PULP HEALING

R. L. GLASS AND H. A. ZANDER

Tufts College Dental School, Boston, Massachusetts

T HE treatment of exposed pulp remains a controversial subject because no

criteria for pulp healing have been established. Pulp capping is performed
to maintain the vitality of a tooth; it is justifiable only if healing results under
the capping material. Most pulp-capping experiments in the past have been
evaluated on a clinical or roentgenological basis only. Such investigations ap-
pear to be concerned with the lack of adverse symptoms rather than the actual
healing process. However, there exists no clinical method by which one can de-
termine whether or not healing results. It is a &ell-known fact that pulp
degeneration and necrosis may occur without any clinical signs or symptoms.
A roentgenogram shows only those gross pathological changes which may or
may not result at the apex of a tooth. Furthermore, vitality tests may indicate
a vital tooth although the entire coronal portion of the tooth may be necrotic.
Therefore, clinical studies using these methods of evaluation give only hazy
results that should be substantiated by histological study.
In general, healing may be defined as the restoration of a tissue to its
normal structure and function. The dental pulp is normally encapsulated by
dentin and an adherent odontoblastic layer. Therefore, in applying this defini-
tion to the pulp, healing means the presence of healthy tissue capable of carry-
ing on the function of the pulp, a continuous odontoblastic layer, and the
erection of a dentin barrier walling off the exposure.
The object of this investigation was to determine whether or not, and
under what conditions an exposed, healthy, young pulp is capable of healing
according to the above definitions.
REVIEW OF THE LITERATURE
Dentists for a long time have believed the pulp to be capable of healing.
The first mention of pulp capping is found in 1756 when Philip Pfaff' attempted
to cap exposed pulps with a small piece of gold carefully adapted to the base of
the cavity. In 1826 Leonard Koeker2 cauterized the exposed portion of the
pulp with a red hot iron wire, then covered the exposure with a piece of lead
foil. Since this date there have been virtually as many technics of pulp capping
as dentists. The earliest attempts to promote pulp healing consisted of placing
different metallic foils against the site of the exposure. This is not illogical,
since certain metallic splints are used effectively in the treatment of bone frac-
tures today. The use of drugs and other materials in close contact with the
This investigation was supported by a Research Grant from the Division of Research
Grants and Fellowships of the National Institute of Health, U. S. Public Health Service.
Presented at the 26th general meeting of the International Association for Dental Re-
search, Rochester, N. Y., June 18-20, 1948 (J. D. Res. 27: 744, 1948).
Received for publication July 9, 1948.

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98 GG LSS AND ZANDER J. D. 1949
April, Res.

pulp gradually came into widespread use. Among the materials recommended
to promote healing of accidental and pathological exposures are the following:
asbestos, l)laster of Paris, powdered ivory, tissue paper (and) Canada balsam,
aseptic sponge, vulcanized rul)ber, court plaster, gutta percha, cork, quill, oiled
silk, gall nuts, beeswax, l)ulverized glass, zinc oxychloride cements, collodion,
boracic acid, iodoform powdeer, iodoformagen, formaldehyde, lactophosphate of
lime, borax, zinc oxide, zinc oxide eugenol, zinc oxide and thymol, Ca3(PO4),
and eugenol, (aCO(),, CaF., Ca:(P04)2, AMg3(PO.1). and eugenol, Ca(OH)2 and
eugenol, AgLO() , Ca F'., and water, and zinc phosphate cements.
In addition to these materials listed, there is a great variety of commercial
preparations wit-h known and unknown formulas. For each of the above drugs,
there is ardent testimony as to ease of manipulation and successful clinical
results. However, there is little or no controlled experimental evidence to sub-
stantiate their use to promote pull) healing. Five to ten years later such articles
are followed by refutations and recommendations for new materials and tech-
nics. One would gather that a dentist finally saw many of his pulp cappings
return to his office as aching and/'or nonvital teeth.
White in 18593 and Grove as late as 1928-1 believed the dental pulp, like
other specialized tissues, to be incapable of regeneration; thus they discarded
attempts at pulp capping as impractical. Their ideas were substantiated in
part in 1927 by Palazzi,5 wcho exposed aseptically the pulps of dog teeth without
causing any hemorrhage. These exposures were capped with asbestos and metal
discs not in contact with the plulp. Palazzi found that the pulp underwent
degeneration and failed to heal. In contrast are the histological studies of pulp
amputations6 which show that the Pulp can heal. There is definite histological
evidence that a bridge of dentin is formed at the line of amputation. Such a
bridge could not be forme(l unless the dental pull) is capable of healing.
EXPE'RIMENXTAL PROCEDURE
To determine whether a sound, young pulp that is deliberately exposed
is capable of healing, the following experiment was carried out. Without
anesthesia, occlusal or gingival third cavities were prepared under a warm
water spray in sound bicuspid teeth to be extracted for orthodontic purposes.
After a classical cavity preparation was made, the pulp was exposed. The tooth
was then isolated with cotton rolls, the cavity dried with compressed air, and the
exposure was capped with one of the following materials: (1) a paste of zinc
oxide and eugenol or (2) a paste of calcium hydroxide and tap water. The
remainder of the cavity in either case was filled with zinc oxide and eugenol.
Only patients losing a minimum of two teeth were included in this study, so that
healing could be studied under different conditions in the same patient. Zinc
oxide eugenol and calcium hydroxide water pastes were used as capping materials
under which to study healing, because of the acceptance of the former as a
bland filling material and the successful results with the latter in amputation
experiments. A total of 40 sound teeth frown children 9 to 15 years of age were
used.

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Volume 28
Number 2
fPUL1jP I \LINU 99

Trhese teeth were extracted at intervals of 24 hours,, 2, 4, 6, 8, and 12 weeks

a after the pulp1 eapjiing wvas perl'oried. The extracted teeth were immediately
ground into lolonitudinal] sIlabI)S, fixed inl Zenker formol, decalcified in 5 per cent
nitric acid, aindi prepared ii t-he usual manner -for celloilin sections, which were
stained with hematoxxlm anti cosim.

.¶, 4. '2.c. .7'a.i

A. .
.'ar4 te.

rig. 1. E'ximesure 2-1 hours after capping with zinc oxide cuuzenal. A. site of exposure, B. den-
tin walls, C. h meni hagie mass, and D. 1)ulp.

i? iRsTMi,

A mi-arked difference in healing capacity is observed between exposed )ulps

capped with zinc oxide enigenol. andt calciui hydroxi(le. An exposure 24 hlours
after it was capped with zinc oxide eugen10ol ]t)aste slows below the site of the
exposure a mnass of red b1loo(1 cells and poloylnorplmollclear leukocytes (Fig. 1).
The hemorrhagic mass is (lemarcated Troin the underly.?-hing pulpl ti ss-ue b)y a zone
of fibrin and infltammatory eells. There is hemorrhage into tihe corommal portion
of the pulp.) and a m-oderate influx of pol-ymoi-phontielear leuluicytes. In sharp
contrast is a 24-hour exposure capl)ed with caleiumii hy-vdroxide (Fia. 2). There
is -no hemorrhagic mass and lint few inflamimiiiatory cells. lloweNver, the super-
ficial portioii of the pull) that wa, s in contact wxxith the calcium hydroxide is
necrotic; there is little or nio cellular detail lpresent. This necrotic area is de-
marcated fronm healthy pulp tissue below b)y a iiew, deeply stainingo zone, a
higlih power view of which is seen in Fig,. 3. This zone is comprised of baso-
philie elements that are )rolbab)ly nmade til) of a calcilln lroteillate. Caleium
lhyidroxide being basic, wvith a hif aroumid 11, ner(otizes the superfieial tissue;

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100 GLASS AND ZANDER J. D. Res.
April, 1949

the location of the proteinate globules probably represents the depth of pene-
tration of the calcium hydroxide, which finally reacts with tissue protein to
form this new structure.
Two weeks after capping with zinc oxide eugenol, degeneration is apparent
at the site of the exposure and a chronic inflammation exists in the pulp tissue
below (Fig. 4). Lymphocytes, plasma cells, and polymorphonuclear leukocytes
are seen around the site of the wound; there is hyperemia and hemorrhage in
the underlying tissue. A two-week-old exposure from the same patient, but
capped with calcium hydroxide, shows a healing process that is well under way
(Fig. 5). A portion of the superficial pulp tissue necrotized by the calcium
hydroxide remains at the site of the exposure. The original proteinate zone of
demarcation seen in a 24-hour calcium hydroxide specimen is still present;
against this zone there is a new area of coarse fibrous tissue, shown in higher
magnification in Fig. 6. This fibrillar structure may be likened to the fibrous
or primitive type bone found in rapid bone healing. Like primitive bone, this
fibrillar structure or primitive dentin is probably only partially calcified, since
calcification tends to lag behind matrix formation. On the periphery of this
new fibrous tissue, cells resembling odontoblasts appear to be lining up. This
is the earliest sign of differentiation of new odontoblasts. The pulp tissue be-
low is normal and is free of inflammation.
An exposure four weeks after capping with zinc oxide eugenol shows at
the site of the exposure an increasingly larger zone of chronic inflammation
(Fig. 7). Polymorphonuclear leukocytes, lymphocytes, and plasma cells are
present. The dentin fragments forced into the pulp are undergoing resorption
in some places; new dentin is being deposited around other areas to join these
fragments together. An exposure from the same patient extracted four weeks
after capping with calcium hydroxide is shown in Fig. 8. The superfiel tissue
necrotized by the calcium hydroxide has fallen out. The pr'oteinate zone of
demarcation seen in the original 24-hour specimen is still visible. Against the
fibrillar structure formed after two weeks, a well-defined zone of new dentin
has been deposited with an adherent layer of new odontoblasts-both continuous
with the walls of pulp chamber. Fig. 9, a high magnification of Fig. 8, shows
in detail the newly formed dentin and odontoblasts. The tissue below is normal.
The pulp has healed.
Even after eight weeks an exposure capped with zinc oxide eugenol has not
healed (Fig. 10). The original site of the exposure is walled off only by chronic
inflammatory cells. The coronal pulp tissue below is mildly infiltrated by
lymphocytes and polymorphonuclear leukocytes. The remainder of the pulp is
essentially normal. New dentin is being deposited around the dentin fragments
forced into the pulp. An exposure from the same patient, caped for eight
weeks with calcium hydroxide, shows an advanced stage in the healing process
(Fig. 11). The same elements seen in a four-week specimen are present; how-
ever, the dentin barrier is thicker and the odontoblasts appear to be more regu-
larly aligned.

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Volume 28
Number 2
PLPIJ HlEALING' MI1

Fig. 2.-Exposure 24 hours after capping with Ca (011)2. A. site of exp)osme, B. dentin walls,
C. necrotic area, ). line of demarcation anl calcium proteinate precipitation, and B. pulp.

Fig. 3.-High magnification of line of demaorca tion showi n in Vig. 2. 1. necrotic ar-t , 1B. line
of demarcation and calcium proteinateIprecipitation, anll C. vitl pulp) tissue.

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102 GLASS AND ZANI\)EjR J. D. Res.
Aprfl, 1949

LMig. 4.- E'XP1)otlle two5wheek-s arftel Capp)inlg xtis zinc oxide eug-enol. A. site, of exposui, .
dentin wA ills, C. area of cihronic inflaninsation. anil I). sires s) l'liy(atminss and hemsorrhsage.

Fig. . -Exposure two weoks sfter eappingiw ithl Ca ( )1-) I. A i site cd exposure, B. slentin w aills,
C. flecI5tic aire5 1). line of (deals retio, F. a sea of fibiu.s pal information, ansi F. vit-l pulp.

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Volume 28 I '1I I-) AINl 108
Number 2

Fig. 6. High niagnitication of areis D) and E in Fig. A.4 line of deemarcation, B.

fibrous proliferation, C. capillary enclosed by tibouo's proliferattion, I). dlignImment of pulp cells
w which ,i f to differentiate into odontobhlrists, A nerve, rind F. c apillhty.

Fig. 7.-Exposure four weeks after capping xwitli zinc oxide eugenol. .4. site of exposure, B.
dentin walls, C. area of chronic inflamnmation, and 1). dentin fragments.

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 Fig. S.-PI-xpoisaue four weeks after capping with Ca (011)2. A. site of exposure, B.
dentin a<llas, C. remnintt of necrotic asrea, D. zone of demnarcation and primlitive dentin, ;and
E. new dentin barrier.

;,MISSISSIPPI

Fig. 9. HIgh magnification of areas D and E in Fig. 8. A. primitive dentin, B. new dentin
barrier, C. predentin, D. odontoblasts, and E. pulp.

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Volume 28 PULP H[EAIJTNG 105
Numuiber 2

I)ISCUSS ION
Originally, healing- of anI exPosed pull) was detited as the walling off or
the exposure by niew dentin formation. Aceo(riinig to this dictum, sound, young
l)ll1ps eal))ped with calcium >dimroxide are healed within- four weeks (Fig. 8).
Zinc oxide eugenol failed to promote healing of exp)ose(d, souind > oungtlc puips.
Aflthlough lll)5s eal)le(1 itlb zine oxi(le eugcenol remained vital an-d without
clinical sympitios duriing the course of this experiment, a elronie inflammatory
readtion- persisted aIt tlhle of the exl)oslmle. This demonstrates thle inadequacy

1 10.-E1X:poSLl'e eight A'ceks (i'elr)pillO

fti slii
it cxo E o
1(l nol. A1. site Of' exposure,
11111tion, 1). dentin tfile
B. dentin walls, C. crea of ('bionic intflm nts, and1 E. norital plpli).

of clinical evaluation ailoew of such. experin X1. SINseeat Ieases, new dentin
was deposited around dentin fr-agments Torced into the pulp. In one ease new
dentin was deposited on the wall of the 1ilj) clamber in an attempt to eon-
striet the diameter of the pulp and join. dentin fracments to form a barrier.
The only sign of healing olserve(1 Nwis this attemp)t of the pulp to join dentin
fragments loreed into the- plmp hy a burr at the time of exposure. In no ease
was an exposure capped wvith zinc oxide euigenol completely walled off by new
dentin formation during the 12-week duration of this study.

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106 G"LASS ANT) Z.\NI)LJ? J. ID. Res.
April, 1949

On the other hand, the lpieviolllsV listed criter-ia for pui]1) lhealingy are seen
in. the healing of exposures treated with calcium. hi-ydroxidle. Withlini ofur weeks,
the continuity of the odontoblastie layer has l)een restored, the exp)osue has
beei wiNlled off- by new dentin formation, and the p)u11) is1 normal. When calcium
hydroxide comes in- contact withi exposed pull) tis-sue, there occurs wvithlin 24
hours a linear (leposition of a calcium ])oitclnate, forming a basophilic zone
that shcarpl)]v demaireates normal p1lp) tissue fr-om the sll-)erficial area neerotized
lby the basic calcium hydroxide. Against the proteinate zone there occurs a
proliferation of coarse, fibrous elements that uindergo calcification to form what
may be called a ''primitive'' type of dentini. After two weeks new odontoblasts
start to (lifterelitiate andl a barrier of new (ientiin is formed to join the walls of
the pu1lp) clhamber to compllete tie healing p)roe8ss.

Fig. 11.-Exp)osure eight weeks after ca-pping ix itl Ca (OH)2-. 4. site of exposure, B.
dentin -w tlls, C. remnant of necrotic area, /). zone of demarcation and primitive dentin, E. neIw
dentin barrier, F. continuous ldontoblastic lay er, and G. vital pulp.

ARY
S UMA t\I

Ptlp) hlealing. t1111eler I}o commoily uised materials, zinici oxide eugenitol and
calcium hydroxide w water hastes, has been studied in exposed, sound young
Iul1ps. N-o healing w-as observed in exposed pulps capped with zine oxide
eLgeoIlV ; Jullp so treated relmaine(l vital, but a chronic inflllmatory reaction
site of the exposure. However, when exposed p)ulps are capped
persisted at. thlei('
with calcium hydroxide a raid healin-o process is seen, relatively free of inflam-
mation. Wit bin four Weeks the orig-inll site of the exposure is completely
walled off liv a niew odontoblastic -lav-er and a new dentin barrier.

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Volume 28 PULP HEALING 107
Number 2

REFERENCES
1. Pfaff, P.: Abhandlung von den Zaehnen des menschlichen Koerpers und deren Krank-
heiten, Berlin, 1756.
2. Koeker, L.: Principles of Dental Surgery, London, 1826, Underwood, p. 433-437.
3. White, J. D.: Practical Hints, D. Cosmos 1: 618, 1860.
4. Grove, C. J.: Capping Vital Pulps, J.A .D.A. 15: 1688, 1928.
5. Palazzi, S.: Experimentelle Untersuchungen uber das Problem der Heilungsvorgange in
de blosstgelegten gesunden Pulpa, Ztschr. f. Stomatol. 25: 91, 1927.
6. Teuscher, G. W., and Zander, H. A.: A Preliminary Report on Pulpotomy, Northwestern
Univ. Bull. 39: 4, 1938.
7. Zander. H. A.: Reaction of the Pulp to Calcium Hydroxide, J. D. Res. 18: 373, 1939.

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