Endodontic Topics 2002, 2, 2434 Copyright C Blackwell Munksgaard

Printed in Denmark. All rights reserved

ENDODONTIC TOPICS 2002
1601-1538
Treatment outcome of vital pulp
treatment
PREBEN HRSTED-BINDSLEV & HENRIK LVSCHALL
Introduction
Vital pulp treatment of permanent teeth in adults in-
cludes, as outlined in this chapter, direct pulp capping
partial pulpotomy and vital pulpectomy.
In clinical practice the methods applied for evalu-
ating the outcome of vital pulp therapy in permanent
teeth and the criteria used to distinguish between suc-
cess and failure have remained almost unchanged for
many years.
Except for a slight tenderness or pain of short dur-
ation during the first couple of weeks after treatment,
absence of pain is taken as a sign of success. The pre-
and postoperative radiographical changes are mostly
minor in diagnosis and treatment of the vital pulp. A
condensing apical periodontitis, widening of the peri-
odontal ligament space and disintegration of the lam-
ina dura may be present with the diagnosis chronic
pulpitis or from time to time immediately after vital
pulpectomy. Success of the pulp treatment is assumed
if the periapical changes disappear. However, persist-
ence of an increased bone density is in general not
expounded as treatment failure. Following direct cap-
ping and partial pulpotomy, success also includes a
positive response to electrical and/or thermal tests.
The reliability and the reproducibility of the tests
are mediocre. As an example, pain may be absent, de-
spite inflammatory changes in the pulp tissue. How-
ever, by adding together information from the differ-
ent sources, an operational basis for estimation of the
outcome may be made. More precise methods to
evaluate the pulpal condition are Laser Doppler flow-
metry, pulse oximetry and dual wavelength spectro-
phometry which all are based on monitoring of the
vascular integrity of the pulp. But these methods are
24
still, although not totally new, at a certain experimen-
tal level and not for use in general practice.
The most precise evaluation ought to be the histo-
logic examination of the tissue. For obvious reasons,
this can only be done in experimental studies. But
also, in such studies, the reproducibility and criteria
are open for discussion and misinterpretation, as was
already been documented in the classical study by
Langeland almost 50 years ago, where he discussed
the risk of misdiagnosis of artefacts (1).
Treatment of exposures
The modern treatment regimen for direct pulp cap-
ping, partial pulpotomy and pulpectomy is most often
based on information from clinical and radiographical
studies and, to a lesser extent, on histological studies.
The strength of controlled longitudinal, clinical and
radiographical studies is that a great number of treat-
ments can be evaluated over a considerable period of
time. Histological studies which may disclose the true
results of the treatments, the so-called usage tests, are
relatively few compared with the clinical and radio-
graphical studies. There are several reasons for this.
Usage tests are costly, and most often performed in
animals. Use of animals may arouse strong feelings in
the population and it is generally desirable to mini-
mize the use of animals for research. Usage tests in
humans are, for various reasons, difficult to perform;
first and foremost for ethical reasons but also because
today only few teeth are available for this purpose.
Less teeth are extracted for orthodontic reasons, and
roots remain in the jaws, even in patients scheduled
for immediate full dentures. As a consequence, most
human histologic studies, especially on pulpectomy,
Treatment outcome of vital pulp treatment
date back 2560years. The weakness of usage tests is
that the number of teeth in the groups are few and,
in addition, teeth may be lost during the histologic
processes. This may cause problems of establishing
statistically significant results.
Thus, when outcome of vital pulp therapy is con-
sidered, we have, by and large, to rely on information
from clinical and radiographical examinations, know-
ing that these may not tell the full story. Often inflam-
matory reactions in the coronal or apical pulp may
prevail following treatment, despite absence of clinical
or radiographical signs of pathosis. This fact is im-
portant to bear in mind when treatment is selected,
prognosis discussed and result of treatment evaluated.
Mechanisms in wound healing of
pulpal tissue
Vital pulp tissue responds to manipulation in several
ways. Exposure or surgical removal of the upper pulp
tissue is a procedure which, even under the best cir-
cumstances, will result in a transient inflammation.
Exposure of the dental pulp as a result of caries or
tooth fracture is a clinical reality that requires optimal
treatment. Experimental evidence suggests that skills,
wound level, choice of instrumentation, choice of
wound dressing, and asepsis, play important roles in
the development of the initial surgical inflammation.
The potential for healing by formation of a dentin
bridge is good, provided that the pulp is not inflamed
(2).
The events taking place after wounding can be di-
vided into the phases of hemostasis, inflammation,
proliferation, and remodeling. Wound healing is,
however, a continuous process where the beginning
and the end of each phase cannot be clearly deter-
mined and phases overlap (3). The observed sequence
of initial pulp reactions is that which is expected when
connective tissue is wounded. Failure to resolve in-
flammation after wounding leads to chronic non-
healing wounds (4), and pulp tissue responds simi-
larly with absence of hard tissue healing.
Initially, the tissue adjacent to the exposure is char-
acterized by varying amounts of necrotic tissue, in-
flammatory cells, and extravasated erythrocytes. The
initial injury triggers exudation of fibrinogen and
blood coagulation and an acute response dominated
by neutrophil granulocytes. Both particles from the
25
capping material and dentin chips are displaced into
the underlying pulp tissue (5).
Inflammation
Both trauma and bacterial infection stimulate release
of pro-inflammatory cytokines in connective tissue.
Vascular alterations and inflammatory cell infiltration
are activated in order to eliminate the irritating mol-
ecules. Adhesion molecule interactions between
blood leukocytes and endothelium enables trans-
migration from inside to outside the vessel wall in
reponse to chemotactic signals (6). Bacterial compo-
nents, such as endotoxin and other cell wall compo-
nents, are implicated as pathogens in the develop-
ment of pulpal inflammation (7).
The host responds to antigens with production of
antibodies and a cell-mediated immune response. The
antibody response involves the production of im-
munoglobins circulating in the body that bind specifi-
cally to the foreign antigen that induced them. The
cell-mediated immune response involves production
of specialized cells that react with the foreign antigens
on the surface of other host cells, e.g. in the lymph
nodes (8). The unspecific defense-mechanism against
bacteria and invading organisms releases enzymes and
toxic metabolites. The complement system is a multi-
factorial protein cascade system and its major function
is activation of cellular defense mechanisms, opsonis-
ation of foreign particles for phagocytosis and the de-
struction of target cells. Released toxic metabolites
leads to generation of highly active species eg oxygen
radicals, halogen and hypochlorous which may also
damage the cells of the host. Generation of reactive
species from accumulated granulocytes and macro-
phages during the inflammatory phase is a critical
event in successful host defense (9).
The wound healing of pulp tissue has primarily
been studied in relation to application of calcium hy-
droxide. Therefore the following discussion of cellu-
lar responses in wound healing will be based on reac-
tions to calcium hydroxide.
Calcium hydroxide
Calcium hydroxide-containing agents which were
used at first by Hermann in 1930 have been widely
used since (1013). The effect of calcium hydroxide
on exposed connective pulp tissue has thus for dec-
Hrsted-Bindslev & Lvschall
ades been studied in experimental animals as well as
in man (11, 1418). Application of calcium hydrox-
ide on exposed healthy pulp tissue results in release
of hydroxide ions with a bactericidal effect, followed
by a combination of lytic and coagulation necrosis in
the wound surface. These necrotic layers repeatedly
form what we interpret to be a biological membrane,
beneath which the inflammatory and reparative pro-
cesses occur. Probably as a result of the high pH of
the calcium hydroxide (19), a bactericidal effect is ob-
tained (20). Previous studies showed that pulp cap-
ping by using a variety of agents, e.g. with a high
(21), low (22, 23) or neutral pH (15) may be fol-
lowed by stimulation of dentin bridging. The benefi-
cial effect of calcium hydroxide has been regarded as
the result of a bactericidal effect and a chemical injury
limited by a zone of necrosis, which caused slight irri-
tation of the vital tissue and stimulated the pulp to
defense and repair (24).
Pulp capping using calcium hydroxide also induces
apoptosis (25, 26) in the underlying pulp. Apoptosis
is a non-inflammatory controlled, cell death mechan-
ism, whereas necrosis induce a pro-inflammatory re-
sponse (27, 28). The balance of their activity after
pulp capping may therefore have crucial influence on
the subsequent inflammatory response. A few hours
after application of calcium hydroxide on pulpal
tissue, inflammatory cells migrate towards the ne-
crotic tissue, and the inflammatory infiltration lasts
for a few days (29). Efforts have been made to find a
formula which minimizes the pro-inflammatory ac-
tions, and at the same time stimulates dentin bridge
formation (2931).
Reparative dentinogenesis
Yamamura (32) summarized the tissue reactions to
pulp capping with calcium hydroxide in dog teeth as
four stages: the exudative stage (15days), the pro-
liferative stage (37days), osteodentin formative
stage (514days), and the tubular dentin formative
stage (14 days and more)
Fibrin exudation takes place under the capping ma-
terial in the pulp tissue for up to 4days (33). After
approximately 36 days, the inflammatory infiltration
is replaced by a migration of granulation tissue orig-
inating from central pulp sites. The granulation tissue
is arranged along the wound surface and consists pri-
marily of newly-formed fibroblasts and capillary
26
blood vessels which proliferate and grow into the
damaged tissue. Layers of fibroblasts increase in thick-
ness around the lesion. Synthesis of new collagen
fibers along the tissue necrosis is detected from 4days
after application of pure calcium hydroxide. Cells sur-
rounded by new matrix, including calcifying nodules,
are found after 7days (16). The initial precipitation
of minerals is associated with detection of matrix ves-
icles, indicating close similarity to mineralization in
bone (34). The minerals are found to originate from
the blood supply (35). After 11days, the new matrix
is associated with cuboidal cells, and some cells with
odontoblast-like differentiation. After 14 days, a clear
odontoblast-like arrangement is observed (36). After
1month, dentin bridges can be seen around the
trauma, representing a defensive interface between
the necrotic zone and the new odontoblast layer (37).
Microscopic evaluation, however, revealed 89% of all
dentin bridges contained tunnel defects (38).
Secretion of matrix from a new generation of cells
implies a discontinuity in tubular structure with sub-
sequent reduction in dentin permeability. The non-
specific response leads to deposition of atubular den-
tinal matrix covered by cuboidal or polygonal pre-
odontoblast-like cells, and inclusions of osteocyte-like
cells are observed in a dense mineralizing matrix
called osteodentin. Deep to the pulp injury, surviving
postmitotic odontoblasts respond with deposition of
reactionary dentin along the dentin walls. In such
situations we observe a reactionary dentin matrix with
less tubular density than in the primary dentin.
Reparative dentinogenesis represents a complex se-
quence of biological processes. Series of wound heal-
ing reactions occur in the pulp tissue simultaneously,
including vascular and cellular inflammatory reactions
and recruitment of competent cells. Interactions of
pulp cells with cytokines and extracellular matrix
components during the complex cascade of wound
healing reactions influence the dentinogenic potential
of the pulp (39).
Stem cells
During dental tissue repair, many of the tooth devel-
opmental processes are mimicked, leading to focal de-
position of reactionary and reparative dentin at injury
sites. The nature and specificity of these responses are
determined in part by the extent of tissue injury (40).
Studies on tooth epithelialmesenchymal signaling in-
Treatment outcome of vital pulp treatment
teractions have greatly increased our understanding
of molecules that regulate dentinogenic events during
tooth development (41). Expression of the odonto-
blast phenotype is characterized by a sequence of
cytological and functional changes which occur at
each site in the pulp chamber according to a specific
pattern (4244). It has been widely recognized that
several forms of reparative mineralized tissues are syn-
thesized by hard tissue-forming pulpal cells which dif-
ferentiate outside the specific temporo-spatial pattern
of tooth development in the absence of dental epi-
thelium and its basement membrane. Different
phenotypic characteristics have been described for
odontoblast-like cells arising from various in vitro and
in vivo experimental or clinical situations (39). The
plethora of confusing terms used to describe physio-
logical and pathological dentin, secreted after primary
dentin formation, has led to a redefinition of tertiary
dentin, which is subdivided into reactionary and re-
parative dentin (45).
The healing of pulpo-dentinal defects requires both
mobilization of connective tissue and differentiation
of a new generation of odontoblast-like cells. Fitzger-
ald et al. (46) studied migration and proliferation in
experimental pulp exposures in monkey teeth after
pulp capping with calcium hydroxide dressing. Con-
tinuous influx of newly differentiating odontoblast-
like cells originating from the deeper pulp was ob-
served at the materialpulp interface. At least two rep-
lications of DNA are required after pulp capping be-
fore cell migration and expression of the new pheno-
type (46).
Within the stromal pulp, e.g. the cell-rich subodon-
toblast layer, undifferentiated mesenchymal cells
could provide the precursor cells. However, perivas-
cular cells and other cell populations, including bone
marrow stem cells migrating via the bloodstream,
have also been proposed as progenitor cells. Never-
theless, it remains open whether odontoblast-like cells
during pulpal repair derive from the original ecto-
mesenchymal dental papilla cell population, which re-
sides at older stages as undifferentiated or fibroblast-
like cells, or from both ecto-mesenchymal and non-
dental cells (39). Whether progenitor cells giving rise
to new odontoblast-like cells for reparative dentinog-
enesis are recruited via the pulpal perivascular area,
from the pulp stroma, or from the subodontoblast
layer remains to be elucidated. Further characteriza-
tion of these cell populations and their developmental
27
history may elucidate not only the origin, but may
also help to understand their specific behavior during
reparative dentinogenesis.
Growth factors
Tissue injury leads to alterations in gene expression
and release of a range of cytokines including growth
factors. Cytokines play a determinant role in regula-
tion of cell proliferation, migration and differen-
tiation during pulp healing. In particular, members of
the transforming growth factor beta (TGF-b) family
have been implicated in reparative dentinogenesis
(4749). Nearly half of the TGFb-1 in dentin matrix
has been reported to be present in active form (50).
However, TGF-b activity decreases with a short half-
life (23min) (51) due to binding of active TGF-b to
extracellular matrix, including, for example, shedded
extracellular betaglycan-residues which bind to TGF-
b receptors (52).
Recent progress in understanding molecular and
cellular changes during tooth development, and how
they are mimicked during dental tissue repair, offers
the opportunity to assess whether this knowledge can
be exploited to design new treatment strategies in vi-
tal pulp therapy. Stimulation of odontoblast differen-
tiation has also been observed after basic fibroblast
growth factor (bFGF) and TGFb-1 implantation
(39), and after insulin-like growth factor I (IGF-I)
implantation enhanced reparative dentinogenesis was
observed (53). Specific molecules appear to be
markers of a dentinogenic response (54). Several
studies have shown that growth factor rBMP-7 im-
plantation markedly stimulates reparative dentin (47,
48, 55) but fails in inflamed pulps with pulpitis (56).
The mechanism whereby foregoing inflammation
may inhibit dentin bridging (57, 58) remains to be
elucidated. Application of exogenous signaling mol-
ecules offers opportunities for development of new
therapies (40, 53), although a number of delivery
considerations must be addressed before these can be
introduced into clinical practice (40).
Direct capping and partial
pulpotomy
As shown above, the pulp tissue is able to respond
positively to external noxious agents. In particular,
animal studies have shown hard tissue formation
Hrsted-Bindslev & Lvschall
without persistent inflammation under exposures fol-
lowing proper treatment (Table 1), whereas human
studies have documented that absence of pain is not
synonymous with success of treatment (59, 60). Clin-
ical and radiographical studies from the last few dec-
ades have shown absence of pain, positive reactions to
electric and thermal stimulation and normal periapical
tissue following direct pulp capping in 8095% of
teeth that, preoperatively, did not show signs of irre-
versible pulpitis (6163).
Discussion has been raised as to the result of direct
pulp capping following pulp exposure through cari-
ous dentin. When carious demineralization of the
dentin has reached the pulp, usually severe inflamma-
tory changes are present in relation to the affected
dentinal tubules. About 95% success after direct cap-
ping and partial or total pulpotomy of carious molars
in adolescents has been reported, even in cases with
periapical changes (6467). The theory has been that
by doing partial or total pulpotomy, the most super-
ficial part of the pulp, which may be characterized
by inflammatory changes and bacterial infiltration, are
removed and therefore the surgical wound would be
situated in sound and reactive connective tissue. In
a retrospective study, Hrsted et al. (63) showed no
statistical significant difference in clinical success be-
tween cappings made following small exposures due
to trauma from cavity preparation or perforation due
to excavation of carious dentin in teeth without pre-
operative pain. In the study, a survival rate of 97%
after 1year was reduced to 82% after 5years. The
authors hypothesize that this reduction may be a
consequence of subsequent operative procedures,
such as replacement of fillings and/or new carious
Table1. Criteria of success versus failure of vital
pulp treatment
Clinical criteria:
O Absence or presence of pain spontaneous, provoked,
duration, dull or sharp
O Sensitivity positive or negative reaction to electric or
thermal stimulation (direct capping and pulpotomy)
O Percussion test positive or negative
Radiographical criteria:
O Changes in appearance of the apical periodontium eg.
widening of the periodontal ligament, changes in tra-
becular pattern, disintegration of lamina dura
28
lesions. Furthermore, at the time of study, only acid
etching was performed and no dentin bonding agent
was used. This may have influenced the marginal leak-
age of some composite restorations, increasing the
risk of failures due to bacterial infection of the dentin
bridge, which is most often characterized by connec-
tive tissue inclusions and channels. The role of bac-
teria for the prognosis has been documented in sev-
eral clinical and animal studies (57, 60, 62, 68).
A higher success rate from capping the teeth of
young individuals with a highly reactive pulpal tissue
is expected to be higher compared to capping of pulp
tissue from older patients where the pulp tissue is rich
in fibers but poor in cells and vessels. Some studies
have supported this view point (63, 64), although
others have failed to show a negative correlation be-
tween age of the pulp and success rate (61, 62, 69).
Capping material
Calcium hydroxide or calcium hydroxide compounds
have, for many years, been the material of choice. But
calcium hydroxide and most calcium hydroxide ce-
ments are liable to dissolution and, in cases of micro-
leakage around restorations, bacteria may gain access
to the exposure site. Therefore, much research has
been devoted to generate alternative materials. How-
ever, the effect of calcium hydroxide has been verified
in numerous histological and clinical studies and each
time a new material for capping or pulpotomy is sug-
gested, the effect of the new material is compared
with the effect of calcium hydroxide (e.g. 70, 71).
Recently, materials as hydroxyapatite, tricalcium
phosphate, mineral trioxide aggregate (MTA), osteo-
genic protein (see BMP-7 above) and dentin bonding
materials are being discussed. Studies on hydroxyapa-
tite have shown very irregular and incomplete hard
tissue formation (72, 73) and that tricalcium phos-
phate to be most active when used in combination
with calcium hydroxide (74). The composition of
MTA is very similar to Portland cement and, as such,
the material sets hard in moist environments. During
the setting reaction, calcium hydroxide is released and
a high alkalinity is present in the exposed area. Histo-
logical studies in animals have shown high sealing
ability and hard tissue inducing capacity (71, 7578).
The material has been recommended for repair of
root perforations, as a root end filling material, for
root-end-closure of permanent teeth and for direct
Treatment outcome of vital pulp treatment
capping and pulpotomy but, although promising, the
documentation from use in humans is primarily based
on case studies (79, 80). At present, however, MTA
seems to be promising candidate as an alternative to
calcium hydroxide.
Hard tissue formation after treatment with dentin
bonding materials has also been shown in animal
studies (8183). The theory behind the use of dentin
bonding materials for direct capping has been that
the most important factor for healing is prevention of
bacterial contamination of the pulpal tissue. If this
can be achieved by sealing of the exposure site, organ-
ization of the injured tissue will start and odonto-
blast-like cells differentiate. Clinical and radiograph-
ical studies in humans have shown positive responses
to vitality testing and absence of pain following direct
capping with dentin bonding materials (70, 8486),
whereas histological results from animal studies have
been inconclusive. Some have shown excellent results
comparable with use of calcium hydroxide, whereas
others have failed to show the same quality of tissue
reactions as when calcium hydroxide is used (81, 82,
8791). Despite the use of adhesives, bacteria have
been found in the pulp, which has been attributed to
problems of controlling hemorrhage and other oper-
ative difficulties. It is remarkable that the histological
studies in humans have shown less success with dentin
bond capping than after capping with calcium hy-
droxide (70, 8486). It can be speculated whether
a difference in species may be of significance in this
respect.
In conclusion: Pulp capping and partial pulpotomy
with calcium hydroxide compounds are realistic treat-
ment alternatives in properly selected cases compared
to the more radical pulpectomy. Performed on teeth
which are without clinical and radiographical signs of
pulpitis and using a gentle operative technique with-
out an interfering blood clot between the capping
material and the pulp and without introducing in-
fected dentin chips and capping material into the
pulp, a high clinical success rate can be expected. In
the long run, prevention of bacterial leakage may be
of decisive importance. The cost of direct capping is
also less compared with the alternatives in both time
and money. It has thus been suggested that with
selection of a pulp capping strategy, instead of a more
radical treatment, the cost savings per year may
amount to 29 million dollars in the United States
(92).
29
Pulpectomy
It is generally accepted that a story of spontaneous or
long lasting provoked pain indicates irreversible and
extended inflammatory changes of the pulp tissue and
a more radical treatment has to be performed. In etio-
logical terms, it is likely that the pulpal infection has
reached a level where its elimination is not possible
without removal of all of the pulp tissue.
Vital pulpectomy gained general acceptance as the
method of choice compared to the previously most
often preferred mortal pulpectomy, following several
studies published in the period from about 194070
(93100). Mortal pulpectomy was abandoned for
several reasons. First, the vital treatment is considered
more biologically acceptable as it is difficult to control
the spread of the mummifying medicaments which
from time to time lead to serious pain and loss of
supporting bone. Second, vital pulpectomy can be
performed in one sitting, thereby reducing dis-
comfort for the patient.
With vital pulpectomy, the clinical aim is removal
of the entire pulpal tissue short of the anatomical apex
followed by a bacteria-tight, biocompatible and stable
root filling. With this treatment, diseased, infected
and often also non-infected and non-inflamed tissue
is removed to an apical level where the wound surface
can be kept to a minimum, the residual pulp tissue is
well vascularized, and the conditions for healing are
optimal, provided the entire treatment can be carried
out under aseptic conditions. The tissue reactions im-
mediately following extirpation and root filling show
inflammatory reactions in the residual pulp with re-
sorption of the canal walls. After a couple of months,
apposition of hard tissue onto the resorption lines and
only few inflammatory cells can be seen close to the
root filling in successful cases.
In vital cases with pulpitis the apical part of the pulp
tissue is normally devoid of bacteria, but deviation
from an aseptic procedure during endodontic treat-
ment may introduce bacteria in the canal, which can
jeopardize the treatment, causing an infection of the
periapical tissue. Studies have provided strong indi-
cations that inappropriate asepsis during treatment of
vital pulps may cause periapical inflammatory reac-
tions (101, 102).
Another factor of importance for the successful out-
come of pulpectomy seems to be the distance from
the anatomical apex to termination of the root filling.
Hrsted-Bindslev & Lvschall
Fig. 1. Capping of healthy pulp tissue in a rat molar with a
calcium hydroxide cement (Dycal) is here observed after 3
days. Necrotic layers form a biological membrane beneath
which the inflammatory and reparative processes occur.
Next to the calcium hydroxide a layer of compression ne-
crosis (arrow) and lytic necrosis (LN) are observed with a
distinct border towards the underlying layer of coagulation
necrosis (CN), which contains numerous dark pyknotic nu-
clei.
Thus, studies have shown that a distance from radio-
graphical apex to root filling exceeding 3mm reduces
the success rate compared to a termination of the fill-
ing 03mm from the radiographical apex (95, 103,
104). Theoretically, a placement of the wound at the
so-called apical constriction is aimed at (105). How-
ever, nature is not always in accordance with theory
and where this place is impossible to define by touch,
a distance of extirpation of 12mm from the radio-
graphical apex is generally accepted. However, it
should be considered that the histological measures
of the residual pulp are most often less than the radio-
graph suggests, and that chronic inflammatory
changes may prevail in the residual pulp despite ab-
sence of clinical and radiographical symptoms (94,
96, 97, 100, 106) (Fig. 1). This emphasizes again the
fact that our normally accepted clinical and radio-
graphical criteria for evaluation may not reflect the
true situation.
Excess of root filling material forced into a radio-
graphically uninflamed periapical tissue may also re-
sult in prolonged healing or persisting inflammation,
probably due to a combination of foreign body reac-
tion and material toxicity (94, 95, 106109).
The effect of quality of the root filling and of root
filling materials on the result will be dealt with in
greater detail elsewhere in this issue.
It should be mentioned here, however, that con-
30
Fig. 2. Apoptosis, a programmed cell death mechanism for
elimination of surplus or damaged cells, is observed here in
the odontoblast layer in rat molar day 7 after capping. The
apoptotic cells are characterized by condensation of chroma-
tine as a result of DNA degradation and formation of apop-
totic bodies (arrows). The programmed cell death plays an
important role as part of the pathophysiological defence sys-
tem.
Fig. 3. Dentin bridge (BD) 80 days following direct capping
of a monkey pulp with a calcium hydroxide cement. The
vacuoles subjacent to the bridge are caused by processing
problems. The empty spaces centrally in the pulp are blood
vessels and a normal structure of the connective tissue can
be seen without inflammatory reactions.
vincing evidence of an apical obturation with hard
tissue following root filling with calcium hydroxide
containing root canal sealers and cements has not
been given. Some studies have shown more hard
tissue modelling following root filling with calcium
hydroxide cements or following packing of sterile
Treatment outcome of vital pulp treatment
Fig. 4. Left: Radiograph of central incisor 12 months after pulpectomy in a patient due for maxillary immediate full denture.
There were no clinical symptoms and pathological periapical changes. Right: Decalcified section of the central incisor shown
to the left. The tissue close to the root filling cement (C) is dominated by numerous inflammatory cells (IN) and resorption
of the canal walls. Further apically few inflammatory cells and apposition of hard tissue can be seen (H) (106).
dentin chips compared to other materials but only in
rare instances a total apical constriction with hard
tissue been shown (110113). One of the reasons
might be that, even though a delicate piece of work
has been done during performance of the pulpecto-
my, the gentle technique in wound treatment that can
be done in the coronal part of the pulp is impossible
to do in the apical darkness.
In conclusion: In controlled clinical and radiograph-
ical studies, success after pulpectomy can be obtained
in about 95% of the cases, which is almost the same
success rate as seen following direct capping and par-
tial pulpotomy. The results following pulpectomy and
necrotic cases without rarefactions are almost the
same, whereas results from root canal treatment of
cases with diagnosed periapical infection are signifi-
cantly poorer (104, 108, 114116). This indicates
31
that the battle against bacteria can be difficult to win.
Thus, the best endodontics may be no endodontics,
as demonstrated by indirect capping. The second best
is endodontics where the healing potential of the pulp
tissue is turned to the best advantage as in direct cap-
pings/partial pulpotomy or if the pulpal wound can
be situated in non-infected tissue as in pulpectomy.
References
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Munksgaard, 1994: 1376.
Hrsted-Bindslev & Lvschall
4. Singer AJ, Clark RA. Cutaneous wound healing. N Engl J
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5. Hrsted P, El Attar K, Langeland K. Capping of monkey
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