentin has been exposed. This may occur as a result of caries, abrasion, consumption of acidic foods, or because the dentist has failed to protect exposed dentin. Fluid communication may result in pain due to touch, sugar, and cold. These warning signals should be heeded. Pain of this nature is a positive reaction, as dentin hypersensitivity implies that the pulp may be in danger and it may bring the patient to the dentist in time to save the pulp. Dentinal tubules are highways along which stimuli can reach the pulp. In the clinic, it is important to realize that whenever we have exposed dentin, the underlying tubules are accessible not only to pain-producing stimuli but also to toxic products elaborated by bacteria. These products can easily diffuse inward and evoke an inflam-
Vol. 12, No. 10, October 1986
matory reaction in the pulp. This will result in sensitivity to the slightest fluid movement, because inflammation has the ability to increase the excitability of the A-fibers located along the pupal wall. In our experiments on human premolars, we exposed dentin by grinding oft the cuspal enamel. The smear plugs disappeared within a couple of days and after 1 wk all of the tubules were open and many were widened due to the removal of peritubular dentin. Many of the tubules had been invaded by bacteria and there were plugs of bacteria in their apertures (Fig. 6) (14-17). The pulps were slightly to moderately inflamed, and there was a loss of odontoblasts and usually a reduction in the width of the predentin. Two weeks following superficial exposure of cuspal dentin, we observed localized pulpal necrosis in 2 of 40 specimens. The pulp horns of these teeth were packed with neutrophilic leukocytes (14). DEFENSE MECHANISMS
Now that you are aware of the high incidence of infection associated with sensitive exposed dentin and beneath restorations, you may wonder how dentin becomes insensitive and how so many pulps have managed to survive. Thanks to the natural defenses of the tooth, the pulp is usually able to survive and the dentin can become insensitive. The term defense is used here in the broadest sense in that it refers to any active or passive change occurring in the tooth which results in the obstruction of dentinal tubules so that the enemy, i.e. bacteria and their toxic products, does not gain access to the pulp, or if it does, it is quickly eliminated.
Postoperative Sensitivity
479
Together with dentinal pain providing a warning signal, pulpal inflammation is the first defense reaction we can expect. Slight to moderate inflammation is a positive reaction. However, if the inflammatory reaction is too strong, it may have a negative effect, as has been shown by Bergenholtz and co-workers (18-20). Thus, in the narrow pulp lumen severe inflammation may lead to localized necrosis. On the other hand, a weak immunological response may also have a negative effect and if pulp necrosis develops, bacteria may invade and colonize the pulp. Consequently, when dentin is exposed and left unprotected, the orifices of the dentinal tubules must be sealed as soon as possible in order to reduce the risk of pulpal infection. In our experiments dealing with exposed dentin in human teeth, we found that in some exposed cusps, even after 2 wks, the dentin was covered by a thin, granulated pellicle that had become mineralized (1). In this way the dentin can become less sensitive, and the grateful patient will be willing to keep the surface of the dentin clean. As a result, fewer toxic products will reach the pulp and the pulp will respond favorably. Inflammation will subside and the leukocytes that have accumulated along the pulpal wall will disappear. Subsequently, cells in the cell-rich zone of the pulp will, if they are still viable, divide, differentiate, and produce irregular dentin in order to block the pulpal ends of the tubules. In this way both ends of the tubules will be obstructed, and bacteria within the tubules will have less opportunity to survive. In addition, deposition of mineral salts within the tubules close to the exposed surface will gradually increase. This obstruction of tubules by calcium phosphate crystals is termed dentinal sclerosis (Fig. 7), and
J
FIG 6. Profile view of base (left) of acid-treated cavity exposed for 1 wk, photographed w~th scanning electron microscope. Microorganisms of varying form in longitudinally fractured, w~dened dentinal tubules. (From Olgart et al., Acta Odontologica Scandinavica 32:6170, 1974.)
FiG 7. Cross-fractured section through the center of the dentin located between the attnted surface and the pulpal lumen. Various degrees of closure of the tubule lumen are observed.
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Branns~om
it seems to develop following the formation dentin. Presumably, sclerosis develops as the ingress of mineral salts, derived from dentinal fluid, that precipitate in the tubules
Journal of Endodontics
of irregular a result of salvia and (21).
TREATMENT OF SENSITIVE EXPOSURES
There are some patients who need our help, as they experience a great deal of pain because dentin has become exposed. In such cases the natural defense mechanisms appear not to be adequate. Too dense an accumulation of inflammatory cells at the pulpal wall may interfere with the formation of irregular dentin, or the salivary "healing effect" (dentinal sclerosis) is not sufficient. Other factors that may contribute to excessive sensitivity include consumption of an excessive amount of acidic foods, mechanical removal of hard tissue due to bruxism, and frequent, energetic use of abrasive toothpastes that expose a large number of tubules each time the affected tooth is brushed. Undoubtedly, a combination of one or more of these factors plus formation of bacterial plaque on the exposed dentin will not allow the pellicle to calcify and, in addition, more tubules will be exposed. Diffusion of irritants from the plaque to the pulp will prevent the pulp from forming a complete barrier of irregular dentin. In addition, when cuspal dentin is exposed, fluid gaps may easily develop at the DEJ, and these gaps will become packed with microbes in the same way and for the same reason that I have described in the case of early enamel caries. Patients suffering from anorexia nervosa may have severe problems with hypersensitive dentin. The teeth of many patients with this disease are exposed to large amounts of acid because of repeated regurgitation of the stomach contents. These patients, usually young girls but occasionally adults with similar problems, need our help. First, we should prescribe proper dental hygiene. The patient should use only nonabrasive, fluoride-active toothpastes which have an efficient cleansing effect. Second, the patient should reduce the consumption of acidic foods and beverages, and if bruxating, a splint should be fabricated. Third, daily rinsing with 0.05% sodium fluoride solution should be strongly recommended. The above measures will often be sufficient to eliminate or greatly reduce dentinal sensitivity and this will allow the patient to better clean the tooth surfaces and remove plaque, thus reducing the risk of acid attack on the exposed dentin. In addition, we may treat sensitive occtusat exposures by impregnating the tubules and gaps at the DEJ with a resin. The rationale and technique for this treatment has been described elsewhere (1,22, 23). When tubules are open and desiccated with a blast of air that is directed parallel to the surface of the dentin and at a right angle to the long axis of the tubules, there will be a rapid outward movement of fluid
in the tubules that will evoke pain. After desiccation for 0.5 to 1 rain, the pain usually subsides. The reason for this is that when the tubules are opened, the outward flow of fluid stops some distance short of the surface. Thus, the outer part of the tubule becomes filled with air. When a resin such as Enamel Bond (3M Co.)is applied to the surface of the dentin, it will quickly flow into the tubules because of capillary attraction. With the same pretreatment procedure, i.e. by producing open, air-filled tubules via desiccation, we can treat sensitive tooth necks by impregnation with 2% sodium fluoride. We may be able to obtain just as high a fluoride concentration within the tubules with this method as with iontophoresis. A fluoride-containing resin, or even better a calcium hydroxide dressing, may then be applied to the surface for a couple of hours. The calcium hydroxide paste should be kept in place with a surgical pack. This actually combines two different techniques which have each been highly recommended. These two components, i.e. fluoride in high concentration and calcium hydroxide, both have antibacterial properties. In addition, precipitation of calcium fluoride should block the tubules. Some fluoride may be released at the surface of the dentin and promote the development of a calcified pellicle. Some will be incorporated into fluorapatite crystals. An alternative to fluoride is potassium oxalate treatment, as suggested by Pashley (see Pashley's article "Dentin Permeability, Dentin Sensitivity, and Treatment Through Dentin Tubule Occlusion" in this issue). I have tested both solutions clinically and found them to be equally efficacious. The disadvantage with the impregnation technique, using either resin or salts, is that it is painful during desiccation and may require local anesthesia. On the other hand, a 1- or 2-min application of agents such as fluoride or oxalate to moistened dentin may result in only limited diffusion of the active ingredients into the tubules. Such a treatment is not likely to produce the desired results. Since the surface layer of dentin is easily removed by attrition, the agents would have to be applied repeatedly over a considerable period of time. Any treatment is likely to be successful if the patient is cooperative and agress to use only a nonabrasive fluoride toothpaste and curtail his or her consumption of acidic foods and beverages. By blocking the tubules as soon as possible, sensitivity of the dentin to touch will be decreased and the patient can then keep the tooth surface clean. By controlling plaque formation and thus limiting the diffusion of irritants to the pulp, pulpal inflammation should gradually subside. However, the tooth may remain sensitive to cold until the pulp is no longer inflamed and can deposit a layer of irregular dentin over the pulpal ends of the tubules. Presented at the F~rst Wodd Co~ference on Dental and Pulpal Pare, New York, NY, October 25-27, 1985
Vol. 12, No. 10, October 1986 Dr Brannstrom is affiliated with the Department of Oral Pathology, Karolinska Institute, Hudd~nge, Sweden
References 1 Brannstrom M Dentin and pulp m restorative dent~sty. London: Wolfe Medical Publ~cat~ens Ltd, 1982. 2 Cox CF, Heall CL, Keall HJ, Ostro E. Biocompatib~lJty of various dental matenals against exposed monkey pulps J Prosthet Dent (in press). 3 Johnson G, Brannstrom M. Pain reaction to cold stimulus m teeth wtth expenmental fillings. Acta Odontol Scand 1971 ;29:639-47. 4 Tobias RS, Plant CG, Browne RM. A comparative pulpal study of two dental amalgam alloys [Abstract 93}. J Dent Res 1985;64(special issue):673. 5. Bergenholtz G, Cox CF, Loesche W J, Syed SA Bactanal leakage around dental restorations, ~ts effect on the dental pulp J Oral Pathol 1982;11:43950. 6 Pashley DH, Nelson R, Kepler EE The effects of plasma salivary constituents on dent~n permeability J Dent Res 1982;61:978-81. 7. Grajower R, B~elak S, E~delman E Caloum hydroxtde I~n~js in retrieved dec~ous teeth [Abstract 40}. J Dent Res 1984;63:550. 8. Cox C, Bergenholtz G, Heys DR, Syed SA, Fttzgerald M, Heys RJ. Pulp cap~ng of dental pulp mechancally exposed to oral mtcroflora' a 1-2 year observation of wound healing ~n the monkey. J Oral Patho11985;14:156-68 9 Brannstrom M, Nyborg H. Cawty treatment with a microblcidal fluonde solution, growth of bactena and effect on the pulp. J Prosthet Dent 1973;30:303-10 10. Torstenson B, Brannstrom M, Mattsson B. A new method for seahng composite resin contraction gaps tn lined ca~ties. J Dent Res 1985,64:450-3.
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11. Nordenvafl KJ, Brannstrorn M, Torstenson B. Pulp reactions and m~croorgantsms under ASPA and Con~se compostte fillings. J Dent Chdd 1979;46.449-53. 12. Watts A, Paterson RC, Gtllespie J, Kelly J. Pulp response to a glass tonomer cement IAbstract 192]. J Dent Res 1984,63:511. 13. Mej~re I, Brannstrom M. Deep bacterial penetration of early proximal canes les~ons m young human premolars. J Dent Child 1985;52:103-7 14 Nordenvall KJ, Malmgren B, Brannstrom M. Desensttizatlon of dentin by resin impregnation: a clin~al and IEjht-microscopic investigation. J Dent Chdd 1984;51 274-6. 15. Lundy T, Stanley HR. Correlation of pulpal htstopatholegy and clinical symptoms on human teeth subjected to experimental ~mtation. Oral Surg 1969; 27187-201. 16 Tronstad L, Langeland K. Effect of attrition on subjacent dentin and pulp. J Dent Res 1971 ;50:17-30 17. Olgart L, Brannstrom M, Johnson G. Invasion of bacteria into dent~nal tubules. Experiments ~n vivo and vttro. Acta Odontol and Scand 1974;32:6170. 18. Bergenholtz G. Effect of bacterial products on inflammatory reactions in the dental pulp. Scand J Dent Res 1977;85:122-9. 19. Bergenholtz G, Ahlstedt S, IJndhe J. Expenmental pulpttis in immunmzed monkeys. Scand J Dent Res 1977;85:396-406 20. Bergenholtz G. Inflammatory response of the dental pulp to bacterial trdtation. J Endodon 1981 ;7.100-4. 21. Brannstrorn M, Garberogllo R. Occulston of dantrnal tubules under superficial attrited dentine. Swed Dent J 1980;4.87-91. 22. Nordenvall KJ, Brannstrom M. In vtvo impregnation of dentinal tubules. J Prosthet Dent 1980;44:630-7. 23. Nordenvall KJ, Brannstr0m M. In wvo resm ~mpregnation of dentin fractures Swed Dent J 1980;4.177-82