Human pulp responses to in-office tooth bleaching

Carlos Alberto de Souza Costa,a Heraldo Riehl,b João Fernando Kina,c

Nancy Tomoko Sacono,d and Josimeri Hebling,d Araraquara, Brazil
ARARAQUARA SCHOOL OF DENTISTRY, SÃO PAULO STATE UNIVERSITY

Objective. To evaluate and compare the responses of human incisor and premolar pulps after bleaching.
Study design. A bleaching agent with 38% hydrogen peroxide (H2O2) was applied on the buccal surface of 10 sound
lower teeth (G1: 6 premolars; G2: 4 incisors) for 45 minutes. Three premolars and 3 incisors that received only rubber/
pumice prophylaxis were used as control groups G3 and G4, respectively. Two days after the bleaching procedure,
the teeth were extracted and processed for histologic evaluation.
Results. Only in G2 (4 incisors) were any changes in the pulp detected. In the coronal pulp there was a large zone of
coagulation necrosis. The radicular pulp showed mild inflammatory changes manifested as an accumulation of
mononuclear cells around congested and dilated blood vessels. No pulpal damage was seen in either of the control
groups (G3 and G4) or in group G1.
Conclusion. Bleaching with 38% H2O2 for 45 minutes causes irreversible pulp damage in lower incisors but not in
premolars. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010;109:e59-e64)

Hydrogen peroxide (H2O2) is a thermally unstable ox-
ygen-derived free radical frequently found within the
cells as the result of a series of intracellular reactions
that occur specifically in the mitochondria.1 High con-
centrations of this chemical agent, which present oxi-
dative power,2-4 have been used to treat discolored
teeth.5 The oxidative reactions and consequent cell
damage caused by free radicals are the main mecha-
nisms responsible for the toxicity of peroxide-contain-
ing compounds.6 Although it is known that free radicals
are capable of degrading complex organic molecules
that are responsible for tooth coloration,4 the exact
mechanisms by which the teeth are bleached are not
completely understood. It has been reported that the
low molecular weight of H2O2 molecules makes them
capable of diffusing across enamel and dentin to reach
the pulpal space.1 Consequently, H2O2 and its degra-
dation products, which play a role in the tooth bleach-
ing, may cause damage to the pulp cells, especially to
odontoblasts that underlie dentin.7 It has been reported
that ⬃70% of patients submitted to bleaching have
complained about postoperative sensitivity, particularly
Supported in part by the Fundação de Amparo à Pesquisa do Estado
de São Paulo—FAPESP (grant nos. 2007/50646-3 and 2008/05890-6)
and Conselho Nacional de Desenvolvimento Científico e Tecnológico—
CNPq (grant no. 301029/2007-5).
a
Department of Physiology and Pathology.
b
Private practice.
c
Department of Restorative Dentistry.
d
Department of Orthodontics and Pediatric Dentistry.
1079-2104/$ - see front matter
© 2010 Mosby, Inc. All rights reserved.
doi:10.1016/j.tripleo.2009.12.002
in their anterior teeth.10 However, although several in
vitro studies have evaluated the cytotoxicity of bleaching
agents to culture of cells,8,9 few data are available con-
cerning the effects of bleaching agents on human pulps.
Therefore, the aim of the present study was to evaluate
and compare the responses of pulps of anterior (incisors)
and posterior (premolars) sound human teeth submitted to
in-office bleaching using a gel with 38% H2O2.
MATERIALS AND METHODS
Sixteen caries-free human teeth scheduled to be ex-
tracted for orthodontic reasons were selected from
young patients. The mean age of the patients was 16.2
years. The parents/guardians as well as the volunteers,
after reading and receiving all necessary explanations
including the experimental rationale, the clinical pro-
cedures, and possible risks, were asked to sign a con-
sent form explaining the research protocol, which was
previously approved by the Ethics Committee.
Sixteen sound teeth were selected for the study and
divided into 4 groups: bleached premolars (G1; n ⫽ 6),
bleached incisors (G2; n ⫽ 4), nonbleached premolars
(G3; n ⫽ 3), and nonbleached incisors (G4; n ⫽ 3). The
latter 2 groups served as control groups and received
only rubber/pumice prophylaxis.
The teeth were cleaned by rubber/pumice prophy-
laxis, thoroughly washed, and dried with an oil-free
air stream. Then, for groups G1 and G2, a light-cured
resin-based gingival barrier (Opal Dam; Ultradent
Products, South Jordan, UT) was used to protect the
soft tissues circumjacent to teeth being whitened and
to protect the adjacent teeth. A 38% H2O2 bleaching
gel (Opalescence Xtra Boost; Ultradent) was handled
according to the manufacturer’s instructions and was

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e60 de Souza Costa et al. April 2010

Table I. Inflammatory cell response Table IV. Absolute frequency (n) observed for each
Score Characterization histopathologic event according to the groups
0 None or a few scattered inflammatory cells present in the Score
pulp area corresponding to the buccal surface of the Histopathologic event Group 0 1 2 3
tooth in which the bleaching gel was applied
Inflammatory cell response G1 6 0 0 0
1 Slight inflammatory cell infiltrate with
G2 0 1 3 0
polymorphonuclear or mononuclear leukocytes
G3 3 0 0 0
2 Moderate inflammatory cell infiltrate
G4 3 0 0 0
3 Severe inflammatory cell infiltrate
Tissue disorganization G1 6 0 0 0
G2 0 0 1 3
Table II. Tissue disorganization
G3 3 0 0 0
Score Characterization G4 3 0 0 0
0 Normal tissue Reactionary dentin formation G1 6 0 0 0
1 Odontoblastic layer disorganized but central pulp normal G2 0 0 1 3
2 Total disorganization of the pulp tissue morphology G3 3 0 0 0
3 Pulp necrosis associated or not with dystrophic calcification G4 3 0 0 0
G1, Bleached premolars (n ⫽ 6); G2, bleached incisors (n ⫽ 4); G3,
Table III. Reactionary dentin formation nonbleached premolars (n ⫽ 3); G4, nonbleached incisors (n ⫽ 3).
Score Characterization
0 Absence
1 Modest hard tissue deposition beneath the buccal surface of
the tooth in which the bleaching gel was applied descriptive analysis according to the criteria presented
2 Moderate hard tissue deposition beneath the buccal surface
in Tables I-III: inflammatory cell response, pulp tissue
of the tooth in which the bleaching gel was applied
3 Intense hard tissue deposition in the pulp tissue disorganization, and reactionary dentin formation.
Using a light microscope (Diastar; Cambridge Instru-
ments, Buffalo, NY) adapted to a video camera (DXC-
107A/107AP; Sony Electronics, Tokyo, Japan), 3 linear
measures from the enamel/dentin junction to the pulp
applied to the buccal surface of the teeth in such a way chamber were carried out to determine the dentin thick-
that a uniform 1-mm layer of material was formed and ness (DT). The video images were loaded into a com-
left undisturbed for 15 min. The bleaching gel was puter and processed using standard software (Mocha;
removed from the tooth surface using a saliva ejector Jondel Scientific, San Rafael, CA). The methodology
with high-power suction, and the bleaching cycle was used in the present study to measure the DT was similar
repeated 2 more times, totaling 3 applications of 15 to that previously used to determine the remaining
minutes each. After the third application, the bleaching dentin thickness between the cavity floor and the sub-
gel was removed from the enamel surface and the tooth jacent pulp tissue.11,12 The 3 readings were averaged to
was copiously rinsed with an air/water spray and gently obtain the mean DT for each tooth. The data regarding
dried with sterile gauze. the DT were submitted to nonparametric Kruskal-Wal-
Two days after the bleaching procedure, the teeth lis test complemented by Mann-Whitney tests at a
were extracted under local anesthesia. The roots were significance level of 5% (SPSS, Chicago, IL).
immediately sectioned midway between the cement/
enamel junction and the root apex with a high-speed RESULTS
handpiece under water spray. The teeth were stored for The scores for each criterion determined by the his-
48 hours in formalin fixative solution at pH 7.2, decal- tologic assessment of the specimens according to
cified in buffered Morse solution (equal volumes of groups are shown in Table IV. The individual and
50% acid formic and 20% sodium citrate), under agi- median DT values are presented in Table V. Regarding
tation, cleared in xylol, vacuum infiltrated with wax the DT, a significant statistical difference was observed
paraffin, and finally embedded in paraffin. Six-micro- between incisors (G1 and G3) and premolars (G2 and
meter-thick serial sections were cut (820; Spencer Mi- G4), with incisors presenting a smaller DT than pre-
crotome, Carson, CA), mounted on glass slides, and molars (P ⬍ .05). No statistical difference was ob-
stained with hematoxylin and eosin (H/E) and Masson served when groups G1 (bleached premolars) and G3
trichrome. Based upon previous in vivo studies,11,12 all (nonbleached premolars) were compared (P ⬎ .05).
sections were evaluated by a calibrated examiner The same lack of difference was seen between G2
blinded to the groups. Using a light microscope (62774; (bleached incisors) and G4 (nonbleached incisors).
Carl Zeiss, Oberköchen, Germany) the following his- The analysis of the radiographs which were taken
topathologic events were evaluated and classified by a immediately before the extractions of all of the teeth
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Volume 109, Number 4
Table V. Dentin thickness (mm) for bleached and nonbleached (control) human premolars and incisors
Specimen (tooth) G1
1 2.99
2 3.21
3 3.10
4 2.98
5 3.10
6 3.24
Mean (SD)† 3.10 (0.11)
Median (P25-P75)‡ 3.10 (2.99-3.22)a
*Group designations as in Table IV.
†Each value represents the mean of 3 measurements taken in the same specimen/tooth.
‡Medians identified with the same letter represent groups that do not differ statistically (Mann-Whitney: P ⬎ .05).
used in the present in vivo study demonstrated no
periapical pathology. The volunteers who had their
inferior incisors bleached (G2) reported postoperative
pain. Therefore, based upon the IRB recommendations,
all teeth were extracted. Conversely, the volunteers
who had their premolars bleached (G1) did not report
any particular postoperative sensitivity. However, to
compare the pulp responses occurring in premolars and
incisors, all premolars also were extracted 2 days after
being bleached.
Overall, the histologic features showed that the pulp
tissue observed in G1 (bleached premolars) and both
control groups, G3 (nonbleached premolars) and G4
(nonbleached incisors), were quite similar. The pulp
responses in G2 (bleached incisors) were different from
those observed in G1, G2, and G3. In G1, all premolars
presented pulp tissue with normal histologic character-
istics, as observed in G3 and G4. Consequently, lack of
inflammatory response and no tissue disorganization
was observed for all specimens (Fig. 1, A and B). The
median of the dentin thickness for this experimental
group was 3.10 mm (mean ⫾ SD ⫽ 3.10 ⫾ 0.11 mm).
In G2, the coronary pulp tissue of the 3 bleached
incisors exhibited a wide zone of coagulation necrosis
(Fig. 1, C and D). Deposition of reactionary dentin was
seen in the root pulp of these incisors, which showed a
moderate inflammatory response mediated by mononu-
clear cells among dilated and congested blood vessels
(Fig. 1, E and F). In only 1 incisor, intense deposition
of reactionary dentin in the coronal and root pulp tissue
was observed. In that tooth, the root pulp exhibited mild
inflammatory response characterized by a few inflam-
matory mononuclear cells. The median of the dentin
thickness for this experimental group was 1.83 mm
(mean ⫾ SD ⫽ 1.82 ⫾ 0.08 mm). In the nonbleached
control groups G3 and G4, all premolars and incisors
exhibited normal pulp tissue. The pulp-dentin complex
exhibited tubular dentin and predentin, intact odonto-
de Souza Costa et al. e61
Group*
G2 G3 G4
1.90 2.80 1.69
1.73 3.22 2.02
1.79 3.02 1.80
1.86 — —
— — —
— — —
1.82 (0.08) 3.01 (0.21) 1.84 (0.17)
1.83 (1.74-189)b 3.02 (2.80-3.18)a 1.80 (1.69-1.94)b
blast layer, cell-free zone, cell-rich zone, and normal cen-
tral part of the pulp tissue (Fig. 2). The medians of the
dentin thickness for G3 and G4 were 3.02 mm (mean ⫾
SD ⫽ 3.01 ⫾ 0.21) and 1.80 mm (mean ⫾ SD ⫽ 1.84 ⫾
0.17 mm), respectively.
DISCUSSION
According to Wataha et al.,13 the risk caused by
dental materials to the dentin-pulp complex depends on
the capability of the components of these products to
diffuse across enamel and dentin to reach the pulp
tissue. Several studies have demonstrated the diffusion
of H2O2 through enamel and dentin,8,14 which is facil-
itated by its low molecular weight as well as its capac-
ity to denature tissue proteins.15 In addition, it has been
reported that the diffusion of H2O2 through enamel and
dentin increases as the concentration of this unstable
free radical in the bleaching gel also increases.6 In the
present in vivo study, the authors did not quantify or
identify the products released from the 38% H2O2
bleaching gel applied on the enamel in the pulp tissue.
However, it was demonstrated that the coronal pulp of
most (3 out of 4) of the bleached incisors exhibited
coagulation necrosis (Fig. 1, C and D). In this experi-
mental group, the mean enamel-dentin junction–pulp
distance was 1.82 ⫾ 0.08 mm. On the other hand, in the
control group G4, in which the incisors were not
bleached, the pulp tissue exhibited normal histologic
characteristics (Fig. 2, C-E). Therefore, it may be sug-
gested that toxic components released from the bleach-
ing agent were capable of diffusing through the thin
enamel and dentin present in the inferior incisors to
cause notable damage to the pulp tissue.
It has been demonstrated that the application of
bleaching agents on enamel increases the porosity of
this highly mineralized dental tissue owing to the dis-
ruption of matrix protein, which causes loss of struc-
tural components by free radical oxidation.16 In addi-
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e62 de Souza Costa et al. April 2010

Fig. 1. Pulp-dentin complex of sound lower human premolar (A and B) and incisors (C-F) submitted to in-office bleaching. A,
Note that both pulp horns of the premolar present normal histologic characteristics. H/E, ⫻32. B, High magnification of the pulpal
horn in A related to the tooth surface in which the bleaching gel was applied. Observe the tubular primary dentin, the defined
odontoblast layer (horizontal arrow), cell-free zone (vertical arrow), and the cell-rich zone (oblique arrow). No inflammatory
response, necrosis, or pulpal calcification can be seen. H/E, ⫻125. C, Dentin-pulp complex of a bleached lower incisor (tooth #3).
Observe the thickness of the dentin (mean 1.793 ␮m) below the buccal surface where the bleaching gel was applied. The pulp
horn exhibits a large zone of coagulation necrosis (N). H/E, ⫻32. D, High magnification of C. Note the transition border (arrows)
between the tubular dentin (TD) and the necrotic pulp tissue (N). H/E, ⫻125. E, Root pulp tissue of a bleached lower incisor which
exhibits notable deposition of reactionary dentin matrix. H/E, ⫻125. F, Detail of E. Note the tubular reactionary dentin matrix
(TRDM), which is poorly calcified, the defined predentin (P), and the remaining pulp tissue (PT) with some mononuclear cells
and a few congested blood vessels (arrows). H/E, ⫻250.

tion, the contact time of the bleaching agent with the
dental tissue influences the transenamel and transden-
tinal diffusion of bleaching components to reach the
pulpal space.3 The increase in hard dental tissue per-
meability may also play a role in postoperative sensi-
tivity or pain after bleaching therapies, which is the
most frequent adverse effect claimed by the patients
submitted to in-office vital tooth bleaching.10 There-
fore, it may be speculated that the pain claimed by the
volunteers in the present in vivo study after bleaching
the incisors was caused, at least in part, by the increase
of the permeability in the enamel and dentin. However,
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Volume 109, Number 4 de Souza Costa et al. e63

Fig. 2. Control groups. Dentin-pulp complex of unbleached lower sound premolar (A and B) and incisor (C-E). A, The coronal
pulps tissue exhibits normal histologic features. Masson trichrome, ⫻32. B, High magnification of the area indicated in A. Note
the pulp tissue with all defined histological zones. Masson trichrome, ⫻250. C, General view of the coronal pulp tissue. Masson
trichrome, ⫻32. D, High magnification of C. No pulp necrosis, inflammatory pulpal response, or significant change is observed
in this specific connective tissue. Masson trichrome, ⫻64. E, Detail of the coronal pulp tissue in D. Note the continuous
odontoblast layer (arrows) and the subjacent pulp tissue with pulp cells and blood vessels. Masson trichrome, ⫻125.

the diffusion of H2O2 to the pulp tissue may also be
involved in postoperative sensitivity or pain caused by
the toxic effects of this chemical agent to the pulp
cells.17 It is known that H2O2 and its degradation prod-
ucts, such as hydroxyl (OH⫺) ions, are reactive species
derived from oxygen, which may cause mutagenesis,
carcinogenesis, cell membrane damage by lipid peroxi-
dation, and protein fragmentation.18,19 Therefore, the
increase in the exogenous levels of these highly reac-
tive free radicals1,18 in contact with cells, as occurs
during tooth bleaching, may result in cell death and
reduced cell proliferation.20-23 These data may explain
the necrosis occurring in the pulp tissue after bleaching
the incisors as well as the postoperative pain reported
by the patients. However, future in vivo studies are
needed to clarify these histologic and clinical observa-
tions.
Vital teeth present dentinal fluid flow produced by
intrapulpal pressure and cytoplasmatic prolongations of
odontoblasts as well as other intratubular components,
which may impede the diffusion of the bleaching gel
components through the dentinal tubules. In addition,
the pulp tissue presents lymphatic drainage which is
capable of moving away toxic products that reach this
connective tissue. Furthermore, owing to the oxidative
stress generated by the presence of free radicals, the
defense system of the pulp cells is activated, releasing
several endogenous antioxidant agents, such as peroxi-
dases and catalases, which promote an enzymatic deg-
radation of H2O2 to avoid excessive tissue damage.24
However, it seems that the outward dentin fluid move-
ment, the complex network of lymphatic vessels
present in the pulp tissue, as well as the protective role
of the defense system of the pulp were not enough to
prevent coronal pulp necrosis when the bleaching agent
with 38% H2O2 was applied on the buccal surface of
lower sound incisors. Perhaps, the different pulpal re-
sponses observed in premolars (Fig. 1, A and B) and
incisors (Fig. 1, C-F) occurred because of the variable
thickness of enamel and dentin. It has been reported
that the dentin thickness plays an important role in the
protection of the pulp tissue against toxic products
released from dental materials.12,14 In the present in
vivo study, the decalcification of the teeth during the
laboratory process resulted in complete enamel loss.
Consequently, only the dentin thickness was micro-
scopically measured. The bleached premolars (G1) and
incisors (G2) presented mean DTs of 3.10 ⫾ 0.11 mm
and 1.82 ⫾ 0.08 mm, respectively. Therefore, it may be
suggested that the protective role of dentin against
diffusion of toxic components leached from the bleach-
ing agent with 38% H2O2 used in the present study

e64 de Souza Costa et al.
increased as a function of the thickness of this tubular
hard tissue. Considering the tooth bleaching procedures
commonly used in esthetic dentistry, it may also be
suggested that the intensity of pulp responses is in-
versely related to the thickness of the enamel. Because
the enamel is thicker in premolars than in incisors, it
may be speculated in the present investigation that the
thickness of enamel plays also an important role in
preventing H2O2 and other products leached by the
bleaching gel from reaching the pulp tissue. However,
this hypothesis needs further investigations. No pulp
damage in bleached premolars was reported by Rob-
ertson and Melfi.25 Those authors demonstrated that
disastrous pulp response in bleached premolars was
observed only when the bleaching agent was heated.
It is known that the continuous deposition of second-
ary and intratubular dentin over time increases the
thickness of this hard tissue and reduces the inner
diameter of the dentinal tubules. Both physiologic
mechanisms, which decrease the dentin permeability,
may impede the diffusion of bleaching agent compo-
nents across dentin to reach the pulp tissue. Therefore,
further in vivo studies are needed to evaluate if similar
pulpal damage, as demonstrated in the present investi-
gation for sound bleached incisors of young patients,
might also take place in teeth of older patients submit-
ted to in-office bleaching.
CONCLUSION
Based on the methodology used in this in vivo study,
it may be concluded that tooth bleaching with 38%
H2O2 for 45 minutes causes irreversible pulp damage in
lower incisors but not in premolars.
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Reprint requests:
Prof. Dr. Carlos Alberto de Souza Costa
Departamento de Fisiologia e Patologia
Faculdade de Odontologia de Araraquara—UNESP
Rua Humaitá, 1680 —Centro
CEP: 14801-903
Araraquara, SP
Brasil
casouzac@foar.unesp.br