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Q U I N T E S S E N C E I N T E R N AT I O N A L

Long-term evolution of a case of direct

pulp capping by adhesion to dentin
Santiago González-López MD, PhD1/Victoria Bolaños-Carmona MD, PhD2

This article presents the long-term follow-up of a female patient who suffered pulp exposure
during removal of a large caries lesion from the mandibular right first molar. The clinical
decision to perform direct pulp capping was made. The tooth was treated with 5% chlorhexi-
dine, etched with 37% phosphoric acid, and then restored with Heliomolar composite after
application of Gluma dentin adhesive. The patient was followed for more than 8 years.
(Quintessence Int 2005;36:797–803)

Key words: clinical follow-up, clinical report, compound resins, conservative treatment,
dentin adhesion, direct pulp capping, pulp exposure, pulp vitality

A 28-year-old female attended our dental
clinic in October 1992 for the treatment of
her mandibular right first molar. The patient
reported food impaction and pain on chew-
ing fibrous food or taking cold drinks that
ceased with the ending of the stimulus.
Examination showed acute caries on the dis-
tal surface (Fig 1). The radiograph showed
deep distal dentinal caries, very close to the
pulp, without periapical lesion. The patient
was informed of the pulpal involvement and
the need for endodontic treatment. The
1
Associate Professor of Operative Dentistry, School of
Dentistry, University of Granada, Spain.
2
Associate Professor of Childhood Integrated Dentistry,
School of Dentistry, University of Granada, Spain.
Reprint requests: Victoria Bolaños Carmona, Facultad de
Odontología, Universidad de Granada, Edificio Máximo, Campus
Cartuja, 18071, Granada, Spain. E-mail: mbolanos@ugr.es
symptoms and the results of a pulp vitality
test raised suspicions about the pulpal
health.
The intervention started with the nerve-
trunk anesthesia and isolation of the opera-
tive field with rubber dam, which included
the complete mandibular right quadrant from
the second molar to the central incisor.
Removal of the caries was done using the
staining technique proposed by Fusayama1
(Fig 2), which was repeated until the dentin
showed no staining. Access to the caries cav-
ity was widened by removing the distal parts
of the buccal and lingual cusps with a 330L
bur (Konet) at high speed (Fig 3).
During the final maneuvers to remove the
softened dentin with the excavator, the pulp
was widely exposed, revealing a red turgid
pulp that immediately stopped bleeding (Fig
4). Cotton wool was used to apply 5%
chlorhexidine (Hibimax) to this area for 1

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Q U I N T E S S E N C E I N T E R N AT I O N A L
González-López/Bolaños-Carmona

Fig 1 Acute caries lesion on the distal surface of the mandibular right first Fig 2 The caries was removed using the staining technique
molar. The patient reported pain on taking cold drinks and chewing fibrous with 0.5% fuchsin in propylene glycol.
foods.

Fig 3 The distal parts of the buccal and lingual cusps were removed to Fig 4 Removal of the carious dentin with an excavator
improve access and allow visual monitoring of the caries removal at the caused a wide pulp exposure.The pulp presented a red turgid
dentinoenamel junction. appearance.

minute (Fig 5). The entire cavity, including the
exposed pulp, was then etched with 37%
phosphoric acid for 30 seconds (Fig 6), and
Gluma dentin adhesive (Bayer) was applied,
according to the manufacturer’s instructions.
A metal matrix on a universal matrix retain-
er-holder was inserted, and a wooden wedge
was placed to the distolingual aspect of the
tooth. The contact point was polished with a
ball-shaped polisher (Fig 7). The cavity was
filled with Heliomolar composite (Vivadent).
The matrix was then removed and the
restoration was finished with occlusal adjust-
ment and polishing (Fig 8).
After the restoration was completed, a
radiograph confirmed a perfect seal and
absence of excess, and showed invasion of
the distal pulp horn. A follow-up examination 1
week later showed absence of symptoms and
competence of the contact point. At 4 months,
the first follow-up radiograph showed that the
distal pulp horn had begun to calcify (Fig 9).
At the 8-month follow-up, caries was diag-
nosed on the mesial surface of the mandibu-
lar right second molar and was restored
during the same session. Radiographic
examination confirmed progressive pulp
calcification of the first molar (Fig 10).

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Q U I N T E S S E N C E I N T E R N AT I O N A L
González-López/Bolaños-Carmona

Fig 5 Disinfection was performed by applying 5% chlorhex- Fig 6 Total etch of the cavity with 37% phosphoric acid for 30 seconds
idine with cotton wool for 1 minute. immediately before the application of Gluma dentin adhesive.

Fig 7 Before the restorative material was applied, a wooden Fig 8 Final appearance of the completed restoration. Heliomolar micro-
wedge was placed to the distolingual aspect, and the contact filled composite was used.
point was polished.

Fig 9 Follow-up radiograph at 4 months shows the perfect Fig 10 Follow-up radiograph at 8 months shows pulp calcification of the
marginal fill of the restoration. Calcification of the distal pulp distal horn.
horn had started.

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González-López/Bolaños-Carmona

Fig 11 Follow-up radiograph at 16 months confirms diagnosis of mesial Fig 12 Cavity preparation after excavation of the mesial
caries and shows the progression of pulp calcification to include the entire caries. Nerve-trunk anesthesia was necessary because of the
pulp horn. high sensitivity of the patient to this intervention.

Fig 13 Follow-up radiograph at 3 years shows that pulp calcification Fig 14 Follow-up radiograph at 5 years. The pulp calcifica-
includes the distal area of the pulp chamber. tion invades the entrance to the distal root canal.

At the 16-month follow-up, mesial caries
was diagnosed on the mandibular right first
molar, which was restored during the same
session. Nerve-trunk anesthesia was admin-
istered because of the high sensitivity of the
patient to this intervention (Figs 11 and 12).
At the next 2 follow-up visits, at 3 years
and 5 years, there were no symptoms and
the radiographs showed that calcification
had progressed to involve part of the distal
area of the pulp and to enter the distal root
canal (Figs 13 and 14).
The patient failed to attend subsequent
follow-up sessions but returned to the clinic
in December 2000, 8 years after the start of
treatment, for discomfort in the same first
molar unrelated to stimuli. Endodontics was
performed at the insistence of the patient,
despite our doubts as to its indication. We
found that the pulp protection procedure 8
years earlier had functioned well and that the
extracted pulp was vital (Fig 15).

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DISCUSSION
The approach to pulp exposure has under-
gone a major revision in recent years. We
now know that healthy pulp can promote its
own tissue repair by cell reorganization and
the production of specialized collagen
matrix–producing cells, which create an ini-
tial substrate for the formation of dentinal
bridge. For this process to occur, the pulp
must be biologically sealed and kept isolated
from bacteria and their toxic components.2–6
Direct pulp capping is a controversial con-
servative procedure. The decision to perform
direct pulp capping is exclusively clinical and
requires a correct diagnosis of pulp status.7
Direct pulp capping is clearly indicated for
minimal pulp exposure of traumatic and
recent origin,8 and teeth with pulp exposure
of accidental or mechanical origin are also
good candidates for this treatment.9,10
Generally, direct pulp capping can be carried
out when the pulp is exposed through unin-
fected dentin, when the tooth has no recent
history of spontaneous pain, and when a cor-
rect antibacterial sealing can be achieved.11
The direct capping of exposed pulp in the
presence of deep caries is considered a high-
risk procedure, and the risk is higher with
greater pulp exposure and the consequent
increased likelihood of pulpal infection.10
Therefore, some of the characteristics of
the present case are considered to worsen
the prognosis of direct pulp capping, since
the pulp exposure occurred during the final
steps of caries removal in an adult tooth, and
the diameter of the exposed area was more
than 1 mm. Although these features are unfa-
vorable, they do not constitute a contraindi-
cation to the procedure.9 The clinical deci-
sion in the present case was based on pre-
operative and intraoperative assessments,
which revealed presence of pain and
absence of negative findings in the physical
and radiographic examinations. Thus, the
appearance of the exposed pulp tissue and
especially the spontaneous cessation of
bleeding indicated that the pulp was healthy
and viable. In our view, when the pulp is
inflamed and the hemorrhage does not read-
ily stop, application of direct pulp capping is
questionable.
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Q U I N T E S S E N C E I N T E R N AT I O N A L
González-López/Bolaños-Carmona
Fig 15 Chamber opening. Vitality of the pulp was confirmed 8 years after
direct pulp capping.
The technique used in this case is of spe-
cial interest. Currently, the most widespread
approaches are the calcium hydroxide tech-
nique and the total-etch technique, with or
without prior protection of the exposed pul-
pal area with calcium hydroxide.7,12–14
Regardless of the technique selected, 3 fac-
tors are essential to the clinical success of
the procedure: asepsis, sealing of the cham-
ber communication, and hermetic sealing of
the cavity. With regard to the first, direct pulp
capping must be performed in conditions of
total isolation, and special care must be
taken to disinfect the cavity and exposed sur-
face. For this purpose, Cox et al5,15 recom-
mended the use of 2.5% sodium hypochlo-
rite. Chlorhexidine has been proposed as an
alternative to achieve the simultaneous
hemostasis and disinfection of the cavity.16
We chose the latter option for the safety and
stability of the product.
Calcium hydroxide has traditionally been
considered the treatment of choice for seal-
ing pulp chamber communication. Currently,
its use has been questioned because of its
lack of specificity for the induction of dentinal
bridge formation2 and the frequent pulpal
reinfection of treated teeth.4,15 This reinfection
has been related to the presence of tunnels
in the newly formed dentinal bridges and,
above all, to the resorption of the calcium
hydroxide within 1 or 2 years.4 On the other
hand, most recent experimental studies3–5,17
have related the inflammatory histologic
801
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Q U I N T E S S E N C E I N T E R N AT I O N A L
González-López/Bolaños-Carmona
response of the exposed pulp to the pres-
ence of marginal microfiltration and have
largely ruled out any toxic effects of the adhe-
sive materials used. Infection control must,
therefore, be our primary concern in achiev-
ing tissue repair.6 In this context, the use of
dentin adhesives may be advantageous
because they prevent bacterial penetration
by producing a hybrid layer that provides a
correct marginal and tubular seal, including
the sealing of tunnel defects present in newly
formed dentinal bridges.4
In the present case, Gluma adhesive was
used. Although it is no longer commercially
available, it was one of the first adhesive sys-
tems to offer predictable outcomes in the
dental setting. The mutagenic capability of
glutaraldehyde and the development of sim-
pler techniques have led to its withdrawal
from the market. However, the clinical suc-
cess of the direct pulp capping in the present
case can be attributed to the achievement
(using Gluma), of an impermeable restora-
tion that allowed pulpal cells to organize and
produce a dentinal bridge. It should be kept
in mind that microfiltration is the main cause
of an inflammatory pulpal response.17
In the present case, pulpal repair activity
was not restricted to the production of a
dentinal bridge at the exposure site, but
rather continued with a pulpal calcification
that progressively invaded the distal part of
the pulp chamber. We do not know the origin
of this reaction, although there may be 2 pos-
sible causes of an unfavorable long-term evo-
lution. The first is the presence of late mar-
ginal microfiltration through deterioration of
the interface in relation to mechanical load
cycling.18,19 However, this would have been
accompanied by the presence of pulpitis,
which was not presented or reported by our
patient. The other possibility may be a calci-
um degeneration process, which may have
produced the nonspecific symptoms pre-
sented by the patient at the last follow-up ses-
sion and that led to the request for endodon-
tic treatment. In our view, the latter is the
most likely explanation, although there are
sparse studies on the effect of dentin adhe-
sives on pulp biology. Heitman and
Unterbrink20 reported normal clinical and
radiologic findings in 8 cases at 2 to 6
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802 VOLUME 36 • NUMBER 10
months after direct pulp capping. Kanca13
describes the stability of pulp chamber size
at 4 years in a traumatized central incisor.
Górecka et al14 had only one failure, due to
pulp necrosis, among 10 cases of incisal
fracture treated with different procedures,
including direct adhesion on the exposed
pulp. None of these authors found the alter-
ations observed in our case. Two recent stud-
ies that used the same fourth-generation
adhesive (All-Bond 2, Bisco) underlined the
dissociation between clinical symptoms and
histologic findings in the pulp healing, even
though there were no clinical symptoms.21,22
CONCLUSIONS
1. Dentin adhesives are a good alternative to
calcium hydroxide in direct pulp capping.
In the present case, the tooth treated by
this procedure has remained vital and
symptom-free for more than 8 years.
2. Asepsis of the operative field and effective
sealing of the pulp chamber communica-
tion and restoration margin are critical to
the success of direct pulp capping using
this technique.
3. A long-term clinical and radiographic fol-
low-up is recommended because the
impact of this direct dentin adhesion tech-
nique is unknown.
4. Further clinical studies are required to
determine the long-term evolution of pulp
status after direct pulp capping with
dentin adhesives.
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1. Fusayama T. Clinical guide for removing caries using
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Biocompatibility of Optibond and XR-Bond adhe-
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Periodontics Restorative Dent 1998;18:86–99.
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