[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.

63]

Review Article

Formocresol, still a controversial

material for pulpotomy: A critical
literature review
Shashidhar Chandrashekhar, Jyothi Shashidhar1
Departments of Conservative and Endodontics, and 1Pedodontics, Modern Dental College and Research Center, Indore, Madhya Pradesh, India

Address for correspondence: Dr. Shashidhar Chandrashekhar, 1663/56, 11th Main Road, Bank Colony, Siddaveerappa Extension, Davangere ‑ 577 004, Karnataka,
India. E‑mail: shashiendo6@gmail.com

ABSTRACT This paper reviews the history, clinical success and concerns regarding the safety of formocresol
as a primary molar pulpotomy medicament. The alternatives to formocresol are discussed and their
advantages and disadvantages are evaluated.

Keywords: Electrosurgical pulpotomy, formocresol, glutaraldehyde, laser surgery

INTRODUCTION success as well as compatibility between pulp and

If any field in pediatric dentistry is more controversial
than others, it is pediatric endodontics.[1] Pulp tissue is
a highly specialized connective tissue necessary for the
immune competence and sensation within a tooth, long
after dentinogenesis is completed.[2] The tissue, located
in a specific rigid environment, has a complex blood
flow[3] and is rich in cellular and neural elements. It is
very difficult for clinicians to diagnose the level of pulpal
inflammation.[2]
This is the reason why pulp therapy in dentistry,
particularly the pulpotomy procedure in pediatric
dentistry, has remained a controversial issue. The ideal
pulp dressing material after pulpotomy should leave
radicular pulp vital, healthy and enclosed within an
odontoblastic‑lined dentine chamber,[4] but such material
has not been found till now. An effective pulpotomy
medicament should show clinical and radiographic
Access this article online
Quick Response Code:
Website:
www.jresdent.org
DOI:
10.4103/2321-4619.143594
surrounding tissue physiologically.[5]
Formocresol
Formocresol has been used in dentistry since 100 years
and for deciduous teeth pulpotomy since 80  years.
The reparative, biologic approach to pediatric pulp
therapy is either devitalization approach of formocresol
pulptomy or pulpectomy. Formocresol was introduced
to treat non‑vital permanent teeth in the United States
by Buckley in 1904.[1] In 1930, Sweet introduced the
formocresol pulpotomy technique. Formocresol has
subsequently become a popular pulpotomy medicament
for primary teeth. Initially, the technique involved five
visits. Sweet reduced the number of visits over the
years, because of economic and behavior management
considerations.[1] Doyle et al.[6] used a two‑visit procedure
in their comparison study of formocresol and calcium
hydroxide. Within a few years, Spedding et al.[7] and
Redig[8] reported the results of a 5‑min formocresol
protocol, and since that time, complete mummification
has been abandoned by the profession.
By 1960, a single visit procedure was advocated.[9] Studies
have shown formocresol therapy to have a success rate
between 70% and 90%.[10] Histologic results have been
variable in contrast to the high clinical success rate.
Formocresol is still considered a gold standard by which
all new modalities are compared.[5]

114 • Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014

[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
Composition
The composition of Buckley’s formocresol is 19%
formaldehyde and 35% tricresol, 15% glycerin and
31% water base.[11] Glycerine is added to prevent the
polymerization of formaldehyde to para‑formaldehyde.
The presence of para‑formaldehyde causes clouding of
the solution.[5] One‑fifth dilution of Buckley’s formocresol
can be prepared by adding 30 ml of Buckley’s formocresol,
90 ml of glycerol and 30 ml of water.[11]
MECHANISM OF ACTION
Formocresol acts through the aldehyde group of
formaldehyde, forming bonds with the side groups of the
amino acids of both the bacterial proteins and those of the
remaining pulp tissue. It is therefore both a bactericidal
and devitalizing agent. It kills off and converts bacteria
and pulp tissue into inert compounds.[11] Its function
is to fasten the live pulps, maintaining them inert and
facilitating the conservation of deciduous tooth until
their physiologic fall. It has a potent antibacterial action
that justifies its use in long curative in endodontic
treatment.
With formocresol as the pulptomy medicament, a zone
of fixation usually is evident where the pulp is in direct
contact with the medicament. Coagulation necrosis of
the tissue occurs at the amputation site and is supported
by the fact that true coagulation necrosis is produced
by poisons such as phenol, formaldehyde or mercuric
chloride, which denatures the protein of the cells.[12] It has
also been shown that formocresol inactivates the oxidative
enzymes in the pulp tissue adjacent to the amputation
site. It may also have some effect on hyaluronidase
action. Therefore, the protein‑binding properties and the
inhibition of the enzymes that can break the pulp tissue
down together result in ‘fixation’ of the pulp tissue by
formocresol and render it inert and resistant to enzymatic
breakdown.[11] Farther away, where the concentration of
formocresol is decreased, there is a zone of poor cellular
definition and necrosis. Apical to this is a zone of chronic
inflammation, which blends into normal tissue.[6,13,14] In
contrast, Berger reported complete loss of vitality with
fibrous granulation tissue in the apical third of the root
canal.[15] In a study to know the effect of formocresol on
polymorphonuclear cells  (PMNs), the lysis of PMNs
was observed with high concentrations of formocresol.
An interesting finding with low concentrations of
formocresol was the significant stimulation of PMN
adherence. The authors postulate that stimulation of
PMNs by pulpotomy medicaments may contribute to the
chronic inflammatory changes seen with their use. Initial
stimulation followed by depressions is a well‑known
response of PMNs following activation by various
stimuli. Same activation‑deactivation phenomenon was
observed clearly with formocresol.[16]
Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014 • 115
Internal resorption may also result in teeth treated
with formocresol might be due to the severe damage
to the residual tissue, also destroying its capacity to
reabsorb. This may be attributed to inflammation of
the residual pulp. On the other hand, pulpotomy
treatment with formocresol in monkeys has been
associated with the formation of reparative dentin.[17,18]
Human studies have not reported the finding of
reparative dentin in association with the formocresol
pulpotomy. [19,20] This might be possibly due to the
production of reparative dentine on light stimulation
like any type of trauma, including formocresol of the
pulpal tissue of monkeys.[17]
PHARMACOKINETICS OF FORMOCRESOL
In addition to the clinical response, biologic effects
of formocresol should also be studied. Formocresol
is toxic to living tissues because of the formaldehyde
component. Formocresol applied to vital pulp tissue
is absorbed readily into the systemic circulation and
distributed throughout the body.[21] A portion of the
absorbed formocresol is metabolized and excreted by
the kidney and lungs.[21,22] The remaining formocresol
is tissue‑bound with the liver, kidney and lungs  the
predominant sites of tissue binding.
Pharmacokinetics of formaldehyde
Formaldehyde exposure occurs daily as it is
present in air, water and food. The World Health
Organization (WHO) has estimated daily consumption of
formaldehyde to be approximately 1.5-14 mg/day (mean,
7.8 mg/day).[23] Assuming a contribution of 9.4 mg/day
from food, 1 mg/day from inhalation and 0.15 mg/day
from water, an adult takes in 10.55 mg of formaldehyde
per day.[24] The estimated formaldehyde dose associated
with 1 pulpotomy procedure, assuming a 1:5 dilution of
formocresol placed on a no. 4 cotton pellet that has been
squeezed dry, is approximately 0.02-0.10 mg.[25]
Hileman has shown that endogenous levels of
metabolically produced formaldehyde range from
approximately 3-12  ng/g tissue.[26] This formaldehyde
is produced by amino acid metabolism, oxidative
d e m e t h yl a t i o n , a n d p u r i n e a n d p y r i m i d i n e
metabolism.[27] Exogenous formaldehyde is taken up
into the human body via ingestion, inhalation and
dermal exposure. Inhaled formaldehyde appears to
be readily absorbed by the upper respiratory tract, but
it is not distributed throughout the body because it is
rapidly metabolized.[28] Ingested formaldehyde is readily
absorbed by the gastrointestinal tract and exhibits little
subacute toxicity after oral exposure.[29] Exogenous
formaldehyde has a biologic half‑life of 1-1.5  minutes
and is quickly cleared from human plasma.[30]
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
Human cells manage formaldehyde exposure
physiologically through multiple pathways of
oxidation of formaldehyde to formate. Cytosolic
alcohol dehydrogenase, mitochondrial aldehyde
dehydrogenase, and glutathione‑dependent and
glutathione‑independent dehydrogenases are
important enzymes in the metabolism of formaldehyde
in hepatocytes, oral mucosa and nasal respiratory
mucosa.[25] Formate is the principal oxidative product
of formaldehyde. Formate is further oxidized to
c a r b o n d i o x i d e a n d wa t e r b y t h e a c t i o n o f
formyl‑tetrahydrofolate synthetase.[25] Formate might
be converted to a soluble sodium salt via alternative
pathways and excreted in the urine, or it might
be incorporated into biologic macromolecules via
tetrahydrofolate‑dependent, 1‑carbon biosynthetic
pathways.[25] Single C‑atoms are released during the
metabolism of formaldehyde and formate. These
C‑atoms deposit in 1 C‑atom pool, which in turn is used
in the biosynthesis of purine, pyrimidine and proteins.
Histological studies demonstrate the true biological
damage after formocresol treatment. Physiologically,
with the vascular damage, the balance between osmotic
pressure and hydrostatic pressure is disrupted in tissue.
As a result, there is absorption of inflammatory fluid
insult by pulp tissue and decrease in the osmotic pressure.
So hemostatic balance is re‑established.[31‑33] When this
occurs, the constricted pulp cavity must dissipate the
pressure changes. If this does not occur, pressure necrosis
of the pulp occurs. In addition, lymphatic and venous
vascular flow from the coronal pulp must dissipate this
excess inflammatory fluid. This excess is distributed
apically and to regional vascular vessels. Therefore, the
local insult results in systemic distribution.
Studies report that formaldehyde labeled with radioactive
carbon  (14C) was apparently distributed among the
muscle, liver, kidney, heart, spleen and lungs. The
quantities of radiolabeled chemical detected, however,
were very small (1% of the total administered dose).[22,34]
Myers et al.[21] and Pashley et al.[35] concluded that [14C]
formaldehyde is absorbed systemically from pulpotomy
sites and formaldehyde is distributed to distant sites, but
did not determine if the labeling of tissues occurred by
metabolic incorporation of the [14C] moiety of the labeled
formaldehyde into macromolecules.
Pharmacokinetics of cresol
The second active ingredient in formocresol, cresol, has
received little attention in investigations of formocresol
efficacy. Cresol has poor solubility, so it is assumed that
it does not enter systemic circulation.[36] Cresol is highly
lipophilic and has been shown to completely destroy
cellular integrity. This would allow deeper tissue fixation
by the formaldehyde component of formocresol.[36,37] No
116 • Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014
data exist regarding cresol metabolism or elimination in
humans or other mammals, and about environmental
sources of cresol to which humans might be exposed.
Benzyl alcohol is a by‑product of tricresol oxidation.[38]
Benzyl alcohol is oxidized rapidly to benzoic acid,
conjugated with glycine in the liver, and excreted as
hippuric acid. It has no carcinogenic or mutagenic
potential, and the allowable daily intake, as established
by WHO is 5 mg/kg.[39,40]
Concerns about formocresol
Concerns about the safety of formocresol have been
appearing in the dental and medical literature for more
than 20  years. Formaldehyde, a primary component
in formocresol, is a hazardous substance.[31] National
Institute for Occupational Safety and Health in USA
states if formaldehyde exposure occurs at a concentration
of 20 ppb  (parts per billion) or higher, it is instantly
dangerous to health and life.[41]
Studies on formocresol therapy have put the clinical
success rate between 70% and 90%. [5] But variable
histologic results were also reported in contrast to the
clinical success rate. Instead of preserving vital pulpal
tissue, chronic inflammation and necrotic tissue were
found.[5,14] Another problem with formocresol is its
systemic distribution from the pulpotomy site. Pruhs
et al. found a relationship between primary teeth
treated with formocresol and enamel defects in the
permanent successors. The allergenic and mutagenic
properties of formaldehyde have been demonstrated
in animal models, but not in humans. Cysts have also
been found to be associated with the pulpotomized
teeth.[5]
The study suggests that full strength formocresol (48.5%
of formaldehyde) absorbed from multiple pulpotomy
sites may initiate tissue injury in kidney and liver
of experimental animals. The author suggests that a
longitudinal study is needed to determine whether the
injured kidney and liver cells would recover as there is
only cell injury, and no evidence of onset of inflammatory
reaction. This study cannot make any direct clinical
implications regarding toxicity of formocresol.[22]
Mutagenicity, genotoxicity and cytotoxicity
Exposure of cells to formaldehyde leads to the formation
of DPX (DNA-protein cross‑links). The most common
types of DNA damage induced by formaldehyde
are clastogenic lesions, including sister chromatid
exchanges  (SCEs), micronuclei and chromosomal
aberrations, and deletions. It has been proposed that
formaldehyde could induce the development of DPX
at distant sites, but no convincing evidence has been
obtained from in vivo experimental studies.[24]
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
The recent research by Heck and Casanova showed
the development of DPX in nasal tissues and
upper respiratory tract associated with high dose
exposure of formaldhehyde.[42] DPX does not persist
in tissues for more than few hours and undergoes
spontaneous hydrolysis or active repair by proteolytic
degradation of cross‑linked proteins. So role of DPX
in formaldehyde‑induced carcinogenesis is again
questionable.[43]
Cytogenetic studies of lymphocytes from rodents
following formaldehyde inhalation with exposures
ranging from 0.5-1.5 ppm for 6 h/day for 5 days failed
to detect either chromosomal aberrations or SCEs at any
of the formaldehyde concentrations.[44]
In vitro experiments with a Chinese hamster cell line
found that DPX and SCE, as a result of formaldehyde
exposure, were associated with cytotoxicity, not
mutation.[45] In addition, no mutagenesis occurred in
cultured human lymphocytes below a formaldehyde
threshold of 5 µg/mL in the culture medium.[46]
In one of the dental studies that do not support
formaldehyde is a mutagenic, Zarzar et al. performed
formocresol pulpotomy on 20 children by using
Buckley’s original formula. Blood samples were
collected from each child immediately before and 24
hours after the pulpotomy. No statistically significant
differences were found between the two groups in
terms of chromosomal aberrations, chromatid breaks
or chromatid gaps. Also, Zarzar et al. concluded that
formocresol is not mutagenic.[47]
Ribeiro et al. reported two studies that assessed the
mutagenic potential of formocresol. With a mouse
lymphoma cell line, cultured human fibroblasts and a
series of formocresol dilutions similar to clinical doses,
these authors found that formocresol did not produce
detectable DNA damage and should not be considered
genotoxic.[48]
The investigations of root canal sealers that contain
formaldehyde and produce cytotoxicity are not
comparable with formocresol pulpotomy studies.
Because large quantities of formaldehyde are produced
from sealers than pulpotomy, large quantities of sealers
are used. Root canal sealer remains in root canal and
forms part of restoration and may lead to further release
of formaldehyde.[49]
It is summarized that DPX development demonstrated
only after a prolonged exposure to formaldehyde at
specific contact sites such as nasopharynx. A  minute
quantity used in pulpotomy for few minutes that will
produce distant site genotoxicity is not evidence‑based.[25]
Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014 • 117
Carcinogenicity
It is concluded that cancer develops after inhalation
of air with large concentrations of formaldehyde. The
cancer can occur after a long‑term direct contact with
susceptible tissues. The toxic effects on initial contact
sites like ulceration, hyperplasia and squamous
metaplasia may subsequently contribute to cancer.[50]
These high‑dose responses are unlikely to occur at
sites distant from the point of initial formaldehyde
contact (such as the bone marrow). Formaldehyde is
not delivered to these distant sites. Those who have
argued against the continued use of formocresol in
pediatric dentistry on the basis that “formaldehyde
causes cancer” have failed to recognize this very
important distinction.[25]
Health Canada and the Organization for Economic
Cooperation and Development have stated on the basis
of CIIT (Chemical Industry Institute for Toxicology
Centers for Health Research) research models that
“taking into account the extensive information on
its mode of action, formaldehyde is not likely to be
a potent carcinogen to humans under low exposure
conditions.”[51]
Two large American studies from National Cancer
Institute (NCI) of epidemiological investigations failed
to show any causal relationship between formaldehyde
and leukemia.[52,53]
In 2004, International Agency for Research on
Cancer  (IARC) reclassified formaldehyde as a known
carcinogen from human probable carcinogen,[54] but
according to them, it is an agent that can increase the
risk of cancer at some doses. They do not undertake
the dose response analyses and possible threshold. The
possibility that inhaled or ingested formaldehyde might
induce cancer at sites distant from the respiratory or
gastrointestinal tracts has been investigated in numerous
long‑term toxicity studies performed in rodents. [49]
Experimental and epidemiologic research do not support
the theory that inhaled or ingested formaldehyde might
induce distant site toxicity.[25]
The facts are that formaldehyde occurs naturally
throughout the body, there are multiple pathways
for detoxification, and only microgram quantities
of formaldehyde are applied to pulp tissues during
pulpotomy procedures for mere minutes. Considering
these facts, exposure of children to the formaldehyde
component of formocresol during a pulpotomy is
insignificant and inconsequential.
Immune sensitization
Pulpotomy in dogs demonstrated that histological
changes where foreign pulp protein is present, host’s
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
necrotic tissues were produced by pulp tissue on reaction
with formocresol. The B cells may produce antibodies
to foreign pulp protein and host necrotic tissue.
Further, non‑specific pro‑inflammatory mediators and
chemotactic cytokines can illicit further immune factor
responses. One response is osteogenic activating factor
that destroys bone. This has not been quantified in either
children or adults.[55]
Experiment on dogs showed that formocresol produces
antigenic activity in pulp tissue.[56] Rolling and Thulin
found no increase in either immune response or
allergic reactions in 128 children who had undergone
formocresol pulpotomy.[57] A Canadian study of urea
formaldehyde foam insulation from products in the
homes of asthmatic subjects found that its long‑term
exposure had no effect on immunologic responses.[58]
Doi et al. found that there is no clinical relevance of
formaldehyde‑specific immunoglobulin E. Hence, the
suggestion that formocresol “sensitizes” children has
not been supported.[59]
Comparing formocresol with other materials
Formocresol versus glutaraldehyde
In recent years, glutaraldehyde has been proposed as an
alternative to formocresol based on its superior fixative
properties, self‑limiting penetration, low antigenicity,
low toxicity and elimination of cresol.[1] It is a colorless
solution that has a mild odor and a boiling point of 183°C
to 187°C, is soluble in water, and produces mild acidity
on contamination.[9] Glutaraldehyde is a chemically
bifunctional reagent, which forms strong intra‑  and
intermolecular protein bonds, leading to superior
fixation by cross‑linkage.[9] Glutaraldehyde produces a
zone of tissue fixation where it is in direct contact with
the pulp, while apical to this is a zone of normal tissue
with few inflammatory cells.[60,61] It has been observed
that inadequate fixation leaves a deficient barrier to
sub‑base irritation, resulting in internal resorption.[62,63]
Penetration into the surrounding peri‑apical tissue is
limited primarily by protein cross‑linkage formation.
Thus, systemic distribution of glutaraldehyde is
limited.[64] Glutaraldehyde is less necrotic, dystrophic,
cytotoxic and antigenic, is a better bactericide, and fixes
the tissue instantly.[9]
Glutaraldehyde appears to produce tissue fixation
without causing tissue necrosis at high concentrations.
Although it depresses PMN adherence at intermediate
concentrations, it does not seem to stimulate PMN
adherence and cause inflammatory tissue damage at
low concentrations.[16]
Prakash et al. concluded that glutaraldehyde is better
fixative and less toxic agent than formocresol. In this
study, they compared the clinical and radiological
118 • Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014
effects of formocresol and glutaraldehyde pulpotomies
in various exposed vital human primary molars.[65] The
2% glutaraldehyde compound was promising when
compared to ferric sulfate and formocresol in an in vivo
study. The only limitations of glutaraldehyde are
instability due to short shelf‑life and it has to be freshly
prepared. In this study, the clinical and radiographic
success of formocresol, glutaraldehyde and ferric
sulfate were compared as a pulpotomy medicament in
primary molars at 3‑month intervals over 1 year. Internal
resorption was found in all the medicaments. Clinical
success was higher than the radiological success.[66]
One study failed to justify recommendation of 2%
buffered glutaraldehyde solution as a substitute to
formocresol as failure was observed within 6  months
of treatment and failure rate was increased even after
and up to 25 months. Internal resorption and external
resorption were listed as failures. Resorption rate of
pulpotomized teeth was similar to that of other teeth.[67]
Long‑term (36  months) success rates of four different
glutaraldehyde preparations  (2%‑buffered and
unbuffered, 5%‑buffered and unbuffered) as a pulpotomy
agent in pulp exposed primary molars were evaluated.
The 5% buffered solution group showed highest success
rate, whereas 5% unbuffered solution showed the lowest,
but as such there was no significant difference found
among the four groups. The canal obliteration was noted
in 22 treated teeth. The relative high failure rate in this
long‑term follow‑up indicates that clinicians should be
cautious before extensively using glutaraldehyde as
pulpotomy agent.[68]
FORMOCRESOL VERSUS
ELECTROSURGICAL PULPOTOMY
Another form of non‑chemical devitalization developed
is electrosurgical pulpotomy.[69] It is a method of cutting
and coagulating soft tissues by means of high‑frequency
radio waves passing through the tissue cells. The
advantages of electrosurgical pulpotomy are similar.[70]
The self‑limiting, pulpal penetration is only a few cell
layers deep. There is good visualization and homeostasis
without chemical coagulation or systemic involvement.
It is less time‑consuming than the formocresol approach.
Electrocautery carbonizes and heat denatures pulp and
bacterial contamination. It may not be suitable if apical
root resorption has occurred.[71] Remarkably, Mack
and Dean[70] reported a very high success rate with the
technique.
Studies show that there is no significant difference
between clinical and radiographic success rates for
electrosurgical and formocresol pulpotomies.[72,73] But
electrosurgery is considered as sensitive technique.[74]
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
Oztas et al. reported that formocresol pulpotomy technique
is histopathologically superior to electrosurgery
pulpotomy technique, as they found presence of
inflammation, fibrosis, necrosis and resorption.
[74]
On the other hand, El‑Meligy et al. showed that
teeth treated by electrosurgery pulpotomy exhibited
less histopathological reaction than formocresol
pulpotomy.[20]
Electrosurgery pulpotomy with either mechanical
coronal pulp removal or electrical coronal pulp
removal induces formation of reparative dentin. This
is in the form of bridging at the pulpal amputation
sites or along the canal walls. It indicates the present
healthy vital pulp efforts to heal the area of insult.[17,74]
This technique also increases the fibroblastic activity
at the middle and apical portions of roots with early
resorption,[17,74] as pulp tissue tries to renew itself with
proliferation of fibroblasts.
On the basis of the use of electrosurgical current
intensity, there is a chance of peri‑apical or furcal
involvement. Ruemping et al. used low intensity
current for electrosurgical pulpotomy during
their research so there was no peri‑apical or furcal
involvement.[18]
In case of electrosurgery, internal resorption was noted
after 4  weeks. This is due to the excess amount of
lateral heat that can accumulate, causing necrosis and
resorption. Heat transfer through accessory canals on
pulpal chamber floor of molars was responsible for
internal resorption. Later, intense inflammatory cells
were observed at coronal third of pulp canals and
complete healing cannot be achieved in the absence of
dentinal bridges.[20]
FORMOCRESOL VERSUS LASER SURGERY
The carbon dioxide laser has wide applications in oral
and general surgery procedures involving soft tissue.[75]
The laser emits an infrared beam at a wavelength of
10.6  m, has an affinity for water, and is capable of
producing well‑localized cautery to soft tissue. Tissue
is removed by ablation through conversion of the laser
beam to heat.[76] Based on these characteristics the carbon
dioxide laser appears to have promise as an alternative
for pulpotomy therapy.
A study conducted to evaluate the response of the
human primary pulp to the carbon dioxide laser and
formocresol for vital pulp therapy showed that there
were no significant differences between the formocresol
and laser groups with respect to symptomatic, clinical
or radiographic findings. The histologic observations in
this study revealed three interesting effects. First, the
Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014 • 119
laser treatment was at least as effective in minimizing
post‑treatment inflammation as the formocresol
treatment. Second, there was no statistically significant
recovery from inflammation between the 28‑ and 90‑day
observation period in either the laser or formocresol
group. Third, there was a strong and statistically
significant inverse correlation between the energy used
during the respective laser pulpotomies and the degree
of inflammation observed at 28 days.[76]
The histological response of dental pulp after different
types of laser irradiation was evaluated in some studies.
The results revealed that laser irradiation caused
carbonization, necrosis and infiltration of inflammation
cells, edema and hemorrhage in the pulp tissue.[77,78]
The pulp can predictably heal itself when the temperature
does not raise more than 5.5oC above physiological
baseline. The higher energy created a thicker char layer
over the remaining pulp, which in some way had a
favorable effect in reducing the initial inflammatory
response in residual pulp.[79]
Laser irradiation was effective for the growth of fibroblast
and induced suppressive effects for macrophage. In
addition, effects of laser irradiation on vital pulpotomy
were investigated. It was observed that laser irradiation
induced enhancement of calcification in wound surface
and stimulated formation of calcified tissue. These
observations indicate that laser irradiation is a useful
method for vital pulpotomy.[80]
FORMOCRESOL VERSUS FERRIC SULFATE
Monsel’s solution, which is a 20% ferric sub‑sulfate, is
widely used as a strong styptic agent in skin and mucosal
biopsies.[66] Ferric sulfate is a non‑aldehyde chemical.
It controls the pulpal hemorrhage and thus prevents
the problems encountered due to clot formation and
minimizes the inflammation and internal resorption.
Shaw et al. (   1987) also found reversible damage to the
connective tissue adjacent to the sulcular gingiva after
application of ferric sulfate. In contact with the blood,
ferric ions form a ferric complex and the membrane of
this complex seals the cut blood vessels mechanically
and provides hemostasis and an agglutinated protein
complex, which produces a blood clot that occludes the
capillary orifices. The hemostatic properties of ferric
sulfate and the favorable pulpal response make it a
promising medicament for pulpotomy.[5]
A clinical research was done by Fie et al. to compare
the clinical and radiographic success of ferric sulfate
and formocresol as pulpotomy medicaments. They
demonstrated that ferric sulfate was clinically and
radiographically successful as a pulpotomy medicament
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
in primary teeth. At the one‑year recall, the success rate
of the ferric sulfate group was actually greater than that
of the traditional formocresol pulpotomy group. In this
study, samples were small and recall period was short.
Although the ferric sulfate technique appeared successful
histologically, the long‑term effect of this drug on the
teeth and the rest of the body was not addressed.[5]
In this study, they used zinc oxide eugenol as a base
material over treated pulp stumps but it is not an ideal
choice as eugenol may irritate the underlying pulpal
tissue. Since formocresol is said to “mummify” or fix
the pulpal tissue in root canals, pulp tissue under this
agent may not be affected by the zinc oxide eugenol.
Garcia‑Godoy et al. found less severe inflammation when
zinc oxide eugenol was placed on formocresol‑treated
pulps.[81] Ferric sulfate may function passively. Since
ferric sulfate is not a fixative agent, the base in direct
contact with the pulpal surface may play an important
role in the healing process. Bases that are inert may
stimulate pulp cell attachment and provide more rapid
and less inflammatory wound healing.[82] The possible
combination of ferric sulfate with different base materials
is certainly worthy of further investigation.
In case of chronic coronal pulpitis, even though tooth is
a good candidate for pulpotomy clinically, inflammation
extension makes it questionable for the procedure. At that
time, formocresol because of its property of mummifying
the remaining pulpal tissue makes the tooth to retain it
for a longer time. Ferric sulfate is nonfixative but has
bacteriostatic properties and may not act on underlying
inflammatory tissue. Thus, it may not be beneficial in
similar situation.[83]
Additional histologic studies are needed to determine
pulpal response to this material. Studies should
determine the potential effects on underlying permanent
teeth and the nature of any absorption and systemic
distribution of ferric sulfate from pulpal tissues.[5]
Jones and Duggal compared the pulpal reactions to
ferric sulfate and formocresol pulpotomies in primary
molars with inflamed pulps of baboons. This study has
shown that both pulpotomy agents produced apparently
successful vital pulpotomies, but both were associated
with pulp necrosis and apical abscesses at a histological
level. No literature has given specific guidelines for
histological success after pulpotomy.[84]
Ideally, healing in primary pulp should be good. The
pulps of primary teeth are known to be quite resilient
and are cell rich and fiber poor.[85] The most important
part of healing of an exposed pulp is formation of a
dentinal bridge. Such finding is rare in the above study
as formocresol destroys those cells that produce healing,
120 • Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014
and the effect of ferric sulfate is unclear apart from
hemostatic properties.
This study suggested that the primary teeth appear to be
clinically functional and not associated with radiographic
changes even though pathological changes can be
seen histologically. Both ferric sulfate and formocresol
pulpotomies produce favorable clinical results in human
primary teeth, which is clear from clinical studies.[5,86,87]
The highest clinical and radiographic success rate (100%)
of ferric sulfate was reported by Prabhu and Munshi.[88]
Another short‑term  (20  months) study showed 100%
clinical and 97.2% radiographic success rate for both
ferric sulfate and formocresol.[89]
There is a study comparing the effects of ferric sulfate
and full strength formocresol as pulpotomy agents in
primary human molars in a long‑term (4 years) follow‑up
clinical trial, which assessed the succedaneous premolar
teeth for any decalcification, abnormal morphology or
any other defects as well. They found overall success rate
of ferric sulfate was almost similar to formocresol and
no delay in eruption of premolars and abnormality were
observed. So the authors concluded that ferric sulfate is
a nontoxic agent to replace formocresol.[90]
It has been stated that success rates may be more
dependent upon the correct choice of teeth, assessment
of bleeding from amputated pulp stumps and adequate
coronal seal as a candidate for vital pulpotomies than
on other factors. Inconsistencies of technique and
microleakage of the restorative material (IRM) may also
limit the success of pulpotomy.
In most of the studies, zinc oxide eugenol is used as
a sub‑base. Zinc oxide is in direct contact with pulpal
tissue, which may cause chronic inflammation and
necrosis. This may lead to internal resorption. Hume
stated that formocresol would fix tissue that may act as a
barrier to the eugenol, but with ferric sulfate the clot is the
only entity separating the eugenol from vital tissues.[91]
Some authors have stated that formocresol pulpotomies
could be considered clinically successful therapies,
as they preserve extremely carious primary molars
until their normal exfoliation.[91,92] The main objective
of pulpotomies must be to maintain the vitality of the
majority of the radicular pulp. The authors who advocate
pulpotomies should be to keep the pulp of primary teeth
vital until their normal physiological resorption, rather
than just “maintaining” teeth.[93]
Formocresol versus calcium hydroxide
Calcium hydroxide was the first agent used in
pulpotomies that demonstrated any capacity to
induce regeneration of dentin. [94] The high pH of
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
calcium hydroxide wounds the pulp in a manner
that permits the intrinsic reparative cascade to begin.
Unfortunately, the stimulus evoked by this compound
is delicately balanced between one of repair and
resorption. The study by Magnusson demonstrated
how often the balance is tilted toward the destructive
pathway.[95]
Schröder emphasized on the importance of avoiding
a blood clot between the amputation site and calcium
hydroxide for clinical success.[96] Calcium hydroxide
adequately controls pulpal hemorrhage, to permit
good contact between medicament and pulpal tissue.
This seems to be important in the prevention of internal
resorption, post‑pulpotomy.[97]
A study conducted to compare the clinical and
radiological outcomes following single‑visit vital pulp
therapy techniques, using two different materials,
formocresol and calcium hydroxide in cariously exposed
primary molar teeth. This investigation confirms the
clinical efficacy of a one‑fifth dilution of Buckley’s
formocresol as an agent in pulp treatment of cariously
exposed, vital primary molar teeth. However, calcium
hydroxide in its pure, powder form is a clinically
acceptable alternative when combined with strict
selection criteria for this method of restorative care. There
was a statistically insignificant difference in successful
clinical and radiological outcome between the two
treatment groups.[98]
The status of radicular pulp tissue may have more
bearing upon the clinical outcome following calcium
hydroxide pulp therapy, since this agent relies on the
tissue itself being able to recover sufficiently to heal, with
or without the formation of a calcific barrier. Therefore,
calcium hydroxide may be more technique sensitive
than formocresol. The inflammatory status of radicular
pulp tissue at the time of treatment, providing effective
coronal seal, is thought to be important to a successful
outcome.
Markovic et al. reported the presence of a dentine
bridge above the pulp amputation site radiographically
in 47% of pulpotomized teeth using calcium
hydroxide. [99] Heilig et al. was performed calcium
hydroxide pulpotomy in 17 carious primary molars
using alternative method of hemorrhage control
i.e., aluminum chloride. This study suggests that the
aluminum chloride‑calcium hydroxide pulpotomy
may be a viable alternative to formocresol pulpotomies
in the primary dentition. Although these findings
encourage continued research, including a long‑term
follow‑up, a histologic study is indicated.[97]
Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014 • 121
Formocresol versus mineral trioxide
aggregate
Mineral trioxide aggregate (MTA) is a fine hydrophilic
powder developed by Mahmoud Torabinejad in Loma
Linda University. It consists of tricalcium silicate,
tricalcium aluminate, tricalcium oxide, silicate oxide and
bismuth oxide.[100] The US Food and Drug Administration
approved MTA in 1998 as a therapeutic endodontic
material for humans.[101]
Torabinejad et al., Bates et al. and Fischer et al. evaluated
the sealing ability of MTA in root canals.[101] MTA is
currently being used in pulp therapy and has been
shown to provide an enhanced seal over the vital pulp
and is nonresorbable. Furthermore, MTA has superior
biocompatibility and is less cytotoxic than other materials
currently used in pulp therapy.
Previous studies showed that MTA stimulated the
release of cytokines and production of interleukin
and induced hard tissue formation. Schmitt et al.
reported that Tulsa Dental provides MTA as ProRoot.
The material can be placed in the tooth with the Tulsa
carrier, an amalgam carrier, Messing gun or a hand
instrument.[101] Advantage of MTA is that it needed less
time for procedures.[102] Some of the main disadvantages
are discoloration,[103] costs and accessibility, which
may block worldwide distribution of MTA where
formocresol is relatively inexpensive and have global
accessibility. MTA has also shown to revascularize and
promote dentin‑like tissue formation in several clinical
situations.[63‑65]
A study comparing three pulpotomy agents in preschool
children suggested MTA success rates were less than
100%. Success rates of 100% can be attributed to smaller
sample size or wider range of patients (5-12 years), which
can reduce validity and reliability of results. Younger
patients showed high radiographic failure rates after 12
months such as external resorption. This is due to wider
pulp canals in younger teeth, which can facilitate the
transfer of stimulatory factors.[100]
A histological study to know the effects of gray
and white MTA on amputated pulp tissue, along
with formocresol as a gold standard suggests that it
preserves and regenerates both hard and soft tissues.
The nearly normal pulp architecture was found to
be intact and continuous odontoblastic layer was
seen. While cases treated with white MTA showed
dentine bridge formation along with inflammatory
cells and areas of partial necrosis, more clinical and
radiographic failures were seen with white MTA. The
minor difference in composition between gray and
white groups accounts for the differences in pulpotomy
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
success rates. The gray MTA contains tetracalcium
aluminoferrite while it is absent in white MTA.[101]
The clinical success of formocresol is attributed to its
bactericidal characters even though it shows poorly
calcified secondary dentin bridging along with complete
necrosis and inflammatory cells.
The normal consequence of pulp treatment is internal
resorption. It was seen in both formocresol and MTA
groups but no explanation for MTA was given as this
consequence is not seen in MTA cases.[102]
Six clinical studies comparing formocresol and MTA
were presented by Fuks.[104] It was noted that five out of
six of these illustrated that MTA was more successful
than formocresol. In the last study they found equal
success between the products.[105] Further, they showed
the ability of MTA to elicit dentin bridges beneath the
pulpotomy site.
Immunologic testing needs to be performed to know the
biological sequelae of MTA. Further studies about its
long‑term efficacy, biological and clinical use should be
done. Nevertheless, the evidence is becoming stronger
that MTA is biologically superior and more clinically
successful than formocresol. There are additional issues
with MTA that need to be rectified. MTA can be difficult
to use and requires a learning curve. Recent concern rose
about the toxicity of aluminum oxide, which is present
in MTA when absorbed systemically.[106]
CONCLUSION
It is highly unlikely that formocresol, when judiciously
used, is genotoxic or immunotoxic or poses a cancer
risk to children who undergo one or more formocresol
pulpotomy procedures. Definitive data to support this
hypothesis are lacking, however, such evidence is needed
before definitive conclusions can be reached.
In keeping with the accepted therapeutic principles,
pediatric dentists who wish to continue to use formocresol
should apply the lowest dose possible for the shortest
time possible to obtain the desired effect. To that end, a
1:5 dilution of Buckley’s formocresol is recommended.
On the basis of the evidence presented in this review,
the risk of cancer, mutagenesis or immune sensitization
associated with the proper use of formocresol in pediatric
pulp therapy can be considered inconsequential.
Until a biologic and reparative alternative has been
identified that is clearly and reproducibly superior to
formocresol, there are no scientific or toxicologic reasons
to discontinue its use in pediatric dentistry. When used
judiciously, formocresol is a safe medicament.
122 • Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014
REFERENCES
1. Ranly DM. Pulpotomy therapy in primary teeth: New modalities
for old rationales. Pediatr Dent 1994;16:403‑9.
2. Levin LG. Pulpal regeneration. Pract Periodontics Aesthet Dent
1998;10:621‑4.
3. Ibricevic H, Heyeraas KJ, Pasic Juhas E, Hamamdzic M,
Djordjevic N, Krnic J. Identification of alpha 2 adrenoceptors in
the blood vessels of the dental pulp. Int Endod J 1991;24:279‑89.
4. Ranly DM, García‑Godoy F. Reviewing pulp treatment for primary
teeth. J Am Dent Assoc 1991;122:83‑5.
5. Fei AL, Udin RD, Johnson R. A clinical study of ferric sulfate as a
pulpotomy agent in primary teeth. Pediatr Dent 1991;13:327‑32.
6. Doyle WA, McDonald RE, Mitchell DF. Formocresol versus
calcium hydroxide in pulpotomy. J Dent Child 1962;29:86‑97.
7. Spedding RH, Mitchell DF, McDonald RE. Formocresol and
calcium hydroxide therapy. J Dent Res 1965;44:1023‑34.
8. Redig DF. A comparison and evaluation of two formocresol
pulpotomy technics utilizing “Buckley’s” formocresol. J Dent Child
1968;35:22‑30.
9. Dummett CO Jr, Kopel HM. Pediatric endodontics. In: Ingle J,
Bakland L, editors. Endodontics. 5th ed. Hamilton: BC Deker;
2002.Vol 1, p. 876, 885‑6.
10. Wright FA, Widmer RP. Pulpal therapy in primary molar teeth:
A retrospective study. J Pedod 1979;3:195‑206.
11. Restorative techniques in paediatric dentistry,. In: Duggal MS,
editor. 2nd ed.; 2002. p. 50‑63.
12. Florey L. General pathology. 4th ed. Philadelphia: WB Saunders
Co,; 1970.Vol. 37, p. 434.
13. Rolling I, Hasselgren G, Tronstad L. Morphologic and enzyme
histochemical observations on the pulp of human primary molars
3 to 5 years after formocresol treatment. Oral Surg Oral Med Oral
Pathol 1976;42:518‑28.
14. Rolling I, Lambjerg‑Hansen H. Pulp condition of successfully,
formocresol‑treated primary molars. Scand J Dent Res
1978;86:267‑72.
15. Berger JE. Pulp tissue reaction to formocresol and zinc oxide
eugenol. ASDC J Dent Child 1965;32:13‑28.
16. Seow WK, Thong YH. Modulation of polymorphonuclear leukocyte
adherence by pulpotomy medicaments: Effects of formocresol,
glutaraldehyde, eugenol, and calcium hydroxide. Pediatr Dent
1986;8:16‑21.
17. Shulman ER, McIver FT, Burkes EJ Jr. Comparison of
electrosurgery and formocresol as pulpotomy techniques in
monkey primary teeth. Pediatr Dent 1987;9:189‑94.
18. Ruemping DR, Morton TH Jr, Anderson MW. Electrosurgical
pulpotomy in primates: A comparison with formocresol pulpotomy.
Pediatr Dent 1983;5:14‑8.
19. El‑Kateb MA. A comparative study and evaluation of formocresol
and glutaraldehyde pulpotomies on primary molars PhD Thesis.
Alexandria University; 1987.
20. El‑Meligy O, Abdalla M, El‑Baraway S, El‑Tekya M, Dean JA.
Histological evaluation of electrosurgery and formocresol
pulpotomy technique in primary teeth in dogs. J Clin Pediatr Dent
2001;26:81‑5.
21. Myers DR, Shoaf HK, Dirksen TR, Pashley DH, Whitford GM,
Reynolds KE. Distribution of 14C‑formaldehyde after pulpotomy
with formocresol. J Am Dent Assoc 1978;96:805‑13.
22. Myers DR, Pashley DH, Whitford GM, McKinney RV. Tissue
changes induced by the absorption of formocresol from pulpotomy
sites in dogs. Pediatr Dent 1983;59:6‑8.
23. World Health Organization. Formaldehyde: Environmental
health criteria 89, International Programme on Chemical Safety,
Geneva, 1989. Available from: www.who.int/Ipcs/publications/
ehc/ehc_numerical/en/[Last accessed on 2006 Mar 13].
24. Federal‑Provincial‑Territorial Committee on Drinking Water.
Formaldehyde: Guidelines for Canadian drinking water quality—
supporting documents. Available from: www.hc‑sc.gc.ca/
ewh‑semt/pubs/water‑eau/doc_sup‑appui/index_e.html [Last on
accessed 2006 Mar 13].
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
25. Milnes AR. Is formocresol obsolute? A fresh look at the evidence
concerning safety issues. J Endod 2008;34:S40‑6.
26. Formaldehyde: Assessing the risk. Environ Sci Technol
1984;18:216‑21a.
27. Squire RA, Cameron LL. An analysis of potential carcinogenic
risk from formaldehyde Regul Toxicol Pharmacol 1984;4:107‑29.
28. Heck HD, Casanova‑Schmitz M, Dodd PB, Schachter EN,
Witek TJ, Tosun T. Formaldehyde (CH2O) concentrations in the
blood of humans and Fischer‑344 rats exposed to CH2O under
controlled conditions. Am Ind Hyg Assoc J 1985;46:1‑3.
29. Johannsen FR, Levinskas GJ, Tegeris AS. Effects of formaldehyde
in the rat and dog following oral exposure. Toxicol Lett
1986;30:1‑6.
30. Bhatt HS, Lober SB, Combes B. Effect of glutathione depletion on
aminopyrine and formaldehyde metabolism. Biochem Pharmacol
1988;37:1581‑9.
31. Kim S, Liu M, Simchon S, Dorscher‑Kim JE. Effects of selected
inflammatory mediators in blood flow and vascular permeability
in the dental pulp. Proc Finn Dent Soc 1992;88 Suppl 1:387‑92.
32. Van Hassell HJ. Physiology of the human dental pulp. Oral Surg
Oral Med Oral Pathol 1971;32:126‑34.
33. Heyeraas KJ, Kvinnsland I. Tissue pressure and blood flow in pulpal
inflammation. Proc Finn Dent Soc 1992;88 Suppl 1:393‑401.
34. Ranly DM. Assessment of the systemic distribution and toxicity
of formaldehyde following pulpotomy treatment: Part one. J Dent
Child 1985;52:4331‑4.
35. Pashley EL, Myers DR, Pashley DH, Whitford GM. Systemic
distribution of 14C‑ formaldehyde from formocresol‑treated
pulpotomy sites. J Dent Res 1980;59:602‑8.
36. Ranly DM. Formocresol toxicity: Current knowledge. Acta Odontol
Pediatr 1984;5:93‑8.
37. Loos PJ, Hans SS. An enzyme histochemical study of the effect
of various concentrations of formocresol on connective tissues.
Oral Surg Oral Med Oral Pathol 1971;31:571‑85.
38. Gruber C. The pharmacology of benzyl alcohol and its esters.
J Lab Clin Med 1923;9:15.
39. International Programme on Chemical Safety. Environmental
health criteria 89: Formaldehyde. Available from: http://www.
inchem.org/documents/ehc/ehc/ehc89.htm [Last accessed on
2007 Mar 13].
40. U.S. Environmental Protection Agency. Integrated risk information
system: Tricresol (CASRN 1319‑77‑77‑3). Available from:
http://www.epa.gov/iris/subst/0030.htm [Last accessed on
2007 Nov 12].
41. The National Institute for Occupational Safety and Health (NIOSH)
Formaldehyde. Available from: http://www.tricornet.com/nioshdbs/
idlh/50000.htm [Last accessed 2006 on Mar 13].
42. Heck H, Casanova M. Pharmacodynamics of formaldehyde:
Applications of a model for the arrest of DNA replication by
DNA‑protein cross‑links. Toxicol Appl Pharmacol 1999;160:86‑100.
43. Quievryn G, Zhitkovich A. Loss of DNA‑protein crosslinks from
formaldehyde exposed cells occurs through spontaneous
hydrolysis and an active repair process linked to proteosome
function. Carcinogenesis 2000;21:1573‑80.
44. Kligerman AD, Phelps MC, Erexson GL. Cytogenetic analysis of
lymphocytes from rats following formaldehyde inhalation. Toxicol
Lett 1984;21:241‑6.
45. Crosby RM, Richardson KK, Craft TR, Benforad KB, Liber HL,
Skopek TR. Molecular analysis of formaldehyde‑induced
mutations in human lymphoblasts and E. coli. Environ Mol
Mutagen 1988;12:155‑66.
46. Kreiger RA, Garry VF. Formaldehyde‑induced cytotoxicity and
sister‑chromatid exchanges in human lymphocyte cultures. Mutat
Res 1983;120:51‑5.
47. Zarzar PA, Rosenblatt A, Takahashi CS, Takeuchi PL,
Costa Junior LA. Formocresol mutagenicity following primary
tooth pulp therapy: An in vivo study. J Dent 2003;31:479‑85.
48. Ribeiro DA, Scolastici C, De Lima PL, Marques ME,
Salvadori DM. Genotoxicity of antimicrobial endodontic
compounds by single cell gel (comet) assay in Chinese hamster
Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014 • 123
ovary (CHO) cells. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 2005;99:637‑40.
49. Huang TH, Ding SJ, Hsu TZ, Lee ZD, Kao CT. Root canal
sealers induce cytotoxicity and necrosis. J Mater Sci Mater Med
2004;15:767‑71.
50. Formaldehyde. IARC Monogr Eval Carcinog Risks Hum
1995;62:217‑375.
51. Organization for Economic Development and Cooperation,
Screening Information Data Set, Initial Assessment Profile.
Available from: http://www.oecd.org/dataoecd/24/22/31744923.
pdf [Last accessed on 2007 Mar 13].
52. Pinkerton LE, Hein MJ, Stayner LT. Mortality among a cohort of
garment workers exposed to formaldehyde: An update. Occup
Environ Med 2004;61:193‑200.
53. Coggon D, Harris EC, Poole J, Palmer KT. Extended follow‑up
of a cohort of British chemical workers exposed to formaldehyde.
J Natl Cancer Inst 2003;95:1608‑15.
54. IARC, WHO. IARC classifies formaldehyde as carcinogenic to
humans: Press release no. 153. Available from: www.iarc.fr/ENG/
Press_Releases/archives/pr153a.html [Last accessed on 2006
Mar 13].
55. Block R. Are you still using formocresol? An update. J Tenn Dent
Assoc 2009;89:14‑7.
56. Block RM, Lewis RD, Sheats JB, Burke SG. Antibody formation
to dog pulp tissue altered by formocresol within the root canal.
Oral Surg Oral Med Oral Pathol 1978;45:282‑92.
57. Rolling I, Thulin H. Allergy tests against formaldehyde, cresol,
and eugenol in children with pulpotomized primary teeth. Scand
J Dent Res 1976;84:345‑7.
58. Pross HF, Day JH, Clark RH, Lees RE. Immunologic studies
of subjects with asthma exposed to formaldehyde and
urea‑formaldehyde foam insulation (UFFI) off products. J Allergy
Clin Immunol 1978;79:797‑810.
59. Doi S, Suzuki S, Morishita M, Yamada M, Kanda Y, Torii S, et al.
The prevalence of IgE sensitization to formaldehyde in asthmatic
children. Allergy 2003;58:668‑71.
60. Tagger E, Tagger M. Pulpal and periapical reactions to
glutaraldehyde and paraformaldehyde pulpotomy dressing in
monkeys. J Endod 1984;10:364‑71.
61. Kopel HM, Bernick S, Zachrisson E, DeRomero SA. The effects
of glutaraldehyde on primary pulp tissue following coronal
amputation: An in vivo histologic study. ASDC J Dent Child
1980;47:425‑30.
62. Garcia‑Godoy F, Ranly DM. Clinical evaluation of pulpotomies with
ZOE as a vehicle for glutaraldehyde. Pediatr Dent 1987;9:144‑6.
63. Lloyd JM, Seale NS, Wilson CF. The effects of various
concentrations and lengths of application of glutaraldehyde on
monkey pulp tissue. Pediatr Dent 1988;10:115‑20.
64. Sun HW, Feigal RJ, Messer HH. Cytotoxicity of glutaraldehyde and
formaldehyde in relation to time of exposure and concentration.
Pediatr Dent 1990;12:303‑7.
65. Prakash C, Chandra S, Jaiswal JN. Formocresol and glutaraldehyde
pulpotomies in primary teeth. J Pedod 1989;13:314‑22.
66. Havale R, Anegundi RT, Indushekar K, Sudha P. Clinical and
radiographic evaluation of pulpotomies in primary molars with
formocresol, glutaraldehyde and ferric sulphate. Oral Health Dent
Manag 2013;12:24‑31.
67. Fuks AB, Bimstein E, Guelmann M, Klein H. Assessment of a 2
percent buffered glutaraldehyde solution in pulpotomized primary
teeth of school children. ASDC J Dent Child 1990;57:371‑5.
68. Tsai TP, Su HL, Tseng LH. Glutaraldehyde preparations and
pulpotomy in primary molars. Oral Surg Oral Med Oral Pathol
1993;76:346‑50.
69. Sheller B, Morton TH Jr. Electrosurgical pulpotomy: A pilot study
in humans. J Endod 1987;13:69‑76.
70. Mack RB, Dean JA. Electrosurgical pulpotomy: A retrospective
human study. ASDC J Dent Child 1993;60:107‑14.
71. Shaw DW, Sheller B, Barrus BD, Morton TH Jr. Electrosurgical
pulpotomy‑‑A 6‑month study in primates. J Endod 1987;13:500‑5.
72. Bahrololoomi Z, Moeintaghavi A, Emtiazi M, Hosseini G. Clinical
[Downloaded free from http://www.jresdent.org on Thursday, January 4, 2018, IP: 178.138.32.63]
Chandrashekhar and Shashidhar: Formocresol‑A review
and radiographic comparison of primary molars after formocresol
and electrosurgical pulpotomy: A randomized clinical trial. Indian
J Dent Res 2008;19:219‑23.
73. Dean JA, Mack RB, Fulkerson BT, Sanders BJ. Comparison of
electrosurgical and formocresol pulpotomy procedures in children.
Int J Paediatr Dent 2002;12:177‑82.
74. Oztas N, Ulusu T, Gygur T, Cokpekin F. Comparison of
electrosurgery and formocresol as pulpotomy techniques in dog
primary teeth. J Clin Pediatr Dent 1994;18:285‑9.
75. Miller M, Truhe T. Lasers in dentistry: An overview. J Am Dent
Assoc 1993;124:32‑5.
76. Elliott RD, Roberts MW, Burkes J, Phillips C. Evaluation of the
carbon dioxide laser on vital human primary pulp tissue. Pediatr
Dent 1999;21:327‑31.
77. Kimura Y, Yonaga K, Yokoyama K, Watanabe H, Wang X,
Matsumoto K. Histopathological changes in dental pulp irradiated
by Er: YAG laser: A preliminary report on laser pulpotomy. J Clin
Laser Med Surg 2003;21:345‑50.
78. Jukić S, Anić I, Koba K, Najzar‑Fleger D, Matsumoto K. The effect
of pulpotomy using CO2 and Nd: YAG lasers on dental pulp tissue.
Int Endod J 1997;30:175‑80.
79. Miserendino LJ, Neiburgerr EJ, Walia H, Luebke N, Brantley W.
Thermal effects on continuous wave CO2 laser exposure on
human teeth: An in vitro study. J Endod 1989;15:302‑5.
80. Kurumada F. A study on the application of Ga‑As semiconductor
laser to endodontics. The effects of laser irradiation on the
activation of inflammatory cells and the vital pulpotomy. Ou
Daigaku Shigakushi 1990;17:233‑44.
81. Garcia‑Godoy F. A comparison between zinc oxide‑eugenol and
polycarboxylate cements on formocresol pulpotomies. J Pedod
1982;6:203‑17.
82. Schroder U. Effects of calcium hydroxide‑containing pulp‑capping
agents on pulp cell migration, proliferation, and differentiation.
J Dent Res 1985;64:541‑8.
83. Schroder U. Agreement between clinical and histologic findings
in chronic coronal pulpitis in primary teeth. Scand J Dent Res
1977;85:583‑7.
84. Cleaton‑Jones P, Duggal M, Parak M, William S, Setze S. Ferric
sulphate and formocresol pulpotomies in baboon primary molars:
Histological responses. Eur J Pediatr Dent 2002;3:121‑5.
85. Ranly DM, Garcia‑Godoy F. Current and potential pulp
therapies for primary and young permanent teeth. J Dent
2000;28:153‑61.
86. Farooq NS, Coll JA, Kuwabara A, Shelton P. Success rates
of formocresol pulpotomy and indirect pulp therapy in the
treatment of deep dentinal caries in primary teeth. Pediatr Dent
2000;22:278‑86.
87. Fuks AB, Holan G, Davis JM, Eidelman E. Ferric sulfate versus
dilute formocresol in pulpotomized primary molars: Long‑term
follow up. Pediatr Dent 1991;19:327‑30.
88. Prabhu NT, Munshi AK. Clinical, radiographic and histological
observations of the radicular pulp following “feracrylum”
pulpotomy. J Clin Pediatr Dent 1997;21:151‑6.
89. Ibricevic H, Al‑Jame Q. Ferric sulfate as pulpotomy agent in
primary teeth: Twenty month clinical follow‑up. J Clin Pediatr
Dent 2000;24:269‑72.
124 • Journal of Restorative Dentistry / Vol - 2 / Issue - 3 / Sep-Dec 2014
90. Ibricevic H, Al‑Jame Q. Ferric sulphate and formocresol in
pulpotomy of primary molars: Long term follow up study. Eur J
Pediatr Dent 2003;1:28‑32.
91. Hume WR. The pharmacologic and toxicological properties of
zinc oxide‑eugenol. J Am Dent Assoc 1986;113:789‑91.
92. Boeve C, Dermaut L. Formocresol pulpotomy in primary molars:
A long‑term radiographic evaluation. ASDC J Dent Child
1982;49:191‑6.
93. Eidelman E, Holan G, Fuks AB. Mineral trioxide aggregate vs.
formocresol in pulpotomized primary molars: A preliminary report.
Pediatr Dent 2001;23:15‑8.
94. Zander HA. Reaction of the pulp to calcium hydroxide. J Dent
Res 1939;18:373‑9.
95. Magnusson B. Therapeutic pulpotomy in primary molars with
formocresol technique‑ clinical and histological follow‑up. I.
Calcium hydroxide paste as a wound dressing. Odont Revy
1970;21:415‑31.
96. Schroder U. A 2‑year follow‑up of primary molars, pulpotomized
with a gentle technique and capped with calcium hydroxide. Scand
J Dent Res 1978;86:273‑8.
97. Heilig J, Yates J, Siskin M, McKnight J, Turner J. Calcium
hydroxide pulpotomy for primary teeth: A clinical study. J Am
Dent Assoc 1984;108:775‑8.
98. Waterhouse PJ, Nunn JH, Whitworth JM. An investigation of the
relative efficacy of Buckley’s Formocresol and calcium hydroxide
in primary molar vital pulp therapy. Br Dent J 2000;188:32‑6.
99. Markovic D, Zivojinovic V, Vucetic M. Evaluation of three
pulpotomy medicaments in primary teeth. Eur J Paediatr Dent
2005;6:133‑8.
100. Neamatollahi H, Tajik A. Comparison of clinical and radiographic
success rates of pulpotomy in primary molars using Formocresol,
ferric sulfate and mineral trioxide aggregate (MTA). J Dent Tehran
Univ Med Sci 2006;3:6‑14.
101. Agamy HA, Bakry NS, Mounir MM, Avery DR. Comparison of
mineral trioxide aggregate and formocresol as pulp‑capping
agents in pulpotomized primary teeth. Pediatr Dent 2004;26:302‑9.
102. Jabbarifar SE, Khademi AA, Ghasemi D. Success rate of
formocresol pulpotomy versus mineral trioxide aggregate in
human primary molar tooth. J Res Med Sci 2004;6:304‑7.
103. Liu H, Zhou Q, Qin M. Mineral trioxide aggregate versus calcium
hydroxide for pulpotomy in primary molars. Chin J Dent Res
2011;14:121‑5.
104. Fuks AB. Vital pulp therapy with new materials for primary
teeth: New directions and treatment perspectives. J Endod
2008;34:S18‑24.
105. Naik S, Hegde AM. Mineral trioxide aggregate as a pulpotomy
agent in primary molars: An in vivo study. J Indian Soc Pedod
Prev Dent 2005;23:13‑6.
106. England MC, West NM, Safavi K, Green DB. Tissue lead levels
in dogs with RC‑2B root canal fillings. J Endod 1980;6:728‑30.
How to cite this article: Chandrashekhar S, Shashidhar J. Formocresol,
still a controversial material for pulpotomy: A critical literature review. J Res
Dent 2014;2:114-24.
Source of Support: Nil, Conflict of Intrest: Nil.