Protection of the Pulp and the Tooth-Restoration Interface
Charles F. Cox, DMD
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
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
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
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
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.
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
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.
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
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
Prevention of Extension With
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
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
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 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
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
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.”
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
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
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.
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.
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
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.
Associate, Department of Biomaterials, University of Alabama School of
Dentistry, Birmingham, Alabama.
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