Endodontics

American Association of Endodontists

I. B. Bender, Editor

Pulp response to externally

applied heat
Leo Znch, D.D.S.,* and Gerson Cohen, D.D.S.,*” New York, W. 1’.
NE\\’ YORK UNIVERSITY COLLEGE OF DEXTISTRY

T he ascending severity of pulpal lesions induced by heat as an isolated stress

is described and illustrated in this study, which is part of a continuing in-
vestigation into the biology of pulpal response. Previous work has described
the reactions of pulp tissue to the complex physical variables of cavity prepa-
ration under many modes of operative procedure.l-” In this portion of the
study, an attempt was made to single out the role of heat as the most signifi-
cant variable,6 without the superimposed effect of cavity preparation, medica-
ments, or fillings on the pulp.
&cry stress that is borne by, or transmitted to, viable dentine induces its
concomitant response within the dental pulp. Not the least of these stresses
is the heat generated during operative procedures, especially when the amount
of coolant is inadequate to prevent dissipation of frictional heat. Pulpal changes
thus far studied in experimental teeth represent the combined effect of severing
dentinal tubules and heating the pulp. Thermogenesis associated with several
operative techniques at high and low speeds, with and without coolants, has been
graphed, and the total pulpal response has been described.7, g Pulp responses
to increased temperatures induced by the application of measured heat sources
to the tooth surface have also been reported .8 Thus far, actual intrapulpal
temperatures correlated with the external heat source have not been reported
in vivo. This study, by applying a known heat source and measuring its effect
intrapulpally in a variety of tooth sizes and shapes, defines the hist,ology of
the heat parameter of pulpal stressors.

This study was supported by Research Grant D-00530, Kationnl Institute of Dental Re-
search, United States Public Health Service.
*Assistant Professor of Pathology, College of Dentistry, New York University.
“*Section Chief, Prosthodontia, Dental Department, Veterans Hospital, New York, N. Y.

515
 The measured rises in intrapnlpal tempcratln-c ~v~~I*cd(~libct~;rtt:l~~ k~I)f, wit Ill11
the range of heat rises which might bc anticipatctl during operntivcb 1II~~w~~~IW.
\VC have re;p~l%~l individual instancxcs 01’ i(~nrl>(‘riltliI’c inrl*(>;ls(ls ])(‘;t killg :IS
high as Go 8’. within the pulp aftti- 20 SccWnds ol’ irppIic2tion of ill1 air-t tirbin(a -
impelled bur using air as the onIy cooIant.!’ 12 SO0 E’. risct was adol)tcd as the
maximum t,o be assayed histologicall- in this study, so that corl*clatcls with a
broader range of clinical opcrativc dental procednros could be considcrctl.

MATERIAL AND METHODS

The test animal was the dLn(~~(l ~hcsus monkey, selected not only because its
teeth are sufficiently large and morphologically similar to the human dentition
hut also because the specific intrapulpal heat rises caused by various types of
drilling procedure had been measured previously in this species. Five adult
animals were used, ranging in weight from 5.8 to 7.6 kilograms. In all instances
the teeth showed no lesion ot,hcr than attrition, which was most marked in the
a,nterior teeth. Intraperitoneal pentoba.rbitaI, 0.5 ml. per kilogram of body
weight, was the anesthetic.
The testing apparatus is diagrammed in Fig. 1. Intrapulpal temperature
rises were induced by applying a soldering iron to the labial or buccal aspects
of the tested teeth approximatelr 1 mm. from the gingival crest. The soldering
iron tips were made slightly concave by grinding so as to conform as closely
as possible to the contour of the enamel. No cavity preparation or other treat-
ment, except scaling to remove sordes, was performed. The soldering iron tips,
measuring 3 by 1.5 mm. on the surface applied to rnamel, reached a temperature

Multichannel
Telethermometer

Thermistor Bead t
Encased in 22ga sealed needle

Fig. 1. Diagram of apparatus usctl to producczand measwc intrapulpal heat rises.

Thermistors,placedagainstthe pulpal wall, are exkemely rnpid and accurate in tjhcir thcmmt~l
responsr.
of 275O C. Contact with the tooth was maintained for periods from 5 to 20
seconds to produce the range of thermal changes studied.
Minute, bea.d-type thermistors, small enough to he seated within 22 gauge
hypodermic needles, were used to detect temperature changes. The end-sealed
needles were inserted into the pulp chambers through small cavities on the
lingual surfaces of anterior teeth and on the occlusal surfaces of posterior teeth.
Mounds of dental cement were packed about the needle as it protruded from
the cavity. This cement performed a dual function; it prevented displacement
of the encased t.hermistors and served as thermal shielding or insulation to rule
out aberrant heat readings caused by heating of the needle itself. The angle of
insertion of the needle into the pulp chamber was regula.ted so that the ther-
mistor-bearing tip was maintained in contact with the pulpal wall at the point
closest to the area of application of the soldering iron tip. These positions were
checked with radiographs.
The temperature-recording device was a multichannel telethermometer,” pre-
calibrated in each channel to a specific thermistor. Several teeth could be “wired,”
and serial recordings of temperature changes could be taken simply by switch-
ing in to the various channels. Minimal lag time and an accuracy of 1.5 per
cent within the range used led to the selection of this instrument.
The number of seconds required to produce the desired temperature increase
within the pulp was recorded for each tooth tested. All thermally measured
teeth were in the same quadrant in each animal. The opposite quadrant was
reserved for histologic study. The test conditions were reproduced on the contra-
lateral teeth at a subsequent experimental session. For the teeth used in the
histologic examination, no cavities were made in the pulp chamber, but the
soldering iron tip was applied for the same number of seconds as on the ther-
mally measured homologous tooth. Within the limits of error caused by size
differences of teeth on the opposite quadrant of the same test animal, it was
assumed that the temperature rise would be approximately the same for the
unmeasured teeth as it was for the thermistor-bearing teeth. One investigator
applied the heat source in all instances, while the other monitored time and
temperature so that replication of test conditions on both sides could be as
accurate as possible. Constancy of the soldering iron heat source was measured
for each experimental run. The iron was preheated in an asbestos-lined Pyres
tube for 5 minutes, and the temperature rise within the tube was recorded when
a maximum reading was maintained for 2 minutes. Ko variation greater than
50’ C. in applied heat source was allowed between the thermally measured and
the histologically examined homologous teeth.
Intrapulpal temperature increases of from 4 to 30° F. were produced in
thermally measured teeth and reproduced on the opposite side of the jaw. Teeth
in which pulp chambers were entered to permit placement of the thermistor
needle were filled with zinc oxide-eugenol paste. Undrilled teeth received no
subsequent treatment whatever. Specimens were obtained at intervals of 2, 7,
11, 56, and 91 days after heat a.pplication.

“Yellowstone Spring8 Instrument Co., Model 4 1C.

518 Inch and Cohen O.S..O..\I.B 0.1’.
.\ljril, lNi.5

The animals wcrc killed by bilatcLra1 perfusion of the carotitl artc:rics wit II
Bouin’s picratc-formalin solution. This technique minimixcs fixation artcfaet
Tooth-bearing blocks of full-thickness mandible and maxilla W(W further fixcttl
and then decalcified in neutral buffered EDTA (sodium salt). Paraffin sections
were cut at 7 microns and stained wit,h hematoxylin-eosin, alcian. blue-PAS
( Schiff) , and Weigert’s reticulin stains. Control sections were also preparrcl
from each animal, using teeth to which external heat was not applied.

RESULTS
lntrapulpal temperature increase of 4O F.
After 2 days this modest temperature increase produced only minimal intra-
pulpal changes confined to the odontoblasts in continuity with the area of ap-
plication of the soldering iron tip. A few small interodontoblastic vacuoles (V)
were evident just below the predentine (PD), as shown in Fig. 2. These micro-
blisters were directly attribut,able to heat rise at a low range. No other changes
were found; the stroma was normal and the predentine was unaffected. Sec-
tions taken at subsequent intervals of 7 days to 3 months after external heat
application disclosed normal pulps with no trace of increased secondary dentine
elaboration. These specimens were histologically unidentifiable from control
unheated specimens.

lntrapulpal temperature increase of loo F.

At this range a considerably more marked intrapulpal response was apparent,
both immediately and after prolonged intervals. Fig. 3 illustrates, in a 2-day
specimen, the destruction of a majority of the odontoblasts and the spatial dc-
rangement and pyknosis of the diminished remainder (0). Large numbers oE
“aspirated” odontoblastic nuclei (AO) were found within the dentinal tubules.
Uncalcified predentine (I'D) was reduced in thickness, with nuclear debris and
microblisters apparent almost in contact with mature primary dentine. The?
subjacent stroma was edematous. Fig. 4, photographed to show the full thick-
ness of overlying dentine in the same specimen, demonstrates the invariable
denaturation of matrix and destruction of Tomes’ fibrils in the area, of dentine
immediately below the region on the enamel which contacted the soldering iron
tip. This lesion, which may be characterized as a burn, was observed in all teeth
in which intrapulpal temperature was elevated loo F. or more upon which the
heat source was allowed to rest longer than 10 seconds. It will be noted that tht
intratubular odontoblastic nuclei (do) are confined to that area, of dcntinc in
direct continuity with the tubules .of the surface burn (R) .
At the end of I week reparative processeswere well under way. Fig. 5 shows
histiocytes (U) engulfing odontoblastic debris. Blood vessels (BV) in close
proximity to the odontoblasts were intensely hgperemic. The stroma was edema-
tous and streaked with protein-rich fluid (P). Elaboration of irritation dentinc
had not pet begun; the dentine was still hordered by fragments of odontoblastic
nuclei.
Two weeks after being heated to IO’ F. the pulp shown in Fig. 6 demon-
strated the initiation of repair phenomena. The normally cell-free zone of Wcil
 Pig. a. Temperature increase of 4’ F., after 2 days. Interodontoblastie vacuoles (V)
just below predentine (PD) are the only signs of disturbance after this modest thermal in-
crease. (Magnification, x250 ; reduced :g.)
Fig. 3. Temperature increase of IO” F., after 2 days. Note destruction of most of the
odontoblasts (0) and displacement of nuclei into the tubules (220). Uncalcified predentinc
(I’D) is lysed. (Magnification, x300; reduced :s.)
Fig. 4. Temperature increase of 10” I?., after 2 days. Same specimen as in Fig. 3, show
ing burn denaturation in dcntine (Zj) and concomit,aut area of ectopic nuclei (AO). (Mag-
nification, x50; reduced ys.)

(ZW) was the site of intense ccllula,r proliferation as preodontoblasts (PO)

migrated from deeper areas. New odontoblasts had begun to line up and resume
their organizer function in the elaboration of predentine (PD). Remnants oi
aspirated cells (AO) persisted in the dentine.
After 56 days, most pulps subjected to the 10’ F. temperature increase had
successfully overcome the thermal trauma, as evidenced in Fig. 7. Although bear-
ing a considerably thick plaque of irritation dentine (ID), the bulk of pulp
substance had reverted to normal. A pulpodcntal membrane (PM) was re-estab-
lished. Odontoblasts had resumed their normal form and positional relation-
ships. A calciotraumatic line (CL) sharply demarcated primary dentine from
the dentinal scar incident to thermal stress. The zone of Veil still showed cellu-
lar activity. Primary dentine continued to bc streaked with cnclaved odonto-
 CM., 0.x. Br 0.1’.
April, 1965

Fig, 5.

Pi!/. 6.

Fiy. 5 Ten lperaturr increase of 10” F., after 1 week. Odontoblastic dt ~bris is being en-
gulfed hv ‘histic jcytes (H). Parked blood vessels (BP) are seen in the rdemz ttous St,1roma ( F).
(Magnifi;:: tti “11, x210 ; reduced :ys.)
Fig. 6 Tern tperature inarease of 10” F., after 2 weeks. Repair has begs m in th .e zone Of
Weil (ZW 5 wit ;h proliferation of preodontoblasts (PO). Predentine (P. j) is i iOl-1 ned wl hile
aspirated odont oblasts persist. (Magnification, x750; reduced :ys.l
Volume 19
Number 4

Rig. Y. Temperature increase of 10” F., after 8 weeks. A thick plaque of scar dentine
(ID) below the calciotraumatic line (CL) is evidence of healing. Pulpodental membrane (Paw)
is re-formed. Lingual wall area (LW) shows relative inactivity. (Magnification, x60 ; re-
duced Vs.)
Fig. 8. Temperature increase of 20” F., after 2 days. Odontoblasts (0) destroyed and
dcntine rich in ectopic nuclei (AO). Blood vessels (BV) are engorged. (Magnification, rlW;
reduced l/s.)
522 Zach and Cohen

blastic nuclei, which remained ax a permanent histologic index 01: previous

thermal trauma. The relative inactivit,v on the unheated lingual pulpal wall
(LTV) was demonstrated by the small size of the unstimulnted odontoblasts
and the total lack of irritation dentine.
At 91 days a 10’ F. intrapulpal temperature rise showed much the same
picture as at 56 days. The pulp bore the stigma of the heat in its irrit!ation den-
tine scar and displaced odontoblastic crll bodies, but the rest of the tissue had
resumed normal appearance. Several pulps of small teeth failed to survirc a
10’ F. heat rise and became necrotic.

lntrapulpal temperature increase of 20° F.

At this level of thermal stress, a critical range in pulpal response was frc-
quently exceeded. Some pulps showed reactions leading to stimulation of ex-
uberant healing mechanisms, while others went on to ultimate necrosis.
Two days after being heated to a peak temperature of 20° F., a typical pulp
(Fig. 8) showed complete destruction and disruption of involved odontoblasts
(0). Numbers of ectopic odontoblasts (80) were found within the dentine,
while the predentine was totally lysed. Vessels (BV) were engorged and packed
with inflammatory cells, some of which had found their way into the stroma.
The affected area was strewn with fragmented nuclear debris, which was par-
ticularly evident below and between t,he necrotic odontoblasts. One week post-
healing, cellular activity of histiocytes had engulfed much of the nuclear debris,
as shown in Fig. 9. Histiocytes (II) abounded in the packed stroma. Entire
odontoblasts, coagulated and “fixed” by the heat application, persist,ed close to
the dentine wall. These dead cells (PO), too large to be removed by the macro-
phages, became embedded in the reparative process. Their persistence will bc
noted later in those few specimens which survive a 20° F. intrapulpal tempera-
ture increase.
Repair was well under way 14 days after the pulp had been heat,ed, as shown
in Fig. 10. In this specimen, preodontoblasts could be observed (YR) undergoing
elongation and orientation as they slipped into position to replace the cells lost
by the heat trauma. Entrapped odontoblastic nuclei, surrounded by their halo
of heat-coagulated cytoplasm, were seen (PO) fixed in position adjacent to the
primary dentinal wall. Disorganized repair dentine (IZD), henceforth to 1)~
termed “stress” dentine, was being formed by maturation of precipitated col-
lagen.
With healing nearly complete 56 days after being heated 20’ F. above nor-
mal intrapulpal temperature, the pulp, as shown in Fig. II, reverted to an
essentially pretreatment st,ate. Odontoblasts (0) were fully formed and tubular
dentine could be observed above them. The zone of Weil still had not returned
to quiescence, but the deeper stroma was completely normal. Beyond the region
of newly laid-down tubules, a ma= of disorganized, nontubular dentine (KU)
demonstrated the whorling pattern of rapidly elaborated matrix. Near the top
of the section numbers of entrapped fragmented cells (PO), remnants of co-
agulated odontoblasts, had been incorporated in the stress dentine. At 91 days
post-heating to 20° F. elevation, a, humped-up, hnlbous mass of st ITSS tlcntinc
 Pulp response to exterdly applied heat 523

Fi g. 3. Temperature increase of 20” F., after 1 meek. Stroma is rich with histiocytes (U)>
while odontoblastic dehris (PO) is “fixed” in the injured pulp. (Magnification, x750 ; re-
dUCd %.I
Pi g. 10. Temperature increase of 20” F., after 2 wwks. Rrpair is proceeding as de tntine
matrix : (RD) is elaborated and preodontoblasts (PR) move into position. Trapped od lonto-
l~lxsts cI’0) persist. Frw pulps withstood a 20 degree rise. (Magnification, x750; rrduwd %.I
 O.S., 0.M. c 0.1’.
April, 1965

Fig. 11. l’m~pcrature increase of 20” I’., after 8 ~ceks. Note successful healing aftct
great stress, with odontoblastic debris (PO) wtrapped within atres3 dentine (ED). Odonto-
blasts (0) have re-formed. (Magnification, x450 ; rcduwd ‘A.)

remained (Fig. 12) as a pcrmant~nt stigma of the thermal trauma (ED). The
pulpodenta,l membrane (Pdl) had Betsy re-formed, and there was reversion to
the elaboration of normal prcdcntint (PD) with regular tubules. The adjacent
stroma was richly vascular, reflcctinp 11le heightened metabolic requirements of
this hyperactive area of pulp.
Teeth which failed to respond with a reparative reaction to this critical level
of a 20° F. intrapulpal heat incremc~nt almost invariably demonstrated an intra-
pulpal abscess. Fig. 13 is typical of the t,hirtccn specimens (out of twenty-one)
so deranged at 20° F. as to respond with irreparable necrosis. The pulp-horn
abscess (A) was bordered by a i’ecble attempt at fibrous walling-off, but thch
deeper stroma was liberally infiltrated with I)c~lymorphonuclear leukocytes (PI;).

lntrapulpal temperature increase of 30’ F.

When intrapulpal tcmpcraturc was elevated 30” F. above normal by the

application of an csternal heat source, all terth so treated showed an over-
whtlming, i~revn+siblc necrotic iwpollse. b’ig. 1-l ~110~s total necrosis 2 days
after SO0 F. htlating. XII pulpal architccturc~ was blanked out by masses of
hemorrhagic and fragmented debris (HD). Predentine had also been lysed in
the rcsponsc. Tn tooth spwinkcns obtainc4 il FtW lollgel* p(lriods, pulp (*ontents
\‘OlUrnC? 19
Number 4

Fig. II. Temperature increase of 20” F., after 12 weeks. End result of hraling with pm-
tuberant scar of stress dentine (RD). Tubular predentine (PD) and pulpodental membrane
(PX) now normal. (Magnification, x200 ; retluacd 3/s.)

had undergone liquefaction. Fig. 15 shows an essentially empty pulp with only
a few necrotic strands persisting in the liquefied mass after 14 days. The deep
burn reaction in dentine at the point of heat application is evident (B). Several
test animals in both this 30 degree series and the 20 degree series experienced
severe dentoalveolar abscesses and had to be maintained with tetracyclines prior
to death. No histologically recognizable pulps were recovered after intrapulpal
heating to 30° F.
A corollary finding in teeth heated to this excessive int.rapulpal measurement
is shown in Fig. 16. On the heated labial wall of the tooth, the root in the region
of the alveolar crest (1lC) showed small lacunar defects (L) which had eroded
through cementum and begun to encroach upon dentine. These eaten-out arcas
were lined by large, osteoclast,-like cells (OC). Vessels in the submucosa ant1
periodontal membrane were swollen. This lytic phenomenon at a site distant
from the point of heat application resembled Bernicr’s “rebound reaction.“3
It is a further example of the potentially powerful effects of severe thermal
irritation.

DISCUSSION
The accumulation of evidence indicating that dental ptllp is a hardier tissue
thiln had been previously b4icvcd has cont,ribnlc~l to t lI(l (5pansion, icl1lal’l> pil’t
 526 %ach und Cohen

Fig. 1s. Temperat ure increase of 20” F., after 1 week. More custc ma I’Y rrs[ lonse to 1this
tennperaturr incremrnl with pulp-horn abscess (A) and arutca inflame :01‘?’ PX udat e II ‘L )
in the surrc mnding stl ‘oma. (Magnification, x50 ; reduced IA.)
Fig. 14. Trmpernt ure increase of 30” F., after 2 days. Total net ,ros is as esvidel riced l,Y
obl !iteration of all nor ma1 pulp with hemorrhagic and fragmented dehl *is (1 ‘11)). ( iif? tgnifi irn-
tio II, x250; reducrd Q .)
v01un10 19
Sumlrcr 4

16. Temperature increase of 30” F., after 2 weeks. Totally necrotic pu IlP stor nary
zie s, with intense burn response on buccal dentine. (Magnification, x40; re :ed 143.1
16. Temperature increase of 30” F., after 2 weeks. Lacunae in root, $1 1 I at line
lar crest, (AC’). Areas linrd by osteoclast-like cells (06’). (Magnificatil :,n. LOO; re-
 Stortin
Level
Safe
-3 > Range
-5

-7

-9

-II

-13

-15

-I 7
0 5 IO I5 20 25 30 35
.tBur Contact

SECONDS OF RUN
Pig. 17. Intrapulpal temperature rises produced by* four types of operative technique.
Group I, air turbine, water-cooled; Group II, air turbine, dry; Group III, low-speed, water-
rooled; Group IV, low-speed, dry.

in the past decade, of operatic tochniqucs and irlstrument;Ltion. Responsesof

dental pulp to various operative techniques were evaluated histologically in
order to establish standards of safety. Heat production was implicated early
as the major stressor in the battery of assaults t,hat the tooth bears when it is
drilled upon. R’esults of this study indicate t,hat healthy pulps, at least in the
species tested, failed to recover from an intrapulpal temperature increase of
YO” F. in about 60 per cent of the eases.Fifteen per cent of the teeth heated
to loo F. failed to recover. Heat rises below this critical level produced renc-
tions, relative in severity to the degree of heat, which almost invariably lrd tn
pulp recovery but which left histologic stigmata. Heat rises above 20” 5’. almost
invariably destroyed the pulp.
It is of some importance to stress that these results were obtain4 in teeth
which were not subjected to the additional trauma of drilling ; nor were the>
pulps previously affected by decay or restorations. These findings, then, as es-
pressed in quantitative terms of degrees of heat rise, must be interpreted as
minimal thermal stresses to which teeth may be subjected with anticipated
pulpal reactions. It seemsreasonable to speculate that these findings might, havcx
quantitative validity when applied to human teeth.
For these findings to have significance in opcrat,ive dentistry, it is neccssar)
to correlate the pulpal responsesto thermal trauma with the heat, rises produced
 Pulp response fo e~fcrnall~y npplied Itent 529

by the various modes of drilling teeth. Ky so doing, it may be possible to offer

an index to clinical operative procedures in terms of anticipated thermal re-
sponse and to delineate those techniques of drilling which fall within the safe
heat range, those in which the p~tlp may receive irrccoverablc shock, and those
in which the pulp is almost doomed to necrosis.
In Fig. 17 the thermal gradicnt,s are divided into segments designated “safe”
and “critical.” Superimposed on these ranges arc the intrapulpal temperature
incrcascs achieved, on the average, by four different methods of tooth prepara-
t,ion. Croup I represents air-turbine drilling with adequate water cooling; Group
I I represents air-turbine drilling, dry; (iroup III represents low-speed drilling
with water cooling; and Group IV rcprcscnts low-speed drilling, dry.

OTHER THERMAL STRESSES

Jt is obvious that under the clinical conditions of actual dental treatment
the pulp is subjected to severe thermal shock from procedures other than rotary-
drill cavit,y preparation alone. The use of thermoplastic substances, such as im-
pression compound, and the insertion of hot gutta-per&a impart quantities of
heat to the already compromised dental pulp which may exceed the safety level.
,1t best, these repeated traumas to exposed dentine, often on the entire clinical
crown (as in full-coverago impression taking), contribute an additive thermal
shock of potentially serious consequence. One studyI indicates that cavit,y-floor
temperature increases of W C. were attained by the insertion of gutta-percha.
If tlic cavities were deep, such a proccdurc might well prodncc an irrcvcrsiblc
pulpitis.
As Robinson and Letkowitz” state, “Excessive heat is the most serious single
insult to the pulp. . . . All possible injuries, one added to the other, must be
avoided.” In this study, the findings relative to the destructive effects of in-
creased intrapulpal tcmperaturc arc reported on intact, undrilled, noncarious
.lLacc~cl ‘rhesus teeth. If to these pulpal rcsponscs arc added the injuries of drill-
ing, decay, medications, impressions, and filling materials, the total pulp reac-
tion may bc expected to be considerably more severe. The indication of a yard-
stick against which pulpal response to thermal shock alone may be evaluated
points up the importance in operative dentistry of minimizing cvcry condition
which contributes to pulpal trauma.

CONCLUSIONS
It is evident from this study that the intact dental pulp responds to mea-
surcd incrcascs in applied heat in a fairly const,ant, predictable manner. Factors
which would serve to modify the thermal response, such as thickness of remain-
ing dentSine, coolant, pre-existing disease, etc., were eliminated in favor of
studying the unmodified “pure” response. It is further evident that many opcra-
tivc procedures performed with little regard for thermal shock result in heat
insult t,o the pulp which enters the critical range. Especially implicated as no-
tcntial thermal irrit.ants are drilling techniques which do not make use of ade-
quatc coolants. Quantity as well as intensity of heat applied to the pulp may
be important. In this regard, it may be fruitful to investigate the effect of the
530 Zaclz md Cohen

\\‘ork continues at this and other laboratories in dforts to dcfinc~ pulpal I*(‘-
sponse and, particularly, the mechanisms involved in pulpal repair. Regeneril-
tion of odontoblasts and formation of the: amorphous scar arc the rcp;lir mwI~-
anisms which are fundamental in retaining vitalit,v of the pulp. Means 01’ unclcr-
standing and perhaps affecting thew prowsscs arc’ important awits 01’ i ti-
vostigation.

The authors wish to thank Mrs. Gloria Turocr and Mrs. Hilde Schmidl, rwearch assistants,
and Miss Elsie Dallas, laboratory twhnician, for their efforts in tissue processing. The
photomicrographs were taken by Mr. Antol Herskovits, staff photographer, ,\ontefiore Hns-
pital, New York. The diagrams were prepared l)y Mrs. Marie Yaw, staff artist, 1furrp and
Loonic Guggenheim Foundation Inst,itutg’ for I)cnntal Rcwarch, Sew York 7:nivcrsitp (‘ollego
of Dentistq.

REFERENCES
1. Br6nnstr6m, M. : Dentinal and Pulpal Rwponsr, ORAT. SLVRG., ORAL 1\IED. & ORAL I'ATH.
15: 203, 1962.
2. Seltzer, S., Bender, I. B., and Kaufman, J. J.: Histologic Changes in Dental Pulps of
Dogs and Monkeys Following Application of Pressure, Drugs and Micro-Organisms on
Prepared Cavities, ORAL SURG., ORAL MED. & ORAL PATH. 14: 327, 1961.
3. Bernier, J. L., and Knapp, M. J.: A New Pulpal Besponse to High-Speed Dental Instru-
ments, ORAL SURG., ORAL MED. & ORAL PATH. 11: 167, 1958.
4. Langeland, K.: Tissue Changes Incident to Cavity Preparation; an Evaluation of Romcx
Dental Engines, Acta odont. scandinav. 19: 397, 1961.
5. Zarh, L., and Cohen, G.: Biology of High-Speed Rotary Operative Procedures: Correla-
tion of Tooth Volume Removed and Pulpal Pathology, J. D. Res. 37: 6i, 1958.
6. Robinson, H. B. G., and Lefkonitz, IV.: Operative Dentistry and the Pulp, J. Pros. I)~~nt.
12: 987, 1962.
7. Hartnett J. E., and Smith, W. F. : The Production of Hc,at in the Dent,al Pulp by .X’s<,
of the Ajr Turbine, J. Am. Dent. A. 63: 210, 1961.
8. PostIt,, H. H., Lefkomitz, W., and McConnell, D.: Pulp Response to Heat, J. I). Xrs. 37:
740, 1959.
9. Zach, and Cohen,
I+ G.: Thermogenesis in Operative Twhnics: Comparison of Four
Methods, J. Pros. Dent. 12: 977, 1962.
10. Jarby, 8. : On Temperature Measurements iu Teeth, Odont. ‘I’idskr. 66: 3Zj 19%.