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BIOLOGICAL BASIS FOR CLINICAL SUCCESS : PULP PROTECTION AND THE TOOTH-RESTORATION INTERFACE
Charles F. Cox, DMD* Abeer A. Hafez, DDS, MS Naotake Akimoto, DMD, PhD Masayuki Otsuki, DMD, PhD John C. Mills, DMD, MSll

This article provides biological and technological information that strengthens clinicians understanding of cohesive hybridization and pulp therapy in order to support their routine use of bonding and resin systems. Utilizing cohesive systems, clinicians should experience several advantages over traditional water-soluble base and liner systems. When properly applied, cohesive hybridization of vital dentin prevents immediate postoperative hypersensitivity under all restorations and completely seals the entire tooth-restoration interface, which provides a reduction in recurrent caries. Key Words: hybridization, acid etching, pulp protection, inflammation, bacteria

or clinicians around the world, the 1991 International Symposium on Adhesives in Dentistry established the acceptance of adhesive bonding.1 The symposium provided scientific documentation regarding hybridization

of vital dentin to develop an interdiffused substrate of the entire cavity interface. Biological data dispelled several myths: the smear layer was inviolate; acid etching of vital dentin killed the pulp; and calcium hydroxide Ca(OH)2 was the ideal pulp protectant. Until then, many researchers and clinicians were reluctant to acid etch dentin; today the smear layer is routinely acid etched or modified in preparation for hybridization of the underlying substrate. Technologies have since unfolded exponentially and knowledge of dentin and pulp has reflected a similar increase. Hybridization of vital dentin is now routinely employed to provide a continuous seal along the entire enamel cavosurface margin to the entire dentin interface and to the pulp. This seal strengthens the underlying tissues, prevents postoperative hypersensitivity, provides a uniform substrate for luting, and provides longterm deterrence of bacterial microleakage and recurrent caries. More recently, hybridization of pulp tissues has been demonstrated to provide a biomemetic substrate for pulp healing and dentin bridge formation. Clinicians

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*Professor, Departments of Biomaterials and Restorative Dentistry, University of Alabama School of Dentistry, Birmingham, Alabama; Visiting Professor, Departments of Operative Dentistry, Tokyo Medical and Dental University, Tokyo, Japan, Tsurumi School of Dental Medicine, Yokohama, Japan.
Research

Associate, Department of Biomaterials, University of Alabama School of Dentistry, Birmingham, Alabama. Department of Operative Dentistry, Tsurumi School of Dental Medicine, Tsurumi University, Yokohama, Japan. Professor, Department of Operative Dentistry, Tokyo Medical and Dental University, Tokyo, Japan.

Assistant,

Associate ll Chair,

Department of Endodontics, University of Alabama School of Dentistry, Birmingham, Alabama. Charles F. Cox, DMD UAB School of Dentistry Depts. Biomaterials and Restorative Dentistry 1919 Seventh Ave. S Birmingham, AL 35294-0007 Tel: Fax: 205-934-1071 205-975-5874

Figure 1. Photomicrograph of resin-capped pulp with ( light pink-stained ) dentin bridge and no inflammation. No Ca(OH)2 was placed for pulp protection.

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Figure 2. Photomicrograph of monkey pulp that was direct capped with Ca(OH)2 (left) and amalgam alloy. Bacteria are evident as gram-negative purple-blue-stained profiles (right) subjacent to the Ca(OH)2.

Figure 3. Photomicrograph of monkey pulp after direct pulp capping with Ca(OH)2. Note the thick dentin bridge. This pulp is subject to microleakage and eventual necrosis.

now practice adhesive bonding to provide immediate patient comfort and to prevent effectual restoration longevity against microleakage. Although acids were originally regarded as pulp irritants that caused inflammation and necrosis, it is now evident that the H3PO4 in acidic cements demineralizes the smear layer and smear plugs. This permits rapid bidirectional fluid flow, particularly when a cold stimulus is applied to a suspected area. Buonocore et al first demonstrated that minimal enamel etching produced a microporous interface for adhesive bonding.2 Due to subsequent studies,3-5 hybridized enamel and dentin are routinely etched for direct and indirect restorations.

Figure 4. Photomicrograph of monkey pulpal fibroblasts 2 years following direct capping. Note the black-stained particles within the cytoplasm of these pulpal fibroblasts remain in the pulp stroma.

Issues of Pulp Protection

The literature describes various considerations for pulp protection barriers to bacterial, thermal, chemical, electrical, and mechanical factors that possess therapeutic and/or stimulatory properties. Pulp protection has historically ranged from placement of a thin (0.2 m to 0.7 m) film liner and a thicker (0.8 m to 25 m) suspension liner to placement of a thick (0.2 mm to 1 mm) base. The majority of the Ca(OH)2 pulp protectants were reportedly endowed with the capacity to prevent postoperative sensitivity, to provide permanent pain relief, and to stimulate reparative dentin formation, soft tissue healing, differentiation of odontoblastoid cells, and dentin bridge formation in an exposed pulp. Liners and bases have been reported to provide only transient bactericidal and/or bacteriostatic properties (at best) and essentially no mechanical seal to the restoration interface due to the physical limitations of their nonadhesive characteristics. Consequently, the scientific validity of these concepts has been seriously questioned.6-10 Film liners are often composed of 10% copal varnish in a nonaqueous chloroform or similar organic solvent that provides a barrier to the underlying substrate against microleakage. Suspension liners may be an aqueous Ca(OH)2 slurry, eugenolic, or polystyrene in composition, and have been reported to provide thermal insulation and therapeutic stimulation to the dentin and pulp. Traditional bases are acid-base mixtures of Ca(OH)2 or ZnOE and, more recently, glass-ionomer cements. For decades, Ca(OH)2 was utilized to protect the pulp if its underlying pink was visible. Eugenol cements were successful for several reasons: eugenol penetrates through dentin to the pulp and denatures the myelin nerve coating, thus blocking the nerve impulse; eugenol also has a microbicidal effect on any remaining bacteria and on those bacteria that may invade the restoration interface via microleakage.

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Figure 5. Right lateral view of tooth #7(12) with a Class V cervical lesion that presents as an ivory-yellow-stained zone of exposed dentin.

Figure 7. Occlusal view of tooth #30(46) following caries detection. Note the stained carious dentin along the dentinenamel junction and areas where the original Ca(OH)2 base had dissolved.

Figure 6. Lateral view of the Class V lesion following staining with a caries detector. The purple-pink-stained infected dentin will be removed for minimal invasive preparation and adhesive restoration.

Although dental pulp was regarded as an inviolate fragile tissue, subject to inflammation and eventual necrosis upon exposure, biological studies have refuted this theory.10 -13 An exposed dental pulp will heal against a pH spectrum of restorative materials that permit new dentin bridge formation as long as a biological or mechanical seal is maintained. In the absence of a Ca(OH)2 base (Figure 1), dentin bridge formation occurs directly adjacent to a composite resin. It must be understood that any material is compromised by its inability to provide a long-term seal against bacterial microleakage. Studies have indicated that certain formulations of Ca(OH)2 become soft and disintegrate over extended service.14 The long-term expectations for commercial Ca(OH)2 formulations have recently become suspect as usage studies demonstrate that certain Ca(OH)2 medicaments dissolve from microleakage,15,16 lose their bactericidal/static

capacity with time, and eventually permit bacterial colonization within the dissolved residue (Figure 2). These formulations have also demonstrated that each underlying dentin bridge contains multiple tunnel defects from persistent pulpal vessels that remain at the initial healing site and can cause several complications (Figure 3). Defects permit multiple avenues for the conveyance of bacteria and their immunogenic factors, which are responsible for recurring pulp infection. Tunnels also permit unchecked migration of dissolved Ca(OH)2 particles to the underlying pulp, which allows constant percolation of dissolved particles into the pulp stroma. These Ca(OH)2 particles can present increased clearance difficulties if they remain in pulpal fibroblast for two years following direct pulp capping with calcium hydroxide agents (eg, Dycal, Dentsply/Caulk, Milford, DE) (Figure 4). From a biological perspective, the increasing physical accumulation of Ca(OH)2 particles in the pulp (without physiological removal) may impose a burden on the pulp vasculature and cause eventual pathology and necrosis. The majority of these agents only adhere to dentin by weak van der Waals forces, without any capacity for mechanical adhesion, and contemporary adhesive systems generally fail to bond to the interface of Ca(OH)2 agents. If one considers the entire surface interface of any Ca(OH)2 liner or base, its presence represents an area that decreases the total adhesive hybridization mechanism. This alone is reason not to use it for adhesive procedures. Various reports have also questioned the use of certain commercial Ca(OH)2 agents as the definitive lining or base material16 -18 and have cautioned clinicians regarding bacterial microleakage as the principal irritant to dentin and pulp substrates when the restorative seal

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fails.19 With proper mechanical and/or biological seal as an objective, adhesive systems can consequently be routinely placed onto vital dentin and pulp tissues with predictable expectations for immediate and long-term success.

Caries Removal: Preparation of the Restoration Interface

Clinicians have traditionally relied upon several strategies for caries identification: visual inspection is a purely subjective consideration; radiographic interpretation depends on technological variables (eg, chemical development and storage). A scientifically documented caries detector solution was developed by Fusayama et al to provide clinical differentiation between infected and affected dentin, thus eliminating the subjective component of caries removal and replacing it with biologically based technology.3 The placement of caries detectors onto a lesion stains and permits immediate differentiation and removal of the outer bacterially infected lesion where a defective collagen zone incapable of remineralization is present (Figures 5 through 7). The underlying zone of transparent dentin is devoid of bacteria and presents a substrate capable of remineralization. Clinicians are now urged to use caries detectors to remove only infected caries with a low-speed bur. The underlying noncarious dentin can then be etched and bonded to establish a continuous hybrid layer that seals against postoperative sensitivity and further recurrent caries.

Figure 8. Photomicrograph of a restored, nonexposed monkey pulp. From left, cavity floor, tubular dentin, calciotraumatic line, and zone of reparative dentin with new odontoblastoid cells are evident.

Amalgam Alloys: A Past Paradigm

Amalgam alloys have been widely used as restorative materials for decades. Traditional amalgam preparations were placed to remove all carious tooth structure and extended into sound dentin to provide retention. Although these materials were placed to provide a long-term seal and prevent recurrent caries, early lathe-cut amalgam alloys corroded along the entire interface. These corrosive products provided a slight mechanical seal and afforded a degree of oxide attachment to the tooth substrate. The cariostatic component of copper oxides against recurrent caries has also been proposed.

Prevention of Extension With Adhesives

The original concept of prevention of extension of decay stated that by extending the cavity preparation toward the buccal and lingual aspects, enamel margins would remain free of contact with the adjoining tooth.20 This promotes cleansing of the embrasure to prevent recurrent caries. From an examination of 10,000 clinical cases, it was reasoned that extension of Class I and II cavities through fissures would permit self-cleansing and placement of all cavosurface margins toward the line angles of the tooth to prevent caries.21 Due to the availability of contemporary adhesive materials, however, Blacks rule of extension for prevention should only be considered as a historical doctrine of the past. These composite resin formulations allow the conservation of sound tooth structure and refute the necessity of using standard outline form. Unfortunately, numerous clinicians and universities continue to employ Blacks design for cavity preparation at the expense of noninfected enamel and dentin.

Preadhesive Restoratives: Did They Seal?

Enamel is the hardest tissue in the body; dentin is the second hardest; dental pulp is a pure low-compliant tissue encased in a hard substrate (ie, dentin). Until adhesive systems were developed, acidic cements luted intra- and extracoronal restorations to the preparation interface. When placed on the hydrophobic substrate of enamel, acidic cements would demineralize the external surface until they set. When an acidic cement is placed on hydrophilic dentin, however, it demineralizes the smear layer and plugs. This permits fluid movement within the dentin tubule complex, which is activated by various thermal and mechanical stimuli. Consequently, not only does H3PO4 increase a patients hydrodynamic pain response mechanism,22 but it also permanently alters the underlying intertubular and peritubular hydroxyapatite and the subjacent collagen without providing a mechanical or biological seal to the underlying hydrophilic

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Figure 9A. Photomicrograph of monkey pulp that was directly pulp capped with Ca(OH)2. Note dentin bridge adjacent to Ca(OH)2 interface. 9B. Odontoblastoid cells have formed from pulpal cells.

substrate. When intra- and extracoronal restorations were luted with H3PO4 cement without any bonding system, however, demineralization occurred. This resulted in hydrolysis of the subjacent substrate and increased the potential for recurrent caries. Various studies have demonstrated that failure to seal the restoration interface results in bacterial microleakage invasion of the underlying dentin tubules and pulp by bacteria, inflammation, and eventual necrosis.23,24 The failure of H3PO4 cements to prevent demineralization of the underlying dentin substrate and the failure of the clinician to provide either a bacterial or mechanical tight seal predisposed the teeth to postoperative hypersensitivity and recurrent caries.

morphology as to their location along the pulp wall, project their processes into the dentin tubule complex oftentimes to the dentin-enamel junction. When caries insults dentin and underlying pulp, tubule sclerosis generally precedes the caries, and when the bacterial insult reaches the pulp, the subjacent odontoblasts below the insult may die. As sclerosis closes the dentin tubules, cells migrate to the interface to form new odontoblastoid cells that will begin to deposit reparative dentin. When a cavity preparation is placed into this dentin-pulp complex, the response is generally the same. Reparative dentin forms to an iatrogenic stimulus (Figure 8), and is deposited at a rate that appears to be independent of any particular restorative material.24 One early investigation demonstrated that specific dental pulp cells proliferate at the wound site and form both a reparative and a new dentin bridge in the absence of bacterial influences and epithelial stimulus.25 This reinforced the concept that the dental pulp possesses an inherent capacity to heal in the absence of a bacterial lesion.

Healing of Nonexposed and Exposed Pulps

The ISO usage guidelines (#ISO 7405:1997-E) recommend the placement of a thin dentin barrier between the cavity floor/pulp interface. Warfvinge and Bergenholtz demonstrated that challenging the dental pulp with a bacterial solution on the cavity floor resulted in several necrotic pulps at one week, and many at one month.26 An additional study has indicated a direct correlation to the presence of stained and anaerobically cultured samples and noted a direct correlation to inflamed and necrotic pulps.27 The thesis of bacterial microleakage has also been cited as the primary factor causing pulp inflammation in numerous reports.28-30 By providing a seal along the entire restoration interface, a reduction of recurrent caries and restoration longevity should be expected. Several ISO Class V studies report a zero to slight pulp response when restored with different adhesive systems. In several of these studies, cavities are placed within 100 m of the dental pulp. At the short-term interval, the odontoblastic layer below the cavities is generally lost due to preparation trauma. By the intermediate ISO time interval, the studies generally reported a thin rim of reparative dentin below the dentin tubules, whereas long-term intervals demonstrated thicker reparative dentin, all without disastrous results. In these studies, tested

Repair Potential of the Dentin-Pulp Complex

The dentin-pulp complex is a biological interdiffusion of odontoblastic processes, fluid, and nerves within the dentin tubules. The pulp is composed of vascular and neural elements, possible lymphatics, fibroblasts, undifferentiated mesenchymal (possible stem) cells, and various immunocompetent cells that terminate at the apical foramen. Dentin is a mineralized hydrophilic tissue of type I collagen and composed of tubules that range in size from 0.3 m at the dentin-enamel junction to 4.0 m or larger at the predentin interface. Under normal conditions, each tubule contains an odontoblastic process nerves that extend approximately 50 m from the pulp and fluid and intertubular dentin that contains collagen fibers and hydroxyapatite crystals. With normal aging, the pulp is reduced in size and the dentin grows in bulk. Primary odontoblasts, which present varying

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adhesive systems present histological data comparable to Ca(OH)2 controls. In order to evaluate the thickness of the remaining dentin, researchers have used an in vitro model that demonstrated HEMA reached the pulp faster than a TEGDMA resin system after one day.31 Release rates depended upon the thickness of the remaining dentin. It would be interesting to follow this study model with bacterial extracts similar in preparation to those of Bergenholtz.27 Nevertheless, it is evident that an intact dentin substrate has the potential to provide substantial protection against the chemical toxicity of materials.32 The term hybrid layer was first used in 1982 to describe the morphologic impregnation of vital dentin with resin.4 Proper adhesive infiltration of acid-etched dentin causes the formation of a hybrid layer. By treating the hybrid layer with HCl and NaOCl in vitro, Nakabayashi demonstrated that the hybrid layer remains intact, which suggested that the hybrid layer seals the entire enamel-dentin-resin interface with a continuous morphologic seal or continuous enamel barrier. Ca(OH)2 has long been considered the paradigm for new dentin bridge formation (Figures 9 and 10). Studies have indicated that high and low pH dental materials are biologically compatible with an exposed dental pulp (Figure 11), which permits an environment for dentin bridge formation. In the literature, however, controversy has persisted. The total etching of exposed primate pulps resulted in sequential death following adhesive capping, and necrosis was observed in 41% of pulps at 26 and 75 days.33,34 Disastrous histological effects were also reported when exposed primate pulps were etched and direct capped with an experimental adhesive.35,36 In contrast, it has been reported that exposed primate pulps healed (Figure 12) and resolved with new dentin bridge formation (Figure 13) following direct capping with three different adhesive systems.37-39 The persistence of the Ca(OH)2 particles has been described as a passing of the marbles on down through successive generations of a family (Gwinnett and Cox, personal conversation). The consistent presence of resin particulates within the dentin-pulp complex was recently reported in a study that demonstrated the formation of resin globules in dentin tubules. These globules were also evident in the primary odontoblastic layer and the macrophage profiles at the initial evaluation period and in multinucleated giant cells at 90 days postcapping with the All-Bond2 adhesive system.40 Their TEM data were similar to those reported by Mjr et al,41 who found phagocytosis of Ca(OH)2 particles within cells subjacent to the exposed pulp. Light microscopic studies of different adhesive systems continue to report variations in final results, as had occurred during pulp capping.33-36,42,43 If all dentin bridges are to be regarded as porous,43 then the longevity of the seal becomes increasingly important with extended function. In order to understand the nature of the clearance of Ca(OH)2 and resin particles from an exposed and capped pulp, long-term TEM pulp studies must be completed to evaluate the biological effects of microleakage
Figure 11. Monkey pulp has been mechanically exposed, pulp capped with an acidic silicate cement, and sealed. A dentin-bridge matrix with odontoblastoid cells is evident along the pulpal interface. Figure 10. Photomicrograph of monkey pulp following exposure and capping. A green-stained dentin bridge is adjacent to Ca(OH)2. New reparative dentin has formed below the cavity exposure.

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Figure 12. Photomicrograph of an exposed monkey pulp that has been direct pulp capped. The healing pulp has migrated. No inflammation is evident, and no Ca(OH)2 was placed.

for clearance of most dentin chips, provides for surgical amputation of the blood clot and damaged cells, and, perhaps most importantly, provides hemorrhage control in the pulp.45 No instances of associated necrosis were observed by these researchers. It has been reported that the presence of dentin chips and fragments disturbed the healing of exposed dental pulp.43 Using 2.5% NaOCl, no in vivo toxicity to pulp cells and no inhibition to pulp healing, odontoblastoid cell formation, or dentin bridge formation were noted. More importantly, a conspicuous absence of dentin chips at the exposure interface was determined at all time periods, which compromised the normal biological healing process and permitted new dentin bridge formation directly adjacent to the adhesive interface. It was concluded by Inoue et al that 4-META was useful in conserving pulp tissues, as the solution maintained a mechanical and biological seal and was not cytotoxic to pulp cells in vivo.46 These investigators demonstrated that 4-META polymerization established a soft tissue hybrid layer (STHL) composed of resin and pulp tissue. They indicated that the resin penetrated into pulp tissue and polymerized therein to create a STHL, which provided a protective function to an exposed pulp, much like that of a dentin bridge. The STHL was thought of as a new biomaterial in the strictest sense of the term, which suggested that the STHL can play a role as a proper substrata for dentinogenesis in situ.

Figure 13. Monkey pulp has been mechanically exposed and direct capped with composite resin. Note the dentin bridge at the adhesive interface. No inflammation occurred due to sealing of hybrid layer.

factors of Ca(OH)2-capped pulps with long-term microleakage.44 In this manner, the long-term capacity of an exposed pulp to heal and clear itself of particulate debris that may cause an immunogenic or giant cell response can be determined. Until such long-term TEM studies are completed on several adhesive systems and Ca(OH)2 controls, the ability of exposed dental pulp to heal and form a new dentin bridge will be ignored.19

Patients Expectations Unlike patients of past decades, contemporary patients demand aesthetic excellence. White teeth and aesthetic smiles are emphasized throughout popular culture and can be successfully delivered without using metallic materials. Due to exponential technological advances in adhesive materials, it is now possible to predictably treat a variety of clinical conditions (eg, cavity forms, stained dentition, diastemata) with metal-free restorations.

Conclusion
The most reliable paradigms for sealing restorations against microleakage (postoperative hypersensitivity and bacterial infection) are the hydrophilic and hydrophobic adhesive systems. Successful bonding of adhesive systems to acid-etched dentin requires the use of hydrophilic resins that bond equally well to peritubular and intertubular dentin.47-49 Consequently, the clinical use of

Factors for Clinical Success

Katoh et al demonstrated that a 6% solution of NaOCl placed on an exposed pulp with a cotton pellet allows

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Ca(OH)2 must remain conservative for adhesive restorations in order to provide maximum dentin interface for bonding and sealing. The presence of tunnel defects in dentin bridges causes one to question if a dentin bridge is the standard for pulpal repair,44 or whether it is simply an abnormal response similar to scar formation in epithelial tissues. It is imperative that clinicians understand the biological importance of hemorrhage control and the technique sensitivity of hydrophilic primers in order to optimize the efficacy of adhesives for clinical success against microleakage of bacterial factors. The dental pulp will maintain its physiological vitality when bacteria and their toxic components are excluded from gaining access to the vital tissues of the dentin and pulp.

References
1. Barkmeier WW, Cooley RL, eds. Proceedings of the International Symposium on Adhesives in Dentistry. July 11 to 13, 1991. 2. Buonocore MG. A simple method of increasing the adhesion of acrylic materials to enamel surfaces. J Dent Res 1955;34: 849-853. 3. Fusayama T, Nakamura M, Kurosaki N, Iwaku M. Non-pressure adhesion of a new adhesive restorative system. J Dent Res 1979;58(4):1364-1370. 4. Nakabayashi N. Resin reinforced dentine due to the infiltration of monomers into the dentine at the adhesive interface. Jpn J Dent Mats and Dev 1982;1:78-81. 5. Inokoshi S, Iwaku M, Fusayama T. Pulpal response to a new adhesive restorative resin. J Dent Res 1982;61(8):1014-1019. 6. Brnnstrm M, Vojinovic O, Nordenvall KJ. Bacteria and pulpal reactions under silicate cement restorations. J Prosthet Dent 1979;41(3):290-295. 7. Brnnstrm M, Nyborg H. Points in the experimental study of pulpal response to restorative materials. Odontol Tidskr 1969; 77:(5)421-426. 8. Bergenholtz G, Cox CF, Loesche WJ, Syed SA. Bacterial leakage around dental restorations: Its effect on the dental pulp. J Oral Pathol 1982;11(6):439-450. 9. Cox CF, Keall CL, Keall HJ, et al. Biocompatibility of surfacesealed dental materials against exposed pulps. J Prosthet Dent 1987;57(1):1-8. 10. Cox CF, Sbay RK, Suzuki S, et al. Biocompatibility of various dental materials: Pulp healing with a surface seal. Int J Periodont Rest Dent 1996;16(3):240-251. 11. Kozlov M. Massler M. Histologic effects of various drugs on amputated pulps of rat molars. Oral Surg Oral Med Oral Pathol 1966;13:455-469. 12. Brnnstrm M, Nordenvall KJ. Bacterial penetration, pulpal reaction and the inner surface of Concise enamel bond. Composite fillings in etched and unetched cavities. J Dent Res 1978;57(1): 3-10. 13. Brnnstrm M, Nyborg H. The presence of bacteria in cavities filled with silicate cement and composite resin materials. Sven Tandlak Tidskr 1971;64(3):149-155. 14. Reinhardt JW, Chalkey Y. Softening effects of bases on composite resins. Clin Prev Dent 1984;5:5-12. 15. Cox CF, Bergenholtz G, Fitzgerald M, et al. Capping of the dental pulp mechanically exposed to the oral microflora A 5 week observation of wound healing in the monkey. J Oral Path 1982;11(4):327-339. 16. Kidd E. Microleakage: A review. J Dent 1976;4(5):199 -206. 17. Lewin DA. The case of disappearing Dycal. Br Dent J 1980; 148:32. 18. McComb D. Comparison of physical properties of commercial calcium hydroxide lining cements. J Am Dent Assoc 1983;107 (4):610-613. 19. Massler M. Preventive endodontics: Vital pulp therapy. Dent Clin N Amer 1967;11:663-673. 20. Webb M. Restoration of Contour and Prevention of Extension of Decay. Dental Cosmos; 1881.

21. Black GV. Management of Enamel Margins. Dental Cosmos; 1985. 22. Brnnstrm M, Lindn LA, Astrm A. The hydrodynamics of the dental tubule and of pulp fluid. A discussion of its significance in relation to dentinal sensitivity. Caries Res 1967;1(4): 310-317. 23. Brnnstrm M, Vojinovic O, Nordenvall KJ. Bacteria and pulpal reactions under silicate cement restorations. J Prosthet Dent 1979; 41(3):290-295. 24. Cox CF, White KC, Ramus DL, et al. Reparative dentin: Factors affecting its deposition. Quint Int 1992;23(4):257-270. 25. Kakahashi S, Stanley HS, Fitzgerald RJ. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Path 1965;20:340-349. 26. Warfvinge J, Bergenholtz G. Healing capacity of human and monkey dental pulps following experimentally-induced pulpitis. Endod Dent Traumatol 1986;2(6):256-262. 27. Bergenholtz G. Effects of bacterial products on inflammatory reactions in the dental pulp. Scand J Dent Res 1982;85:122-129. 28. Qvist V. Correlation between marginal adaptation of composite resin restorations and bacterial growth in cavities. Scand J Dent Res 1980;88(4):296-300. 29. Torstenson B, Nordenvall KJ, Brnnstrm M. Pulpal reaction and microorganisms under clearfil composite resin in deep cavities with acid etched dentin. Swed Dent J 1982;6(4):167-176. 30. Qvist V. Pulp reactions in human teeth to tooth colored filling materials. Scand J Dent Res 1975;83(2):54-66. 31. Hamid A, Hume WR. Diffusion of resin monomers through human carious dentin in vitro. Endodon Dent Traumatol 1997;13(1):1-5. 32. Hume RW. Are restorative materials and procedures harmful to the pulp? Transactions of the Academy of Dental Materials. 1998;12:105-119. 33. Stanley HR. Trashing the dental literature-Misleading the general practitioners: A point of view [editorial]. J Dent Res 1996;75 (9):1624-1626. 34. Stanley HR, Pameijer CH. Sequential death of exposed pulps with total etch bonding treatments. J Dent Res 1997;76(Abstract No. 2334):305. 35. Pameijer CH. The disastrous effects of the total etch technique in vital pulp capping in primates. J Dent Res 1997;76(Abstract No. 1899):251. 36. Pameijer CH, Stanley HR. Pulp reactions to resin cements. Am J Dent 1992;5(2):81-87. 37. Akimoto N, Momoi Y, Kohno A, et al. Histologic observation of direct capped pulps with liner bond 2 adhesive system. J Dent Res 1997;76(Abstract No. 519):78. 38. Otsuki M, Tagami J, Kanca J, et al. Histologic evaluation of two Bisco adhesive systems on exposed pulps. J Dent Res 1997;76(Abstract No. 520):78. 39. Cox CF, Hafez AA, Akimoto N, et al. Biocompatibility of primer, adhesive and resin composite systems on non-exposed and exposed pulps of non-human primate teeth. Am J Dent 1998;1: (special issue):55-63. 40. Gwinnett AJ, Tay FR. Early and intermediate time response of the dental pulp to an acid etch technique in vivo. Am J Dent 1997;10:35-44. 41. Mjr IA, Dahl E, Cox CF. Healing of pulp exposures: An ultrastructural study. J Oral Path Med 1991;20(10):496-501. 42. Pereira JC, Segala AD, Costa CAS. Human pulp response to direct capping with an adhesive system: Histologic study. J Dent Res 1997;76(Abstract No. 1329):180. 43. Stanley HR. Criteria for standardizing and increasing credibility of direct pulp capping studies. Am J Dent 1998;1(11)(special issue):17-34. 44. Cox CF, Sbay RK, Ostro E, et al. Tunnel defects in dentin bridges: Their formation following direct pulp capping. Oper Dent 1996;21(1):4-11. 45. Katoh M, Kidokoro S, Kurosu K. A study on the amputation of pulp using sodium hypochlorite (NaOCl). Jpn J Pediat Dent 1978;16:107-116. 46. Inoue T, Miyakoshi S, Shimono M. Dentin pulp/adhesive resin interface: Biological view from basic science to clinic. Quint Int 1995;(special issue):217-220. 47. Pashley DH, Horner JA, Brewer PD. Interactions of conditioners on the dentin surfaces. Oper Dent 1992;5(suppl):137-150. 48. Fusayama T. Factors and prevention of pulp irritation by adhesive composite resin restorations. Quint Int 1987;18(9):633-641. 49. Cox CF, Suzuki S. Re-evaluating pulp protection: Calcium hydroxide liners vs. cohesive hybridization. J Am Dent Assoc 1994; 125(7):823-831.

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CE
27

CONTINUING EDUCATION
NEW YORK UNIVERSITY
College of Dentistry Center for Continuing Dental Education New York City, NY

To submit your CE Exercise answers, please use the answer sheet found within the CE Editorial Section of this issue and complete as follows: 1) Identify the article; 2) Place an X in the appropriate box for each question of each exercise; 3) Clip answer sheet from the page and mail it to the CE Department at Montage Media Corporation. For further instructions, please refer to the CE Editorial Section. The 10 multiple-choice questions for this Continuing Education (CE) exercise are based on the article Biological basis for clinical success: Pulp protection and the tooth-restoration interface by Charles F. Cox, DMD, Abeer A. Hafez, DDS, MS, Naotake Akimoto, DMD, PhD, Masayuki Otsuki, DMD, PhD, and John C. Mills, DMD, MS. This article is on Pages 819-826.

Learning Objectives:
This article provides an overview of reliable paradigms for sealing restorations against microleakage. Upon reading the article and completing this exercise, the reader should: Be aware of the adhesive systems that are recommended by the authors. Understand the rationale for the selection of particular adhesive systems.
1. Each of the following common beliefs were challenged at the 1991 International Symposium on Adhesives in Dentistry EXCEPT: a. The smear layer is inviolate. b. Acid etching of vital dentin kills the pulp. c. Calcium hydroxide is the ultimate pulp protectant. d. Vital dentin can be hybridized to provide a clinical seal at the pulp/dentin interface. 2. Traditional bases typically comprise all of the following EXCEPT: a. Acid-base mixtures of Ca(OH)2. b. Acid-base mixtures of ZnOE. c. Glass-ionomer cements. d. Eugenol. 3. Which of the following conditions are necessary for the exposed dental pulp to heal? a. A biological or mechanical seal is maintained. b. Ca(OH)2 is used as a base. c. Copal Varnish is used as a liner. d. A dentin bridge is formed. 4. Failure to adequately seal the restorative interface results in each of the following EXCEPT: a. The production of exudate. b. Bacterial microleakage. c. Inflammation. d. Eventual necrosis. 5. Which of the following effects occur with the use of adhesive systems in nonexposed and exposed pulps? a. The pulp is extremely irritated and necrotic pathology occurs. b. The adhesive is incompatible with any exposed pulpal tissue. c. The adhesive bonds with the entire surface interface of any Ca(OH)2 liner or base. d. A hermetic seal forms and prevents bacterial microleakage. 6. Which of the following is considered the hardest tissue in the human body? a. Dental pulp. b. Dentin. c. Enamel. d. Bone. 7. Each of the following statements is an accurate reflection of the results of recent studies EXCEPT: a. Certain Ca(OH)2 formulations dissolve due to microleakage. b. Certain Ca(OH)2 formulations grow harder and increase in strength over time. c. Certain Ca(OH)2 formulations lose their bactericidal/static capacity with time. d. Certain Ca(OH)2 formulations stimulate reparative dentin formation and prevent postoperative sensitivity. 8. The dentin pulp complex is a biological interdiffusion of each of the following items EXCEPT: a. Nerves. b. Odontoclastic processes. c. Odontoblastic processes. d. Fluid. 9. Which of the following strategies has been most effective with exposed primate pulps? a. Etching and direct capping with an experimental adhesive. b. Direct capping with an adhesive system. c. Use of Ca(OH)2 as a base or liner. d. Total etching of exposed tissue prior to capping. 10. What factor is most important in the clinical and biological success of a direct pulp capping? a. Use Ca(OH)2 to control hemorrhage of the exposure. b. Use of 2% Xylocaine to control hemorrhage of the exposure. c. Controlling hemorrhaging prior to material placement. d. Use of an agent such as NaOCl to control hemorrhage of the exposure.

PPAD

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