Clinical Review

By Dr Jeff Ward BDS, Postgraduate, Endodontics, School of Dental Science, The University of
Melbourne, 71 1 Elizabeth Street, Melbourne, Victoria, 3000.
Vital Pulp Therapy In Cariously
Exposed Permanent Teeth And
Its Limitations
Abstract
Vital pulp therapy for cariously exposed permanent
teeth remains one of the most controversial areas in
dentistry. Because a vital, functioning pulp is capable
of initiating several defence mechanisms to protect
the body from bacterial invasion, it is beneficial to
preserve the vitality and health of an exposed pulp
rather than replace it with a root filling material
following pulp exposure. There is no consensus on
the survival rate of formerly cariously exposed pulps.
Observation time, judgement criteria,
pulpotomy/pulp capping technique and, most
importantly, pulpal status at the time of treatment,
vary to a great extent amongst studies.
In mature teeth, a pulp exposed by caries is usually
removed and the root canals are cleaned, shaped and
filled. Amongst the methods for preservation of a
cariously exposed pulp, partial pulpotomy has yielded
a markedly high success rate in young teeth. Major
limitations in the success of vital pulp therapy in
cariously exposed permanent teeth exist. The lack of
predictability and long-term success greatly influence
decision-making. The decision-making itself is
unreliable primarily due to the difficulty of accurately
diagnosing the ability of the pulp to repair.
While there are indications for vital pulp therapy in
young permanent molars, it must be remembered
that ultimately, none of these procedures enjoy the
long-term success of complete root canal therapy.
Introduction
The treatment of the cariously exposed permanent tooth should
result in arresting the carious process and keeping the vital pulp free
of inflammation ( I ) The aim of vital pulp therapy is to preserve the
vitality and function of the coronal or remaining radicular pulp tissue
(2) Carious lesions involving the pulp, if not treated will lead to
pulpal necrosis and often involvement of the periradicular tissues,
with pain and discomfort for the patient (3) The treatment of the
cariously exposed pulp is dependent upon the maturity of the
tooth In deciduous teeth, treatment is aimed at removing the
infected, coronal pulp and fixing or mummifying the radicular pulpal
tissue, thereby preserving the tooth, not the pulp (4) In mature
permanent teeth, pulpectomy and obturation of the root canal
system is usually the treatment of choice.
In young permanent teeth, pulpotomy is classically undertaken
to promote apexogenesis (5). Apexogenesis refers to a vital pulp
therapy procedure performed to encourage physiological develop-
ment and formation of the root end (6). The objective is to pro-
mote root development and apical closure. An open, divergent
apex presents the challenge of producing an apical stop or
constriction for placement of a hermetically sealed root canal filling
(6). Because the pulp is necessary for the formation of dentine, the
loss of vitality in young permanent teeth before completion of root
formation leaves a thin, weak root that is prone to fracture and
difficult to treat endodontically (7). The prognosis for permanent
retention is limited when compared with fully developed teeth.
Every effort must be made to maintain the vitality of the pulp in
teeth with incomplete apices to achieve root development. Once
root development is achieved and apices have closed, root canal
treatment is completed. The need for root canal treatment was
based on the premise that possible necrosis, continued calcification
or internal resorption will occur following pulpotomy. Recent
studies have proposed that as long as a hermetic seal is ensured,
root canal treatment is not needed following pulpotomy (8).
Partial pulpotomy aimed at preserving pulpal vitality has been
shown to be successful in traumatically exposed permanent teeth
(9). This treatment regimen has been applied and showed some
success in the treatment of cariously exposed young permanent
molars ( 10, I I ). The excellent blood supply of a young permanent
tooth with incompletely formed roots may contribute towards this
success (7). In contrast, the decreased resistance of the aged pulp
may become significant when one considers that the vascular
reaction to inflammation is considered a protective mechanism of
the pulp against invading factors ( 12). From the clinical point of view,
the vitality of the dental pulp of an aged person appears to be
weaker than that of a young person (I 2).
Considerable literature emphasises the negative aspects of vital
pulp therapy and discourages its practice. Many clinicians and
researchers continue to condemn vital pulp therapy for the same
reasons reported in the literature 80 years ago, despite the
advances made in pulp biology (I 3).
The immediate and long-term success of root canal therapy is
well known, but clinicians are less certain of the success of vital pulp
therapy. Cvek ( 9) reported a 96% success rate for partial
pulpotomy in traumatically fractured teeth with an open apex that
were healthy before trauma. Barthel et al (14) in comparison,
found a success rate of only 13% ten years after capping cariously
exposed, asymptomatic, vital pulps. Whilst observation time,
pulpotomy technique and judgement criteria vary between studies,
AUSTMLIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002
29
the status of the pulp at the time of capping is the predominant
factor in determining the healing of exposed pulps (I 4).
The long-term prognosis and the ability to restore a tooth are
the overriding factors when assessing whether vital pulp therapy
should be undertaken (15). The amount of crown destruction
usually associated with a pulp exposure in an immature molar
means that the tooth involved would require significant restorative
maintenance in the long term.
Basic Concepts In Vital Pulp Therapy Of
Cariously Exposed Permanent Teeth
The treatment objective following pulp exposure is to obtain
healing of a pulp wound in order to preserve a vital tooth with a
healthy pulp. Kakehashi et a1(I 6), clearly showed that the key factor
in pulpal healing after exposure is the absence of infection. Failures
are caused by infection due to either remaining bacteria, or the
exposure to new bacteria from leakage (17). Heys et al (18)
demonstrated that exposed pulps heal even against an inert material
such as Teflon, when bacterial contamination is eliminated.
Vital pulp therapy aims to treat reversible pulpal injury. There IS a
difference in the outcome between treating an inflamed and a non-
inflamed pulp (I 7). The chance for successful outcome is markedly
higher in the non-inflamed pulp exposed by trauma, than in the
inflamed pulp exposed during caries excavation. Treatment will be
successful only if the pulp, at the time of treatment, is sound or
not seriously enough inflamed to result in a continuation of the
inflammatory response (I).
Caries causes pulpal inflammation, even if the carious process
has not reached the pulp tissue, because bacterial by-products will
reach the pulp via the dentinal tubules. Consequently, with the
majority of deep carious lesions, the dentine is often supported by
an injured pulp that itself must undergo repair and remain clinically
asymptomatic for vital pulp therapy to be considered a success ( 19).
The presence of pain does not always indicate that a pulp injury is
irreversible, although certain patterns and intensities of pain tend
to suggest a greater likelihood of an irreversible change. The
inflammatory status of the pulp during a pulpal exposure is a major
factor in determining whether vital pulp therapy will be successful
and is also extremely difficult to accurately diagnose.
For teeth in which the caries process is aggressive or in which the
pulp may have a reduced repair potential because of chronologic or
physiologic aging, there is generally a progressive inflammation and
necrosis of tissue resulting in the loss of the pulp as a functioning
organ (I 9). The inflammation in such cases is classified as irrever-
sible. If the pulp can recover from the inflammation induced by
a caries attack with appropriate treatment, the inflammation is
referred to as reversible. Seltzer et al (20) showed that the
correlation between diagnostic and actual histologic findings in the
pulp is not strong and that this classification should be considered
clinical rather than histopathologic. A low-grade, asymptomatic
chronic inflammation leading to pulpal necrosis often exists long
after caries had been removed and the tooth restored (20).
Reversible inflammation is more common in young permanent
teeth than in mature permanent teeth ( I 9). Growth, maturation
and inflammation all cause the pulpal vasculature to undergo
significant morphological changes. The superficial layer of the young
pulp consists of a characteristic three-layer vascular network ( 12).
After teeth grow into occlusion, the pulp cavity narrows and this
vascular network undergoes reconstruction. Two of the three
vascular layers disappear, leaving a coarse terminal capillary network
( 12). As these morphological changes progress with time, the
protective vascular reaction to inflammation diminishes, influencing
30
the pulp's ability to successfully protect against invading factors.
The success of vital pulp therapy techniques in cariously exposed
permanent teeth is dependent upon the technique employed, the
inflammatory status of the pulp tissue, the type of pulp therapy
agent used, the period of observation and the criteria used to
determine success (2 I ). Accurate diagnosis of the pulp status prior
to treatment, caries removal, leakage prevention and use of an
aseptic technique, are key determinants in a successful treatment
outcome.
Techniques
Vital pulp therapy techniques that are used for treatment of
cariously exposed permanent teeth include:
Indirect pulp capping
Direct pulp capping
Full coronal pulpotomy
Partial pulpotomy.
These procedures have been employed for carious, mechanical,
and traumatic exposures of the pulp. A high incidence of success
has been reported, asjudged radiographically and by the absence of
clinical signs and symptoms (22). However, large variations in
success rate between studies exist. Differences in case selection,
length of study, and type of investigation are responsible for these
variations (22).
Indirect pulp therapy is a technique for avoiding pulpal
exposure in the treatment of teeth with deep carious lesions in
which there exists no clinical evidence of pulpal degeneration or
periapical disease (22). This technique is based on the theory that a
zone of affected demineralised dentine exists between the outer
infected layer of dentine and the pulp (23). When the infected layer
is removed, the affected dentine can then remineralise and the
odontoblasts form reparative dentine, avoiding a pulp exposure.
Carious dentine left in the tooth undoubtedly contains some
bacteria but calcium hydroxide and/or zinc oxide-eugenol cement
can greatly diminish their numbers (24). The remaining soft dentine
is covered and after two months the degree of remineralisation is
tested and any residual softened dentine removed (24). If caries has
reached the pulp, endodontic treatment is initiated. If there has
been a favourable response and the dentine is hard, a permanent
restoration can be placed. Some studies report repair in 74% to
99% of cases ( I 3, 25). Other authors state that there is a low
expectation for success and that failures increase with time ( I 7).
A difficulty with this technique is clinically determining what is
infected or just afected dentine. To intentionally leave infected
material is definitely not recommended as it leads to further pulpal
inflammation and likely failure. From a practical standpoint, it is
strongly advised to excavate carious dentine until the remaining
dentine feels hard to a dental explorer and reflects light (I 7). The
use of caries indicator dye may be of benefit also.
Direct pulp capping is a procedure in which an exposed
dental pulp is covered with a protective dressing or cement that
protects the pulp from additional injury and permits healing and
repair (26). The outcome for direct pulp capping following a carious
exposure is considered, at best, unpredictable (27, 28). During the
direct capping procedure the capping agent is placed on tissue that
has been exposed to microorganisms and where inflammation is
present ( I 7). Histologic examinations have shown chronic
inflammation under many cariously exposed pulp caps and
diminished success rates (22). Direct capping procedures should
only be carried out on fresh, traumatic or mechanical exposures,
before bacterial plaque has established on the exposure and the
underlying pulp has become inflamed ( 17, 29).
AUSTRALIAN ENDODONTIC IOURNAL VOLUME 28 No. I APRIL 2002
Pulpotorny has become the treatment of choice for cariously
exposed vital teeth ( 17). Pulpotomy is described as a procedure that
involves the amputation of the coronal portion of the affected or
infected dental pulp and treating the remaining vital pulp to preserve
its vitality and function (30). Pulpotomy allows for the pulp wound
to be placed in healthier tissue than at the site of exposure.
Full coronal pulpotorny involves the complete removal of the
coronal pulp and the placement of a wound dressing at the canal
orifice(s). Many different chemical compounds have been used as
wound dressings. Wound dressings containing formaldehyde,
phenol, creosotes and other highly toxic materials were advocated
to "mummify" the remaining pulp tissue ( I 7). The short-term
clinical outcome for these materials is usually acceptable. On the
other hand, with increasing time there is a decreasing success rate
following pulpotomy with formaldehyde-containing materials ( I 7).
Due to the short lifespan of primary teeth, this form of pulpotomy
is popular in paediatric dentistry.
The use of materials such as formocresol in the full coronal
pulpotomy of permanent teeth with pulp exposures has been
recommended (3 I). This goes against all modern endodontic
principles as the remaining chemically necrotised tissue can serve as
a substrate for bacteria as a result of leakage ( 17). In addition, Fuks
et al (32) found a high incidence of internal resorption in
formocresol-pulptomised permanent monkey teeth and Rolling
et al (33) found that the portion of canal apical to the fixed plug of
tissue beneath formocresol pulpotomies in permanent teeth with
pulp exposures, is often tortuous and extremely difficult to
instrument when endodontic treatment is often needed years later.
Formorcresol pulpotomies are not recommended in teeth with
mature root formation unless there are behavioural and/or socio-
economic constraints to performing root canal therapy ( 15).
Pulpotomy agents such as formocresol and glutaraldehyde are
associated with systemic toxicity and carcinogenic potential, sotheir
safety is questioned (34).
Partial pulpotorny has achieved very high success rates in
the treatment of complicated crown fractures (95%) (32), and
in young, posterior, symptom-free permanent teeth with carious
exposures (9 I-93%) ( 10, I I , 35). Partial pulpotomy as described
by Cvek in I978 (9), is the aseptic, surgical removal of the exposed
pulp and dentine surrounding the exposure to a depth of 1.5-2.0
mm. This aims to surgically remove tissue that is irreversibly
inflamed and exposed to microorganisms leaving a clean-cut wound
surface on healthy tissue ( I 7). The pulp wound is irrigated with
sterile saline until physiologic haemostasis is achieved and then the
pulp wound is covered with a paste of calcium hydroxide and water.
An alternative irrigant is sodium hypochlorite (055.25%). This has
been shown to be effective at haemorrhage control and surface
disinfection and flushing, without any detrimental pulpal effects (5,
18). The wound dressing is then carefully dried and sealed with a
suitable material. The direct apposition of the calcium hydroxide
paste on the non-bleeding pulp tissue is essential, as an extra-pulpal
blood clot will diminish the chances for hard barrier formation and
long-term success ( 17). Partial pulpotomy creates a retentive cavity
for the covering materials and the use of calcium hydroxide in
combination with removal of blood clot gives predictable healing
with a continuous hard tissue barrier (9).
With calcium hydroxide treatment, a dentine bridge will pre-
dictably form over healthy, remaining pulp tissue (13). In the
absence of a bridge, the wounded pulp tissue is much closer to the
surface and is more easily invaded by subsequent attacks of oral
bacteria and their by-products (36). A dentine bridge allows more
predictable repair by giving underlying pulp tissue something to
attach to (I 3). Without a bridge, pulp tissue remains unattached,
undergoes degeneration, atrophy and shrinkage away from
dentine. Dentine bridges contain tunnels and porosity. The number
and size of these tunnels reflects the degree of trauma to the pulp
(I 3). Cellular inclusions and empty vascular spaces create porosity,
and in combination with tunnels, contribute to the permeability of
every dentine bridge. Dentine bridges have been condemned as
ineffective protective barriers because of their permeability,
although regular tubular dentine is itself, permeable ( 13). Even
though the quality of a dentine bridge may be suspect as to its
integrity, it nevertheless provides a physical barrier of some sub-
stance to protect the pulp. Dentine bridge formation is the best
solution for healing of the underlying pulp ( 13).
Current Research
The success of vital pulp therapy in cariously exposed permanent
teeth is the subject of much debate. The scepticism towards vital
pulp therapy originates from an historical context, where treatment
decisions were based on empirical reasoning (26). Strindberg in
1956 (37) reported a success rate for direct pulp capping with
calcium hydroxide of 64%, compared to a success rate of 83% for
root canal treatment. Since then, knowledge of pulpal physiology
has broadened, leading to a better understanding of the conditions
necessary to take advantage of the good potential of the pulp to
heal. Recent clinical studies indicate that vital pulp therapy of
cariously exposed young permanent teeth can produce success
rates that compare favourably with the success rate of root canal
treatment (2, 3, 10, I I , 26, 38).
Conflicting views have been expressed when relating pulpal
changes to caries progression and clinical symptoms (20, 27, 39,
40). In 1968, Langeland and Langeland (41) showed that deep
carious lesions might be found with relatively normal pulps or with
only a slight increase in chronic inflammatory cells. Trowbridge (42)
suggested that the pattern of pulpal inflammation is determined by
the permeability of dentine and the proximity of the carious lesion
to the pulp. Lin and Langeland (43) stated "whereas the repair
capacity of pulp tissue following removal of all carious dentine
without pulp exposure is excellent, after carious exposure it is
questionable and unpredictable". Seltzer et al (20) histologically
considered up to 79% of permanent teeth with clinical pulp
exposures to be in the non-treatable category.
It is generally accepted that in advanced stages of a carious lesion,
just prior to or soon after pulp exposure, bacterial components
cause only localised irreversible damage beneath the exposure,
while the remaining pulp is infiltrated with inflammatory changes to
a varying degree. The bacteria only seem to gain access to the pulp
lumen after some part of the pulp has become necrotic (39, 40).
These views seem to be confirmed by the studies of Zilberman et
al ( I I ) and Mejire and Cvek ( 10). The removal of the superficial
layers of pulp tissue together with the contaminated dentine and the
prevention of microleakage, sufficed to ensure healing in most of
the treated teeth.
Seltzer et al (20) showed that under small carious lesions only
an increase in reparative dentine formation is induced, whilst in
moderately large cavities, macrophages and lymphocytes are
observed under the involved dentinal tubules of the coronal pulp.
In very deep lesions, chronic inflammatory exudate develops.
When the pulp is exposed by caries, acute localised inflammation
and liquefaction necrosis can be observed under the exposure site.
Langeland (39) postulated that in order to preserve the remaining
heatthy pulp, it is necessary to remove this infected, necrotic and
disintegrated pulpal tissue.
AUSTPALIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002
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Farooq et al(30) showed that a carious primary tooth diagnosed
with pain from reversible pulpitis could be successfully treated with
either an indirect pulp treatment or a formocresol pulpotomy.
Success rates of 85% and 76% respectively were observed for
these two techniques over a four-five year follow up. Gruythuysen
and Weerheijm (44), in a similar study over a two-year period,
achieved an 80% success rate with the placement of calcium
hydroxide as a base after pulpotomy of carious primary teeth with
signs of reversible pulpitis. Both these studies (30, 44) showed a
high failure rate of all vital pulp therapy when a preoperative
diagnosis of irreversible pulpitis or pulpal necrosis was formed.
Careful history taking, together with symptoms and clinical/
radiographic findings should help form the final diagnosis and
determine the final treatment to be provided.
Formocresol pulpotomy in permanent teeth has shown good
success rates. Hosseini (45) showed a 92% success rate after 10
years. Teplitsky (46) showed evidence of continued apical devel-
opment following formocresol pulpotomy procedures on young
permanent teeth with incompletely developed apices. Initially it was
thought formocresol pulpotomy had more appeal than calcium
hydroxide pulpotomy as calcification of the remaining pulp tissue
was not seen (22). Contrary to these thoughts, calcification of canals
with formocresol pulpotomy was shown. Full strength formocresol
pulpotomy has been shown to produce obliteration of the root
canal in up to 80% of teeth treated (47). Fuks and Bilstein (48) using
a one-fifth dilution of full-strength formocresol found radiographic
obliteration in only 29% of treated teeth. This obliteration by
calcification may preclude future root canal treatment. Although this
treatment has been reported to be partly successful, it cannot be
routinely recommended until further research showing this
technique to be successful has been completed (22).
As stated earlier, Cvek (9) reported a 96% success rate for partial
pulpotomy in traumatically fractured teeth with an open apex that
were healthy before trauma. Mejare and Cvek ( lo), using the partial
pulpotomy technique adopted from Cvek (9), achieved a 93.5%
success rate after carious pulp exposure of young permanent teeth
exhibiting no clinical or radiographic symptoms. Zilberman et al ( I I )
found I 4 of I 5 deeply carious permanent young molars exhibited a
vital pulp response at 12-99 months following partial pulpotomy.
Mass and Zilberman (35) achieved a success rate of 9 I .4% after a
minimum of 12 months, using partial pulpotomy and careful
inclusion criteria in the treatment of young permanent molars with
carious pulp exposure. Barthel et al (14) in comparison, found a
success rate of only 13% ten years after capping cariously exposed
asymptomatic, vital pulps.
Matsuo et al (38) showed a success rate of 80% at >6 months
following direct pulp capping of permanent carious teeth with some
symptoms of irreversible pulpitis. Unlike most other studies, teeth
with lingering pain to thermal stimuli and with sensitivity to
percussion were included in the study. Caligan (2) showed that
periapical involvement did not necessarily preclude cariously
exposed permanent teeth from vital pulp therapy. Twenty-six
permament vital molars with carious pulp exposures and radio-
graphic periapical involvement were treated using a full coronal
pulpotomy, with calcium hydroxide placed directly on the radicular
pulp tissue once bleeding had stopped. Of these, twenty-four teeth
showed resolution of radiographic periapical involvement and
dentine bridge formation after 16-72 months. The presence of
radiographic periapical change accompanying reversible pulpitis can
best be rationalised as a sequel to reversible pulpal neurogenic
inflammation, rather than as a direct response to an infected, dying
Pulp,
It was traditionally believed that the primary cause of pulp
damage after direct pulp capping was direct toxic effects from dental
materials. Animal studies however, have demonstrated that
restorative materials do not cause pulp inflammation or necrosis
when directly placed on the exposed pulp if bacteria are sealed off
at the margins (49).
In recent years there have been many publications illustrating
healthy pulps without dentine bridges in teeth treated with a total
etch and bond technique. The concept is that these bonding
techniques adequately seal the exposure sites from bacterial
invasion and consequently a dentine bridge is not needed. Long-
term success of this seal has not been established ( I 3). Kitasako (49)
found that because pulp tissue protruded into the cavity around the
exposure site, direct resin pulp capping might permit oral bacteria
to eventually access the pulp via microleakage. Exudation from the
exposed pulp may also prevent the moisture sensitive resin
materials from adhering to peripheral dentine (49). Hebling et al
(50) showed a persistent inflammatory reaction and lack of
complete pulp repair or dentine bridging 60 days after direct
capping of non-inflamed pulpal exposures with an adhesive system,
compared to pulp repair with complete dentine bridging with
calcium hydroxide. At present, there is little long-term data available
to support this technique.
The Future
Pulp therapy for cariously exposed teeth remains one of the
most controversial areas in dentistry. No clear-cut diagnostic
indication or therapeutic method exists. Current protocols are
based on the empiricism of ages past. Much of this controversy is
because scientific research has not provided us with the technology
to overcome two great shortcomings in dentistry. Firstly we are
unable to directly treat pulp infection and save the pulp. Secondly,
we have no predictable inductive agent for stimulating reparative
dentine (5 I ) . Also, we cannot predictably diagnose the
inflammatory status of the affected pulp.
Pulp studies are very difficult. The anatomy of the pulp cannot be
duplicated in vitro, pulp cells in culture quickly lose their phenotypes,
animal teeth do not react like human teeth and clinical studies are
often long and arduous (5 I ). Molecular biology though, has made
it possible to ask the questions that have never been asked.
Odontoblast and pulp cell lines will now maintain their charac-
teristics despite many passages in cell lines. Tooth specific proteins
enable us to identify the differentiation state of cells and knowledge
is increasing about dentine inducing Bone Morphogenetic Proteins
(BMPs) and Transforming Growth Factor-Beta VGF-P). Many of
these bioactive molecules are expressed in the dental tissues during
odontogenesis and systemically play a role in signalling cellular
processes during health and disease (52).
Advances in material and biological sciences should offer at least
two therapeutic approaches (5). Firstly, the development of dental
adhesives for pulp capping procedures should offer greater success
with pulpotomies. With diseased tissue removed, the response of
the remaining pulp should be more favourable. Secondly are the
recent advances in the field of BMPs. These growth factors have
proven to be inductive for bone and dentine (5). The demon-
stration that reparative dentine can be induced by direct or indirect
contact with a biologic agent, and its thickness determined by dose,
elevates pulp therapy to a new level (5). Someday we might treat a
pulpotomised permanent molar with growth factors and predictably
induce sound dentine bridges, leaving the remaining pulpal tissue
completely enclosed in healthy tissue, eliminating the need for root
canal therapy.
32 AUSTRALIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002
Recombinant human BMP-2, -4 and -7 has been shown to
induce reparative dentine formation in experimental models of large
direct pulp exposures in permanent teeth (53-55). New reparative
dentine replaces the stimulating agents applied directly to the
partially amputated pulp. This new tissue forms contiguous with,
and not at the expense of, the remaining vital pulp tissue. This
permits the induction of a predetermined and controlled amount of
reparative dentine.
These results provide experimental support for the potential of
biologic agents to stimulate reactionary dentine formation (53-55).
Further development of proper carrier vehicles that will optimise
clinical handling characteristics and delivery will add to further
possible uses (53). In the future, pulpotomies for primary and
permanent teeth may be handled in exactly the same way (5).
Pulpal innervation has traditionally been regarded to serve a
purely nociceptive function. This concept is being challenged by
increasing evidence that sensory nerves also serve important
effector functions (56). Rodd and Biossonade (56) showed a caries-
induced dynamic increase in neural density in both primary and
young permanent teeth and speculated that this may be critical for
the regulation of pulpal inflammation and healing.
In endodontics, it has been proposed that the laser has an
application in direct pulp therapy as well as i-oot-end preparation
and canal disinfection (57). Moritz et al (57) used a CO, laser at I W
to irradiate non-inflamed pulps for 0. I sec pulses at I sec intervals
until exposed pulps were completely sealed. A hard setting calcium
hydroxide cement and a glass ionomer restoration were then
placed over the pulp. In the control group, a hard setting calcium
hydroxide cement and a glass ionomer restoration were placed
directly on the pulp without prior laser treatment. At I 2 months,
laser Doppler flowmetry assessed 89% of the laser treated cases to
be vital as compared to 68% of the non-laser treated cases.
The amount of data that has been accumulated over the years
on the biology and the clinical behaviour of the dental pulp are
impressive (58). Yet there are considerable gaps in our knowledge
of the defence and repair mechanisms of the dentine-pulp complex
that future research should address.
Limitations
Research data on vital pulp therapy can be misleading and
confusing ( I 3) In categorising success and failure of vital pulp
therapy, many more factors need to be considered than just
the presence or absence of microorganisms ( 13) In addition to the
presence of microorganisms, degrees of inflammatory response
and dentine bridges one must differentiate between true tissue
necrosis and mummification, t ecognise the potential for washout
of microorganisms, leukocytes and loss of extruded pulp tissue
elements, the influence of impaction of particles of pulp therapy
agents and dentine chips, the control of haemorrhage and
embolisation of particles of pulp therapy agents, the size of the pulp
exposure, the final location of the dentine bridge, and the quality of
its formation ( 13) A distinction between failure of the pulp therapy
and failure of the overlying resoration must also be made
While there are indications for vital pulp therapy in young
permanent molars, it must be remembered that ultimately, none of
these procedures enjoy the success of complete root canal therapy
( I 5) In the mature permanent tooth, pulpectomy and root filling
are the preferred treatment (I 7) This is because firstly, pulpectomy
with a subsequent root filling has a high success rate (90-96%), and
secondly, with the wound placed apically, inflammatory responses
to infection can radiographically be detected early When vita pulp
therapy has been performed, problems may develop later and
periodic monitoring is essential (I 5).
Generally, partial pulpotomy of carious permanent teeth, most
often with calcium hydroxide, serves to maintain the vitality of
radicular tissue until apexogenesis is complete (5). Once the apex is
closed, root canal treatment is performed. This practice is based
on anecdotal evidence that calcium hydroxide will precipitate
dystrophic calcification in the canals and prevent endodontic
treatment later, if needed (5). This obliteration of the root canals
results in diminished blood supply, which could lead to pulp necrosis
(35). This relates to full coronal pulpotomy where too little pulp
tissue is confined with too much calcium hydroxide. With partial
pulpotomy, where the objective is to remove only infected tissue,
dentine bridging is stimulated in the coronal area and canals are free
of dystrophic calcification (5). Stanley (36) proposes that the
negative side effects of inorganic calcium hydroxide, such as
dystrophic calcification, have been eliminated in the lower pH,
hard-setting, commercial calcium hydroxide preparations.
Success
A limit to determining success of vital pulp therapy in permanent
teeth is the ability to recall patients regularly to determine success.
Although histologic success cannot be determined, clinical success is
judged by the absence of any clinical or radiographic signs of
pathosis and the presence of continued root development in teeth
with incompletely formed roots (22). Success rates decrease with
time. Barthel et al (14) showed a success rate of 37% at 5 years,
which dropped to 13% at 10 years. Canal calcification, internal
resorption and/or pulpal necrosis are potential sequelae of vital pulp
therapy and careful monitoring is needed to diagnose these
potential problems as early as possible.
Age
The patient's age may be another limiting factor in the success
of vital pulp therapy in cariously exposed permanent teeth. In
older patients, the histological state of the pulp may affect its ability
to overcome an insult. Pulpal vasculature constantly undergoes
morphological changes incident to various conditions such as
growth, maturation and inflammation. Over time, owing to the
apposition of secondary and tertiary dentine, this leads to the pulp
cavity becoming narrower and the vasculature within undergoes a
reconstruction ( 12). The resistance of the pulp becomes reduced
with age ( 12). This becomes significant when one considers that the
vascular reaction to inflammation is considered a protective
mechanism of the pulp against invading factors ( I 2). Horsted et al
(59) demonstrated a significantly lower tooth survival rate in the
older age group (50-79 years of age) over longer observation
periods. From the clinical point of view, the vitality of the dental pulp
of an aged person appears to be weaker than that of a young
person ( I 2). Mass and Zilberman (35) achieved a 9 I .4% success
rate in a sample limited to children, teenagers and young adults and
suggested that vital pulp therapy of cariously exposed permanent
teeth be limited to children or young adults. Chronological age does
not always reflect physiological age, and neither one should be seen
as an absolute contraindication for vital pulp therapy in permanent
teeth (26).
Controversy exists as to whether the pulp should be re-entered
after the completion of root development in the pulpotomised
tooth (22). Root canal therapy is recommended because of the
chance that calcification would render the canals non-negotiable at
a future date. Recent research has shown that with good case
selection, a gentle, aseptic technique and careful placement of
calcium hydroxide onto the pulp, progressive calcification is an
infrequent sequela of pulpotomy (22).
AUSTRALIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002 33
Size Of Exposure
The size of the carious pulpal exposure can influence the
prognosis for vital pulp therapy. This is because generally the larger
the exposure, the greater the bacterial penetration of the pulp (35).
Also, the larger the exposure, the harder it is to seal. Long-term
success is certainly less predictable with large carious exposures
than with small carious exposures (60). It has been proposed that
vital pulp therapy be limited to exposures less than 2 mm in
diameter (35).
State Of The Pulp
The inflammatory status of the cariously exposed pulp is a major
determining factor in the success of vital pulp therapy. The success
of vital pulp therapy is dependent upon the ability of the pulp to
recover from its inflammatory state (I). Ideally, the status of the pulp
should be known before therapy is started (39). The diagnosis
of pulpal inflammatory status is based on subjective signs and
symptoms, which have been shown to be inconsistent, unreliable
and do not correlate well with actual histologic data ( 19, 20). Mass
and Zilberman (35) proposed that an ultimate pulpal diagnosis be
made immediately after removing 2-3 mm of the pulp during a
partial pulpotomy procedure. A continuously bleeding pulp wound
would contraindicate vital pulp therapy. A success rate of 9 I .4%
was achieved at a minimum of 12 months following partial
pulpotomy in cariously exposed young permanent molars using this
criteria (35). Mass et al (29) proposed that due to the difficulty in
accurately diagnosing pulp status, vital pulp therapy in cariously
exposed young, vital permanent teeth should only be carried out
when there are no symptoms at all. Because there is no single
reliable technique of determining pulp status clinically, a careful
interpretation of multiple tests is the most reliable method (26).
In general, clinicians agree that radiographically demonstrable
periapical involvement is always associated with total pulp necrosis
or irreversible pulpitis (22). The first recommended treatment in
irreversible pulpal pathological conditions is root canal therapy or
extraction. Caliqkan (2) showed that this irreversible pulpitis may be
limited to the coronal pulp, because vitality of the radicular pulp and
resolution of radiographic periapical involvement after full coronal
pulpotomy with calcium hydroxide dressing was achieved. The
dangers of dystrophic calcification of the root canals and prevention
of later root canal treatment, if necessary, must be considered with
use of this technique.
Extra-Pulpal Blood Clot
Stanley (36) concluded that the control of bleeding and the
contact of calcium hydroxide with pulp tissue seems to have an
influence on the success of the procedure. Matsuo et al (38)
reported a significantly higher incidence of failures when the pulps
showed heavy bleeding dc-ing the procedure, compared with
moderate or poor bleeding. Excessive bleeding usually indicates a
hyperaemic pulp with little chance of recovery (60). If clinical
success is expected, bleeding from exposed pulp tissue should be
minimal and stop soon after the exposure (60). Persistence of the
coagulum-clot has been demonstrated as detrimental to pulp
healing (61). The blood clot or its degradation products may
interfere with healing and act as a bacterial substrate, as well as
preventing the action of the capping material on the pulp (26). It
must be removed before any definitive seal is placed. The presence
of dentine chip fragments, dead cells, bacteria and restorative
material particles in the wound site will also be detrimental to pulp
healing (6 I). Five percent sodium hypochlorite solution will
chemically amputate the blood coagulum at the exposure-pulp
interface, arrest pulp haemorrhage and will remove most dentine
chips, bacteria and damaged pulp cells (6 I). Most importantly,
sodium hypochlorite will not cause damage to normal underlying
tissues (6 I ).
Choice Of Capping Material
The choice of a capping material can influence the success of vital
pulp therapy (35). Calcium hydroxide has been the gold standard
for direct pulp capping since the 1930s (6 I). This opinion has been
based on the premise that calcium hydroxide was unique in its
ability to stimulate dentine bridge formation. More recently it has
been shown that many materials are biologically compatible against
exposed pulps and permit an environment that is conducive to
dentine bridge formation (I 6, 6 I , 62). The ideal medicament for
pulp dressing after pulpotomy should be non-toxic, and possess
antimicrobial activity and an anti-inflammatory potential to control
pre-existing inflammatory states and surgically induced inflammation
(34). Currently available agents possess two of these three require-
ments but none include all three. Cox and associates (62),
investigated the biocompatibility of silicate cement, zinc phosphate
cement, amalgam and composites on monkey pulps, with and
without an additional surface seal of zinc oxide-eugenol. Their
results indicate that the healing of dental pulp exposures is not
dependent on the type of pulp capping material, but is related to the
capacity of these materials to prevent bacterial leakage. Even inert
materials such as Teflon@, show pulpal healing when used as a
direct pulp capping material, as long as bacterial contamination is
eliminated ( I 8).
Mineral trioxide aggregate (MTA) has been shown to prevent
dye and bacterial leakage and has a high level of biocompatibility
(63, 64). Pitt Ford et al(65) used MTA as a pulp capping material on
I 2 mechanically exposed pulps of monkeys and all but one showed
pulpal healing and dentine bridge formation adjacent to the pulp.
Torabinejad and Chivian (63) speculate this is due to MTPs sealing
ability, biocompatibility, alkalinity, or other properties associated with
this material. Based on these results, MTA has been considered as
a suitable pulp capping material (63-65).
Anti-inflammatory agents have been examined but to date all
are far too toxic or ineffective (34). Anti-inflammatory compounds
used in general medicine, such as Tetrandrine, have been studied
and whilst they have shown less inflammation than other anti-
inflammatory agents such as corticosteroids, no long-term data exist
(34). Corticosteroids have been tried and have shown reasonable
short-term success, but again, no favourable long-term results exist
Total etch techniques with resin bonding have shown mixed
results (66-68). Short-term experiments have shown that modern,
resin-based composite systems may be as effective as calcium
hydroxide (67). Total cavity etching with 10% phosphoric acid
seems to be safe for the exposed pulp, but 35% phosphoric acid
may be disastrous (66-68). The cytotoxicity of the resin-based
composites and the temperature rise during polymerisation seems
not to be of concern, but microleakage, sensitisation and allergic
reactions may pose problems (67). Pulp capping with resin-based
composites is promising, but long-term research is mandatory
before the method can be recommended (66, 67).
Lederrnix@ (Lederle Pharmaceuticals, Cyanamid GmbH,
Wolfratshausen, Germany), a combination of an antibiotic and a
corticosteroid, has been proposed as a pulp placement material
(70). It was recommended that Ledermix be placed directly on the
radicular pulp following full coronal pulpotomy of traumatically or
cariously exposed vital teeth (70). This proposal was based on
evidence that Ledermix will not induce a calcific bridge but will allow
(34).
34
AUSTRALIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002
dentinogenesis to continue around the radicular pulp. This is a
temporary procedure to aid in apexogenesis before root canal
treatment is begun. Ledermix cementB, a compound containing
zinc oxide, eugenol and calcium hydroxide, as well as an antibiotic
and corticosteroid, has shown some promise as a pulp capping
material (7 I , 72). Concern has been expressed though, that the
corticosteroid agent, triamcinolone, may suppress local repair as
well as inflammation (73). Hume and Testa-Kenney (7 I ) showed
that 70% of the steroid is released in the first 24 hours after direct
placement on the pulp and that during this period, steroid con-
centration is at a level that would be expected to reduce local
inflammation and local repair. However, this inhibitory effect is likely
to have little effect on long-term healing as the steroid concentra-
tion drops to below an effective inhibitory concentration after 24
hours (7 I ).
Calcium hydroxide, which accelerates the deposition of a
dentine bridge and possesses antibacterial properties, is the material
of choice (74). Schroder (75) proposed that the firm, limiting
necrosis caused by calcium hydroxide irritates the pulp, which
stimulates the pulpal cells to defence and repair, and the firm
necrosis may also induce minerals from the tissue fluid to calcify. Veis
(76) suggests that the necrotic layer presents a surface to which the
pulp cells attach and polarise, and then begin to express their
odontoblastic potential. Calcium hydroxide is generally used in one
of three forms: as a powder, as a paste mixed with saline or
aqueous methylcellulose, or incorporation into a setting cement.
Kirk et al (77) showed that calcium hydroxide in paste form
produces reparative dentine sooner than in cement form, but
proposed that the cement form may be a more effective physical
barrier to bacterial ingress than the softer, porous paste form.
Of the many calcium hydroxide cements, Dycal@ (L.D. Caulk,
Dentsply Int. Inc., Milford, DE, USA), and LifeB (Kerr Manuf. Co.,
Romulus, MI, USA), have been shown to be satisfactory and
associated with dentine bridge formation across pulp exposures
(76, 78-80). Heys et al (74) showed that when bacterial micro-
leakage occurred around an unlined amalgam restoration, the
complex, setting calcium hydroxide formulations such as Dycal and
Life, were associated with a higher incidence of pulpal healing,
when compared with the non-setting calcium hydroxide formu-
lations. The non-setting, simple calcium hydroxide formulations
were more consistent in promoting dentine bridge formation
where bacterial microleakage was controlled (74). A dentine bridge
generally forms directly against the capping material when calcium
hydroxide cements such as Dycal and Life are used (79, 80), but
forms at a distance from the capping material with a necrotic layer
between the two, when the paste or powder formulations are used
(78). This may be due to the increase in inflammation that is
produced by the more alkaline paste and powder formulations.
Stanley (36) proposes that the negative side effects of inorganic
calcium hydroxide such as dystrophic calcification have been
eliminated in the lower pH, hard-setting, commercial calcium
hydroxide cements and recommends their use over the powder or
paste preparations.
Bacterial Contamination
Bacterial contamination is the main factor that determines the
prognosis of vital pulp therapy (26). Bacterial contamination of
the pulp can occur directly through caries or through exposure to
salivary contamination. Following caries removal and the aseptic
removal of superficial pulp, it is important to control bacterial
contamination of the pulp by microleakage at the tooth restoration
interface (8 I). Cox et al (62) showed that three weeks after res-
torations were placed over a pulp exposure, pulpal reorganisation
and hard tissue repair occurred when a surface seal preventing
marginal leakage was placed over the restoration. Without this
surface seal, severe pulpal inflammation and necrosis were noted,
with bacteria often found at the pulp-restoration interface. Barthel
et al ( 14) found that placement of a definitive restoration within the
first two days after carious pulp exposure contributed significantly to
the survival rate of these teeth. Partial pulpotomy improves pulp
sealing by creating a retentive cavity for the capping and restorative
material (35).
The long-term prognosis and the ability to restore a tooth are
the over-riding factors when assessing whether vital pulp therapy
should be undertaken ( I 5). The amount of crown destruction
usually associated with a pulp exposure in an immature molar
means that the tooth involved would require significant restorative
maintenance in the long term. Extraction and orthodontic treatment
may be preferable.
Conclusion
It is beneficial to preserve the vitality and health of an exposed
pulp rather than replace it with a root filling material following pulp
exposure. A vital, functioning pulp is capable of initiating several
defence mechanisms to protect the body from bacterial invasion
( 14). Pulp exposure without involvement of microorganisms can
clearly be overcome by repair mechanisms, such as dentinal
bridging. There is no consensus on the survival rate of formerly
exposed pulps. Observation time, judgement criteria, pulpotomy/
pulp capping technique and most importantly, pulpal status at the
time of treatment, vary to a great extent among the studies. This is
shown in the success rate of vita pulp therapy of cariously exposed
permanent teeth varying between 13% and 93% ( I 0, 14). Among
the methods for preservation of a cariously exposed pulp, partial
pulpotomy has yielded the highest success rate in young teeth
From the clinical point of view, the vitality of the dental pulp of an
aged person appears to be weaker than that of a young person
( I 2). In the future, more efficient wound dressings containing per-
haps growth factors, together with improved local antimicrobial and
anti-inflammatory materials will combine with the improved sealing
ability of restorative materials, to preserve the vitality of the cariously
exposed pulp in permanent teeth.
Major limitations in the success of vita pulp therapy in cariously
exposed permanent teeth exist. The lack of predictability and long-
term success greatly influence decision-making, The decision-
making itself is unreliable primarily due to the difficulty of accurately
diagnosing the ability of the pulp to repair.
The success demonstrated in various clinical studies justifies
recommending partial pulpotomy as a treatment option for asymp-
tomatic, cariously exposed, young permanent molars (29).
However, due to the lack of long-term success, these cases have to
be monitored on a regular basis to avoid unnoticed necrosis of the
pulp with invasion of bacteria into the root canal system.
(3, 10).
References
I . Koncke A. Treatment of deep carious lesions. Int Dent J 1970;
20: 338-43.
2. @o$kan M.K. Pulpotomy of carious vital teeth with periapical
involvemet. Int Endod J 1995; 28: 172-6.
3. Nosrat I.V. Nosrat C.A. Reparative hard tissue formation
following calcium hydroxide application after partial pulpotomy
in cariously exposed pulps of permanent teeth. Int Endod J
1998; 3 I : 22 1-6.
AUSTRALIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002
35
4. Ranly D. M. Pulp therapy at the turn of the century. Paed Dent
1999; 2 I : 384-6.
5. Ranly D.M., Garcia-Godoy F: Current and potential pulp
therapies for primary and young permanent teeth. J Dent
2000; 28: 153-64.
6. Goldtein S. , Sedaght-Zandi A, , Greenberg M. , Freidman 8.
Apexification and Apexogenesis. New York State Dent J 1999;
23-5.
7. Fuks A.B. Pulp therapy for the primary and young permanent
dentitions. Dent Clin North Am 2000; 44: 57 1-96,
8. Subay R.K., Suzuk, S. , Kaya H. , Cox C.F: Human pulp response
after partial pulpotomy with two calcium hydroxide products.
Oral Surg Oral Med Oral Pathol 1995; 80: 330-7.
9. Cvek M. A clinical report on partial pulpotomy and capping
with calcium hydroxide in permanent incisors with
complicated crown fracture. J Endod 1978; 4: 232-7.
10. Mejare l . , Cvek M. Partial pulpotomy in young permanent teeth
with deep carious lesions. Endod Dent Traumatol 1993; 9:
238-42.
I I . Zilberman U. , Mass E. , Sarnat H. Partial pulpotomy in carious
permanent molars. Am J Dent 1989; 2: 147-50.
12. Takakashi K. Changes in pulpal vasculature during inflam-
mation. J Endod 1990; 16: 92-7.
I 3. Stanley H.R. Criteria for standardising and increasing credibility
of direct pulp capping studies. Am J Dent 1998; I I : S 17-35,
14. Barthel C.R., Rosenkranz B. , Leuenberg A, , Roulet /-F: Pulp
capping of carious exposures: treatment outcomes after 5 and
I 0 years: a retrospective study. J Endod 2000; 26: 525-8.
15. Cameron A.C., Widrner R. P A Handbook of paediatric dentistry.
Westmead Hospital, Sydney, 1996; pp. 65-76.
16. Kakehashi S. , Stanley H.R., Fitzgerald R. L. The effects of surgical
exposures of dental pulps in germ-free and conventional
laboratory rats. Oral Surg Oral Med Oral Pathol 1965; 20:
340-9.
17. 0ntavik D., fi tt Ford TR. Essential endodontology: prevention
and treatment of apical periodontitis. Blackwell Science,
Oxford, 1998; pp. 192-2 10.
18. Heys D.R., Fitzgerald R.J., Cox C.F, Avery / . K. The inherent
healing capacity of the dental pulp. J Dent Res 1985; 64: 22 I .
19. Walton R. E. , Torabinepd M. Principles and practice of
endodontics. W.B. Saunders Company, Philadelphia, 1989;
pp. 353-70.
20. Seltzer S. , Bender I . b , Ziontz M. The dynamics of pulpal
inflammation: correlations between diagnostic data and actual
histologic findings in the pulp. Oral Surg Oral Med Oral Pathol
1963; 16: 846-7 I ,
2 I . Waterhouse g., Numm J. H. . Whitworth J.M., Soames / . V.
Primary molar pulp therapy - histological evaluation of failure.
Int J Paed Dent 2000; 10: 3 13-2 I .
22. Cohen S. , Burns R.C. Pathways of the pulp. Mosby Year Book,
6th ed., St Louis, 1994; pp. 682-7 19.
23. Dannenberg J.L. Pedodontic-endodontics. Dent Clin North
Am 1974; 18: 367-77.
24. Fairbourn D.R., Charbeneau G. 1, Loesche W/ . Effect of
improved Dycal and I.R.M. on bacteria in deep carious lesions.
J Am Dent Assoc 1980; 100: 547-52.
25. Ninchl RE , Avery D.R. Evaluation of new pulp capping agent in
indirect pulp therapy. J Dent Child 1983; 50: 25-30.
26. Lim K.C., ffirk E.E.J. Direct pulp capping: a review. Endod Dent
Traumatol 1987; 3: 2 13-9.
27. Baume L.J. Dental pulp conditions in relation to carious lesions.
Int Dent J 1970; 20: 309-37.
28. Bergenholtz G. Effect of bacterial products on inflammatory
reactions in the dental pulp. Scand J Dent Res 1977; 85:
122-9.
29. Mass E., Zilberrnon U. , Fuk A. 8. Partial pulpotomy: Another
treatment option for cariously exposed permanent molars. J
Dent Child 1995; 62: 342-5.
30. Farooq N.S., Coll/.A., Kuwabara A. , Shelton P Success rates of
formocresol pulpotomy and indirect pulp therapy in the
treatment of deep dentinal caries in primary teeth. Paed Dent
3 I . Rothman M.S. Formocresol pulpotomy: a practical procedure
for permanent teeth. Gen Dent 1977; 25: 39-4 I .
32. Fuks A.B., Binstein E. , Bruchim A. Radiographic and histologic
evaluation of the effect of two concentrations of formocresol
on pulpotomised primary and young permanent teeth in
monkeys. Paed Dent 1983; 5: 9- 13.
33. Rolling I . , Hosselgren G. , Tronsrad 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: 5 18-28,
34. Kim Seow !A!, Thong YH. Evaluation of the novel anti-
inflammatory agent tetrandrine as a pulpotomy medicament in
a canine model. Paed Dent 1993; 15: 259-66.
35. Mass E. , Zilberrnan U. Clinical and radiographic evaluation of
partial pulpotomy in carious exposure of permanent molars.
Paed Dent 1993; 15: 257-9.
36. Stanley H.R. Pulp capping: conserving the dental pulp - can it
be done? Is it worth it? Oral Surg Oral Med Oral Pathol 1989;
68: 628-39.
37. Strindberg L.Z. The dependence of the results of pulp therapy
on certain factors. An analytical study based on radiographic
and clinical follow-up examinations. Acta Odontol Scand 1956;
14: I75 Suppl 21.
38. Matsuo T , Nakanishi T , Shimizu H. , Ebisu 8. A clinical study of
direct pulp capping applied to carious-exposed pulps. J Endod
1996; 22: 55 1-6.
39. Langeland K. Tissue response to dental caries. Endod Dent
Traumatol 1987; 3: 149-7 I .
40. Reeves R. . Stanley H.R. The relationship of bacterial
penetration and pulpal pathosis in carious teeth. Oral Surg
Oral Med Oral Pathol 1966; 22: 59-65.
41. Longeland K. , Longeland L.K. Indirect capping and the
treatment of deep carious lesions. Int Dent J 1968; 18:
3 26-80.
42. Trowbridge H.O. Pathogenesis of pulpitis resulting from dental
caries. J Endod I98 I ; 7: 52-60.
43. Lin L., Langeland K. Light and electron microscopic study of
teeth with carious pulp exposures. Oral Surg Oral Med Oral
Pathol I98 I ; 5 I : 292-3 16.
44. Gruythuysen R.J., Weerheijm K.L. Calcium hydroxide
pulpotomy with a light-cured cavity-sealing material after two
years. J Dent Child 1997; 64: 25 1-53,
45. Hosseini A.A. A clinical evaluation of root resorption by
formocresol treatment in 120 cases of pulpotomy in
permanent molars. J Clin Paed Dent 1992; 17: I I - 13.
46. Teplitsky FIE. Formocresol pulpotomies on posterior per-
manent teeth. J Can Dent Assoc 1984; 50: 623-7.
47. Willard R.M. Radiographic changes following formocresol
pulpotomy in primary molars. J Dent Child 1976; 43: 4 14-6.
48. Fuks A.B., Bimstein E. Clinical evaluation of diluted formocresol
pulpotomies in primary teeth of school children. Paed Dent
1981; 3: 321-4.
2000; 22: 278-86.
36 AUSTRALIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002
49. Kitasako Y, lnokoshi S. , Tagarni /. Effects of direct resin pulp
capping techniques on short-term response of mechanically
exposed pulps. J Dent 1999; 27: 257-63.
50. Hebling /,, Giro E.M.A., Costa C.A. Biocompatibility of an
adhesive system applied to exposed human dental pulp. J
Endod 1999; 25: 676-82.
5 I . Ranly D.M. Pulp therapy at the turn of the century. Paed Dent
52. Tziafas D. , Smith A.]., Lesot H. Designing new treatment
strategies in vital pulp therapy J Dent 2000; 28: 77-92.
53. Rutherford R.B., Fitzgerald M. A new biological approach to
vital pulp therapy. Crit Rev Oral Biol 1995; 6: 2 18-29,
54. Rutherford R.B., Wahle ]., Tucker M., Rueger D., Charette M.
Induction of reparative dentine formation in monkeys by
recombinant human osteogenic protein- I . Arch Oral Biol
1993; 38: 57 1-6.
55. Smith A,/., Tobias R.S., Cassidy N., Plant R.B., Browne R.M.,
Begue-Krn C., et a/. Odontoblast stimulation in ferrets by
dentine matrix components. Arch Oral Biol 1994; 39: 13-22,
56. Rodd H. D. , Biossonade EM. Innervation of human tooth pulp in
relation to caries and dentition type. J Dent Res 200 I ; 80:
389-93.
57. Moritz A., Schoop U., Goharkhay K. , Sperr W The CO, laser as
an aid in direct pulp capping. J Endod 1998; 24: 248-5 I .
58. Bergenholtz G. Pathogenic mechanisms in pulpal disease. J
Endod 1990; 16: 98- I0 I .
59. Hosted P, Sondergaard B. , Thylstrup A. U Attar K., Fejenkov 0.
A retrospective study of direct pulp capping with calcium
hydroxide compounds. Endod Dent Traumatol 1985; I :
29-34.
60. Christensen GJ . Pulp capping 1998. J Am Dent Assoc 1998;
6 I . Cox C.E, Hafez A.A. Biocomposition and reaction of pulp
tissues to restorative treatments. Dent Clin North Am 200 I ;
45: 3 1-48,
62. Cox C.E, Keall C.L., Keall H/., Ostro E., Bergenholtz G.
Biocompatibility of surface-sealed dental materials against
exposed pulps. J Pros Dent 1987; 57: 1-8.
63. Torabinejad M. , Chivian N. Clinical applications of mineral
trioxide aggregate. J Endod 1999; 25: 197-205.
64. Torabinejad M. , Higa R.K., McKendry D./., Pitt Ford TR. Dye
leakage of four root end filling materials: effects of blood
contamination. J Endod 1994; 20: 159-63.
65. Pitt Ford TR. , Torabinejad M., Abedi H.R., Bakland L.K.,
Kariyawasarn S.P Using mineral trioxide aggregate as a pulp
capping material. J Am Dent Assoc 1996; 127: I49 1-4.
1999; 2 I : 384-6.
129: 1297-9.
66. de Souza Costa C.A., HeblingI., Honk C.T Current status of
pulp capping with dentin adhesive systems: a review. Dent Mat
67. Schuun A.H.B., Gruythuysen RJ .M., Wessehk PR. Pulp capping
with adhesive resin-based composite vs. calcium hydroxide: a
review. Endod Dent Traumatol 2000; 16: 240-50.
68. Cox C.E, Hafez A.A., Akrnoto N., Otsuk M., Suzuk S. , Tarirn 6.
Biocompatibility of primer, adhesive and resin composite
systems on non-exposed and exposed pulps of non-human
primate teeth. Am J Dent 1998; I I : S55-63.
69. Parneijer C.H., Stanley H.R. The disastrous effects of the "total
etch", technique in vital pulp capping in primates. Am J Dent
1998; I I : 545-54.
70. Ehrrnann E.H. Pulpotomies in traumatised and carious
permanent teeth using a corticosteroid-antibiotic preparation.
Int Endod J I98 I ; 14: 149-56.
7 I . Hurne WR., Testa Kenney A,. Release of 3H-triamcinolone
from Ledermix. J Endod I98 I ; 7: 509- 14.
72. Clarke N.G. The corticosteroid-antibiotic dressing as a capping
for inflamed dental pulps. Aust Dent J I97 I ; 16: 7 1-6.
73. Uitto V/ . , Antrla R., Ranto R. Effects of topical glucocorticoid
medication on collagen biosynthesis in the dental pulp. Acta
Odontol Scand 1975; 33: 287-98.
74. Heys D.R., Cox C.E, Heys R./., Avery / . K. Histological
considerations of direct pulp capping agents. J Dent Res 198 I ;
75. Schroder U. Effects of calcium hydroxide-containing pulp
capping agents on pulp cell migration, proliferation, and
differentiation. J Dent Res 1985; 64: 54 1-8.
76. Veis A. The role of the dental pulp -thoughts on the session
on pulp repair processes. J Dent Res 1985; 64: 552-4.
77. Kirk E. E. , Lirn K.C., Khan M.O.G. A comparison of
dentinogenesis on pulp capping with calcium hydroxide in
paste and cement form. Oral Surg Oral Med Oral Pathol
1989; 68: 2 10-9.
78. Heys D.R., Heys R.J., Cox C.E. Avery / . K. The response of four
calcium hydroxides on monkey pulps. J Oral Pathol 1980; 9:
372-9.
79. Stanley H.R., Lundy T: Dycal therapy for pulp exposures. Oral
Surg Oral Med Oral Pathol 1973; 34: 8 18-27,
80, Pitt Ford TR. Pulpal response to a calcium hydroxide material
for capping exposures. Oral Surg Oral Med Oral Pathol 1985;
59: 194-7.
8 I . Mjor I.A., Tronstad L. The healing of experimentally induced
pulpitis. Oral Surg Oral Med Oral Pathol 1974; 38: I 15-2 I .
2000; 16: 188-97.
60: 1371-9.
AUSTRALIAN ENDODONTIC J OURNAL VOLUME 28 No. I APRIL 2002 37