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Protection of the Pulp and the Tooth-Restoration Interface

For clinicians around the world, the 1991 International Symposium on Adhesives in Dentistry established the acceptance of adhesive bonding.1 Biological data presented therein 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; the smear layer is now 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 long-term 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 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.

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 µm to 0.7 µm) film liner and a thicker (0.8 µm to 25 µm) 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; 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.

Although dental pulp was regarded as a 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 (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.

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 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 5-6-7). 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.

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, Black’s 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.

Amalgam Alloys: A Past Paradigm

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.

Preadhesive Restoratives: Did They Seal?

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 patient’s 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 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.

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 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 µm at the dentin-enamel junction to 4.0 µm or larger at the predentin interface. Under normal conditions, each tubule contains an odontoblastic process—nerves that extend approximately 50 µm 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 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. By providing a seal along the entire restoration interface, a reduction of recurrent caries and restoration longevity should be expected. It is evident that an intact dentin substrate has the potential to provide substantial protection against the chemical toxicity of materials.26

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.27,28 Disastrous histological effects were also reported when exposed primate pulps were etched and direct capped with an experimental adhesive.29,30 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.31-33

Light microscopic studies of different adhesive systems continue to report variations in final results, as had occurred during pulp capping.27-30,34,35 If all dentin bridges are to be regarded as porous,35 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 factors of Ca(OH)2-capped pulps with long-term microleakage. 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

Factors for Clinical Success

Katoh et al demonstrated that a 6% solution of NaOCl placed on an exposed pulp with a cotton pellet allows 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.36 It has been reported that the presence of dentin chips and fragments disturbed the healing of exposed dental pulp.35 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.37 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.

Conclusion

The most reliable paradigms for sealing restorations against microleakage (ie, 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. Consequently, the clinical use of 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, 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.

 

*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.

 

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