Current concepts

in vital primary pulp therapy

A.B. FUKS

ABSTRACT. Review Recent progress in understanding the molecular and cellular changes during tooth
development and how they are mimicked during tissue repair, offers the opportunity to assess the biologic validity
of the various vital pulp treatments. Under this light, indirect pulp treatment can be an acceptable procedure for
primary teeth with reversible pulp inflammation, provided that this diagnosis is based on a good history, a proper
clinical and radiographic examination, and the tooth had been sealed with a leakage-free restoration. Several
articles report the success of this technique of direct pulp capping (DPC) and calcium hydroxide has been widely
used with high success rates in young permanent teeth, but the results in primary teeth are less satisfactory. Recent
studies have reported successful results with direct adhesive capping of exposed pulps, while others showed pulp
inflammation and unacceptable results using this technique. Thus, the traditional rationale for the use of calcium
hydroxide should be maintained, and this treatment modality reserved for iatrogenic exposures in asymptomatic
teeth that are expected to exfoliate within a short period of time. In younger children, iatrogenic or carious
exposures should be treated by pulpotomy. Formocresol has been the most popular pulp dressing material for
pulpotomized primary molars for many years but, due to its deleterious effect, the use of formocresol is decreasing
considerably worldwide. Ferric sulphate has been proposed as a substitute to formocresol, and the success rates
were comparable to those of formocresol. More recently, considerably better results have been obtained with MTA
(Mineral Trioxide Aggregate), and statistically significant differences were reported when compared with
formocresol. Internal root resorption, a finding seen both in ferric sulphate and formocresol, was not observed in
the MTA treated teeth. MTA is commercially available, but its cost is very high, and cannot be kept once opened.
Thus, ferric sulphate can still be a valid and inexpensive solution for pulpotomies in primary teeth.

KEYWORDS: Indirect pulp, Direct pulp capping, Pulpotomy

Introduction during tooth development and how they are mimicked

The primary objective of pulp treatment is to
maintain the integrity and health of the oral tissues.
Although a tooth can remain functional without a vital
pulp, it is desirable to attempt to maintain the vitality
of the pulp [American Academy of Pediatric Dentistry
Reference Manual, 2001-2002]. Thus, the objective of
vital pulp therapy (indirect pulp treatment, direct pulp
capping and pulpotomy) is to treat reversible pulp
injury [Tziafas et al., 2000]. Recent progress in
understanding the molecular and cellular changes
Presented at the Pre-Congress Symposium
6th Congress of the European Academy of Paediatric Dentistry
Dublin, Ireland - June 2002, Sponsored by Ultradent
Department of Pediatric Dentistry
Hebrew University – Hadassah School of Dental Medicine
Jerusalem, Israel
during tissue repair offers the opportunity to assess the
biologic validity of the various vital pulp treatments.
The present article reviews briefly the dentinogenesis
process during tooth formation, throughout life and in
response to injury. Under this light the various vital
pulp treatments will be analyzed.
Dentinogenesis in healthy state. The odontoblasts
are cells derived from the ecto-mesenchymal cells of
the dental papilla. During the post-mitotic state the
odontoblasts line the formative surface of the matrix,
and start secreting primary dentine. The other cells of
the pulp (in the sub-odontoblastic layer and in the pulp
core), although supporting dentinogenesis, do not play
a direct role in primary dentine secretion [Linde and
Goldberg, 1993]. After secretion of the bulk of dentine
during primary dentinogenesis, physiological
secondary dentine is secreted at a much slower rate
throughout the life of the tooth, leading to a slow
reduction in the size of the pulp chamber [Baume,

EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 3/2002 115

A.B. FUKS
1980]. The original post-mitotic odontoblasts,
responsible for primary dentinogenesis, survive for the
life of the tooth, unless subjected to injury. These cells
remain in a resting stage after primary dentinogenesis,
and the physiologic secondary dentine formation
represents a basal level of cell activity in the resting
stage [Linde and Goldberg, 1993].
Dentinogenic response to injury. The pulp-dentine
complex responds to injury by formation of new hard
tissue, mainly tertiary dentine, increasing the
distance between the injury and the pulp cells and
sometimes decreasing the dentine permeability
[Tziafas et al., 2000]. The nature and quality of the
tertiary dentine depends on its tubular structure,
influencing the dentine permeability of the area.
Thus, in case of a mild injury, the odontoblasts
responsible for the primary odontogenesis can
frequently survive the challenge, and are stimulated
to secrete reactionary dentine beneath the injury site
[Smith et al., 1995]. Since the original odontoblasts
are responsible for this matrix secretion, there will be
tubular continuity and communication with the
primary dentine matrix [Mjor, 1983].
Reactionary dentine might be considered as an
extension of physiological dentinogenesis. However,
since it is a pathological response to injury, it should be
regarded as distinct from the primary and secondary
dentinogenesis.
When the injury is severe, the odontoblasts
beneath the injury may die but, if suitable conditions
exist in the pulp, a new generation of odontoblasts-
like cells may differentiate from underlying pulp
cells, secreting a reparative dentine matrix. As this
dentine is formed by a new generation of cells, there
will be discontinuity in the tubular structure, with a
subsequent reduction in permeability [Byers et al.,
1999].
A critical question that arises is what are the factors
responsible for triggering the stimulation of
odontoblastic activity? Although much still has to be
learnt of the molecular control of cells activity in
general and of odontoblastic activity in particular, one
family of growth factors, the TGFb superfamily, has
been reported to have extensive effects on the
mesenchymal cells of many connective tissues
[Messagne, 1990]. During tooth development, the
odontoblasts secrete TGFbs, and some of them remain
sequestrated into the dentine matrix. These TGFbs
may be released during any process leading to tissue
dissolution, such as dental caries [Tziafas et al., 2000].
Thus, dentine matrix should not be considered as an
inert dental hard tissue, but rather as a potential tissue
store of a cocktail of bioactive molecules (particularly
116
growth factors) waiting to be released, if appropriate
tissue conditions prevail [Tziafas, 2000].
In contrast to reactionary responses, reparative
dentinogenesis represents a more complex sequence
of biological processes. Migration and differentiation
of pulpal progenitor cells must take place, creating a
new generation of odontoblast-like cells, prior to
matrix secretion. A series of stereotypic wound
healing reactions will be occuring in the pulpal
connective tissue, including vascular and cellular
inflammatory reactions. In vitro and in vivo
experiments on reparative odontogenesis demonstrate
that the non-inflamed pulp constitutes an appropriate
environment where competent pulp cells (potential
preodontoblasts) can differentiate into new
odontoblast-like cells, forming reparative dentine
[Nakashima et al., 1994a; Magloire et al., 1996;
O’Kane and Ferguson, 1997].
Review of clinical strategies in vital pulp therapy.
A variety of clinical procedures have been used
traditionally in restorative dentistry, with a
considerable degree of success, although somewhat
empirical and not always directed to the initiation of
particular tissue events. The improvement in
knowledge of molecular and cellular processes in
dentine and pulp allows a better understanding the
traditional procedures on these tissues.
Indirect pulp capping. Indirect pulp treatment is
recommended for teeth that have deep carious lesions
approximating the pulp, but no signs or symptoms of
pulp degeneration. In this procedure, the deepest layer
of the remaining carious dentine is covered with a
biocompatible material to prevent pulp exposure and
additional trauma to the tooth. Two materials are most
commonly used in indirect pulp treatment: calcium
hydroxide (CH) and zinc oxide-eugenol paste (ZOE).
Presently, glass ionomer cements are also
recommended. Treatment of dentine with various
cavity conditioning agents has shown their ability to
solubilize TGFb from the matrix. It seems probable
that this solubilizing effect of cavity conditioners
results in the release of TGFb from the tissue,
diffusing down the dentinal tubules, promoting a
reactionary dentinogenic response in the underlying
odontoblasts [Smith and Smith, 1998]. The rationale
for indirect pulp treatment is that few viable bacteria
remain in the deeper dentine layers, and after the
cavity has been sealed properly they will be
inactivated. Stainless steel crowns (SSC) are
frequently recommended after indirect pulp treatment,
particularly if the tooth has to function for several
years (Fig. 1). These facts argue against a two-step
procedure, in which the tooth is reentered for the
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 VITAL PULP TREATMENT

a b

c d
FIG. 1 - Mandibular primary molar with extensive caries to be treated by indirect pulp treatment. a) Tooth isolated with rubber
dam prior to caries removal. b) Remaining carious tissue over the pulpal floor. c) Carious area covered by glass ionomer
cement. d) Final restoration with a stainless steel crown.

purpose of excavating the previously carious dentine
and to confirm the formation of reparative dentine.
This procedure risks creating a pulp exposure and
further insult to the pulp [Dumshat & Hovland, 1985].
A practical judgement would advise reentry in
permanent teeth or in primary teeth that will be
maintained for long periods of time, as the
restorations may eventually leak and lead to a
reactivation of the carious process and pulpal
involvement [Camp, 1984].
The ultimate objective of this treatment is to
maintain pulp vitality [Eidelman et al., 1965], by
arresting the carious process, promoting dentine
sclerosis (reducing permeability), stimulating the
formation of tertiary dentine, and remineralizing the
carious dentine. Success rates of indirect pulp
treatment have been reported to be higher than 90% in
primary teeth [Farooq et al., 2000; Straffon et al.,
2000; Falster et al., 2002], and thus its use is
recommended in patients where a preoperative
diagnosis suggests no signs of pulp degeneration.
Direct pulp capping. Direct pulp capping is a
procedure that is carried out when a healthy pulp has
been inadvertently exposed during an operative
procedure. The tooth must be asymptomatic, and the
exposure site must be pinpoint in diameter and free of
oral contaminants. A CH medicament is placed over
the exposure site to stimulate dentine formation and
thus “heal” the wound and maintain the vitality of the
pulp [Levine et al., 1988]. The ability of the TGFbs
and BMPs (Bone Morphogenetic Proteins) to induce
reparative dentinogenesis in pulp capping situations in
vivo [Rutherford et al., 1993; Rutherford et al., 1994;
Nakashima, 1994c; Tziafas et al., 1998; Hu et al.,
1998] provides the basis for development of a possible
new generation of biomaterials. As the specificity of
these growth factors to induce reparative processes is
not clear, further studies are required to fully
understand the kinetics of growth factor release and
the sequence of growth factor-induced reparative
dentinogenesis.
Direct pulp capping of a carious pulp exposure in a
primary tooth is not recommended, but can be
successful in immature permanent teeth. The direct
pulp cap is indicated for small mechanical or
traumatic exposures when conditions for a favourable
response are optimal. Even in these cases the success
rate in primary teeth is not particularly high. Failure

EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 3/2002 117

A.B. FUKS
a b
FIG. 2 - Radiograph of maxillary primary incisors with mesial caries. a) Iatrogenic pulp exposure capped with Dycal. b)
Extensive internal root resorption observed six months later.
FIG. 3 - Histologic section of an exfoliated primary molar
after direct capping with an acid etch and composite restora-
tion. Notice the absence of a dentin bridge and the presence of
a microabscess.
of treatment may result in internal resorption (Fig. 2)
or acute dentoalveolar abscess. Kennedy and Kapala
[1985] claim that the high cellular content of the
primary pulp tissue may be responsible for the
increased failure rate of direct pulp capping in
primary teeth. These authors believe that
undifferentiated mesenchymal cells may differentiate
into odontoclasts, leading to internal resorption, a
principal sign of failure of direct pulp capping in
primary teeth.
The use of dentine bonding agents for direct pulp
capping has been advocated by some investigators
[Kashiwada and Takagi, 1991; Kanka, 1993]. The
rationale for this is based on the belief that if an
effective, permanent seal against bacterial invasion
is provided, pulp healing will occur. Animal research
has shown good compatibility of mechanically
exposed pulps to visible-light-activated composite
when bacteria are excluded [Cox et al., 1987].
118
Araujo et al. [1996] reported good clinical and
radiographic results in cariously exposed primary
teeth, one year after acid etch, capping with a
bonding agent and restoring with a composite resin.
In another publication, one year later, Araujo et al.
[1997] examined histologically primary molars with
micro-exposures that were successfully treated with
a composite acid etch technique and were extracted
or exfoliated. These authors observed
microabscesses adjacent to the exposure site; no
dentine bridge was formed in any specimen (Fig. 3).
These results were confirmed by Pameijer and
Stanley [1998, 1999], who concluded: “The belief
that any material placed on an exposed pulp will
allow bridge formation as long as the cavity is
disinfected, is a fallacy”. Conversely, high success in
direct pulp capping has been observed by the same
group in monkeys employing a modified Bioglass
formula, encouraging clinical studies [Clark et al.,
1999].
Presently, direct pulp capping should still be looked
upon with some reservations in primary teeth.
However, this treatment could be recommended for
exposed pulps in older children, one or two years prior
to normal exfoliation. In these children, a failure of
treatment would not imply a need for a space
maintainer following extraction, as it would be the
case in younger children.
Pulpotomy. The pulpotomy procedure is based on
the rationale that the radicular pulp tissue is healthy or
is capable of healing after surgical amputation of the
affected or infected coronal pulp [Fuks and Eidelman,
1991]. The presence of any signs or symptoms of
inflammation extending beyond the coronal pulp is a
contraindication for a pulpotomy. Thus, a pulpotomy
is contraindicated when any of the following are
present: swelling (of pulpal origin), fistula, pathologic
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 3/2002

mobility, pathologic external root resorption, internal
root resorption, periapical or interradicular
radiolucency, pulp calcifications, or excessive bleeding
from the amputated radicular stumps. Other signs,
such as a history of spontaneous or nocturnal pain,
tenderness to percussion or palpation, should be
interpreted carefully.
The ideal dressing material for the radicular pulp
should be bactericidal, be harmless to the pulp and
surrounding structures, promote healing of the
radicular pulp, and not interfere with the physiologic
process of root resorption. A good deal of
controversy surrounds the issue of pulpotomy agents
and, unfortunately, the “ideal” pulp dressing material
has not yet been identified. Formocresol (FC),
usually as Buckley’s solution, has been the most
popular pulp dressing material for pulpotomized
primary molars for many years but, due to its
deleterious effect, the use of formocresol is
decreasing considerably worldwide.
Some biologic materials have been proposed as
pulp dressings on the theory that they would promote
physiologic healing of the pulpotomy wound: freeze-
dried bone [Fadavi et al., 1989]; autolyzed, antigen-
extracted, allogenic dentine matrix; allogenic bone
morphogenetic protein [Nakashima, 1989]; enriched
collagen solutions [Fuks et al., 1984]. All have led to
varying levels of success in early experimental
stages. Recent clinical studies have reported
promising results using ferric sulphate (FS), a
hemostatic agent, in pulpotomized human primary
teeth [Davis and Furtado, 1991; Fei et al., 1991].
Fuks et al. [1997] reported a success rate of 93% in
teeth treated with FS and 84% in those where dilute
formocresol (DFC) was employed. These teeth were
followed-up 6 to 35 months. Success rates
comparable to those of FC were also reported by
Smith et al. [2000]. The results of other FC clinical
studies were presented by Papagiannoulis [2002]
separately in this symposium.
More recently, considerably better results have
been obtained with Mineral Trioxide Aggregate
(MTA), and statistically significant differences were
reported when compared with FC [Eidelman et al.,
2001]. Internal root resorption, a finding seen both in
FS and FC, was not observed in MTA treated teeth.
MTA is commercially available as Proroot MTA
(Dentsply, Paris), but its price is very high. As the
material cannot be kept once the envelope is opened,
its clinical use in pediatric dentistry practice becomes
almost prohibitive. Thus, FS can still be considered a
valid and inexpensive solution for pulpotomies in
primary teeth.
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 3/2002
VITAL PULP TREATMENT
Acknowledgements
The author wishes to thank Dr. Lloyd Straffon and
Dr. Fernando Borba Araujo for their courtesy in
providing part of the figures in this manuscript.
References
American Academy of Pediatric Dentistry, Reference Manual
2001-2002: clinical guidelines for pulp therapy for primary and
young permanent teeth. pp. 58-61.
Araujo FB, Barata JS, Garcia-Godoy F. Cinical and radiographic
evaluation of the use of an adhesive system over primary dental
pulps. J Dent Res 1996;75:280, abstr. 2101.
Araujo FB, Barata JS, Costa CAS, Garcia-Godoy F. Cinical,
radiographical and histological evaluation of direct pulp capping
with a resin in primary teeth. J Dent Res 1997;76:179, abstr. 1327.
Baume LJ. The biology of pulp and dentine. In: Myers HM, editor.
Monographs in oral science. Basel: S Karger AG; 1980.
Byers MR, Narhi MV. Dental injury models: experimental tools for
understanding neuroinflammatory interactions and polymodal
nociceptor functions. Crit Rev Oral Biol Med 1999;10(1):4-39.
Camp JH. Pulp therapy for primary and young permanent teeth.
Dent Clin North Am 1984 Oct;28(4):651-68.
Clark AE, Pameijer CH, Stanley HR, Louw NP. Pulp capping
with a modified Bioglass formula. J Dent Res 1999;78:219,
abstr. 910.
Cox CF, Keall CL, Keall HJ, Ostro E, Bergenholtz G.
Biocompatibility of surface-sealed dental materials against
exposed pulps. J Prosthet Dent 1987 Jan;57(1):1-8.
Davis J, Furtado L. Ferric sulfate a possible new medicament for
pulpotomies in the primary dentition: the first year results from
a 4 year study in Fortaleza, Brazil. Thirteenth Congress of
International Association of Dentistry for Children, Kyoto,
Japan, Program and Abstracts, September 27-30, 1991.
Dumsha T, Hovland E. Considerations and treatment of direct and
indirect pulp-capping. Dent Clin North Am 1985
Apr;29(2):251-9.
Eidelman E, Finn SB, Koulourides T. Remineralization of carious
dentine treated with calcium hydroxide. J Dent Child
1965;32:218-225.
Eidelman E, Holan G, Fuks AB. Mineral trioxide aggregate vs.
formocresol in pulpotomized primary molars: A preliminary
report. Pediatr Dent 2001;23:15-18.
Falster AC, Araujo FB, Straffon LH, Nor JE. Indirect pulp
treatment: in-vivo outcomes of an adhesive resin system vs.
calcium hydroxide. Pediatr Dent 2002;24:241-256.
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 Jul-Aug;22(4):278-86.
Fei AL, Udin RD, Johnson R. A clinical study of ferric sulfate as
a pulpotomy agent in primary teeth. Pediatr Dent 1991 Nov-
Dec;13(6):327-32.
119
A.B. FUKS
Fuks AB, Michaeli Y, Sofer-Saks B, Shoshan S. Enriched collagen
solution as a pulp dressing in pulpotomized teeth in monkeys.
Pediatr Dent 1984 Dec;6(4):243-7.
Fuks AB, Eidelman E. Pulp therapy in the primary dentition. Curr
Opin Dent 1991 Oct;1(5):556-63.
Fuks AB, Holan G, Davis JM, Eidelman E. Ferric sulfate versus
dilute formocresol in pulpotomized primary molars: long-term
follow up. Pediatr Dent 1997 Jul-Aug;19(5):327-30.
Hu CC, Zhang C, Qian Q, Tatum NB. Reparative dentine formation
in rat molars after direct pulp capping with growth factors. J
Endod 1998 Nov;24(11):744-51.
Kanca J 3rd. Replacement of a fractured incisor fragment over pulpal
exposure: a case report. Quintessence Int 1993 Feb;24(2):81-4.
Kashiwada T, Takagi M. New restoration and direct pulp capping
systems using adhesive composite resin. Bull Tokyo Med Dent
Univ 1991 Dec;38(4):45-52.
Kennedy DB, Kapala JT. The dental pulp: biological
considerations of protection and treatment. In: Braham RL,
Morris E (eds): Textbook of Pediatric Dentistry. Baltimore:
Williams & Wilkins; 1985.
Levine N, Pulver F, Torneck CD. Pulpal therapy in primary and
young permanent teeth. In Wei SHY (ed): Pediatric Dentistry-
Total Patient Care. Philadelphia: Lea & Febige; 188.
Linde A, Goldberg M. Dentinogenesis. Crit Rev Oral Biol Med
1993;4(5):679-728.
Magloire H, Joffre A, Bleicher F. An in vitro model of human
dental pulp repair. J Dent Res 1996 Dec;75(12):1971-8.
Massague J. The transforming growth factor-beta family. Annu
Rev Cell Biol 1990;6:597-641.
Mjor IA. Dentine and pulp, Reaction patterns in human teeth. New
York: Boca Raton, FL: CRC Press; 1986.
Nakashima M, Nagasawa H, Yamada Y, Reddi AH. Regulatory role
of transforming growth factor-beta, bone morphogenetic
protein-2, and protein-4 on gene expression of extracellular
matrix proteins and differentiation of dental pulp cells. Dev Biol
1994 Mar;162(1):18-28.
120
Nakashima M. Induction of dentine formation on canine
amputated pulp by recombinant human bone morphogenetic
proteins (BMP)-2 and -4. J Dent Res 1994 Sep;73(9):1515-22.
Nakashima M. Induction of dentine in amputated pulp of dogs by
recombinant human bone morphogenetic proteins-2 and -4 with
collagen matrix. Arch Oral Biol 1994 Dec;39(12):1085-9.
O’Kane S, Ferguson MWJ. Transforming growth factor bs and
wound healing. Int J Biochem Cell Biol 1997;29:63-78.
Pameijer CH, Stanley HR. The disastrous effects of the "total etch"
technique in vital pulp capping in primates. Am J Dent 1998
Jan;11 Spec No:S45-54.
Pameijer C, Stanley HR. Pulp capping with “total etch” and other
experimental methods. J Dent Res 1999;78:219, abstr. 911.
Rutheford RB, Wahle J, Tucker M, Rueger D, Charette M.
Induction of reparative dentine formation in monkeys by
recombinant human osteogenic protein. 1. Arch Oral Biol
1993;38:571-576.
Rutheford RB, Spanberg L, Tucker M, Rueger D, Charette M. The
time-course of the induction of reparative dentine formation in
monkeys by recombinant human osteogenic protein. 1. Arch
Oral Biol 1994;39:833-888.
Smith AJ, Cassidy N, Perry H, Begue-Kirn C, Ruch JV, Lesot H.
Reactionary dentinogenesis. Int J Dev Biol 1995 Feb;39(1):273-80.
Smith AJ, Smith G. Solubilization of TGFb1 by dentine
conditioning agents. J Dent Res 1998;77:1034 abstr. 3224.
Smith NL, Seale NS, Nunn ME. Ferric sulfate pulpotomy in
primary molars: a retrospective study. Pediatr Dent 2000 May-
Jun;22(3):192-9.
Straffon LH, Loos P. The indirect pulp cap: A review and
commentary. J Israel Dent Assoc 2000;17:7-14.
Tziafas D, Alvanou A, Papadimitriou S, Gasic J, Komnenou A.
Effects of recombinant basic fibroblast growth factor, insulin-like
growth factor-II and transforming growth factor-beta 1 on dog
dental pulp cells in vivo. Arch Oral Biol 1998 Jun;43(6):431-44.
Tziafas D, Smith AJ, Lesot H. Designing new treatment strategies
in vital pulp therapy. J Dent 2000 Feb;28(2):77-92.
EUROPEAN JOURNAL OF PAEDIATRIC DENTISTRY • 3/2002