Invited author

T i s s u e r e s p o n s e t o d e n t a l c a r i e s
Langeland K. Tissue response to dental caries. Endod Dent
Traumatol 1987; 3: 149-71.
Abstract - Caries still represents the most widespread hutnan dis-
ease. The pulp tissue sequelae of dentin caries are of utmost im-
portance, because prevention ofpulpal damage considerably re-
duces the need for extensive restorations and endodontic therapy.
There is, however, considerable disagreement in the literature re-
garding how early the pulpal response to caries can be detected. The
material in this article, gathered from the author's and his co-
authors' earlier investigations, deals with pulp reactions from in-
itial caries to increasingly extensive caries; caries in combination
with attrition; the effect of carious dentin in experimental cavities of
intact dentin; the effect of medicaments, restorative procedures
and materials, and indirect pulp capping in the treatment of deep
caries; microbiologic aspects of dentin caries; diagnosis criteria for
treatment; light and electron microscopic study of teeth with cari-
ous exposure; periodontal disease and root caries in the geriatric
population; pulp biopsies of teeth with periapical lesions, and the
breakdown ofthe remaining pulp and its periapical sequelae. Pul-
pal reactions to initial caries detected as early as bacteria reach the
dentinal tubules arc also discussed. As in medium and deep caries,
this can be reversible following the removal ofthe infected dentin,
except for irritation dentin and calcifications on the canal walls or
free in the lumen. Bacteria remaining in dentinal tubules combined
with iatrogcnesis may be the reason for pulpal disintegration under
deep restorations. Indirect pulp capping is not an acceptable pro-
cedure. Pain (or lack thereof) is not a predictable indicator ofthe
inflammatory stage ofthe pulp. Root caries must be treated early to
prevent pulpal destruction. Vital pulp tissue can he found in the
roots of teeth with periapical radiolucencies that will ultimately
show the presence of bacteria.
Ka a r e La n ge l a n d
Department of Endodontics, John Dempsey Hospi-
t a l , University of Connecticut Health Center, Far-
mington, Connecticut, USA
Key words: caries, coronal and radicular; micro-
organisms; inflammation, pulpal and periradicular;
calcification; immune response; pain/no pain; pulp,
vita i and non-vital; pulp capping, indirect and direct.
Kaare Langeland, DDS, PhD, Department of Endo-
dontics, John Dempsey Hospital, University of
Connecticut Health Center, Farmington, CT 06032,
USA.
Accepted for publication 12 March 1987.
Caries - despite all prophylactic measures - is still
the most widespread human disease. Akhough die
disease has heen considerahly reduced in the popula-
tions of the West, caries causes tooth destruction of
considerable significance, placing great demands on
human labor and materials. According to the 1979
ADA Survey of Dental Practice (1) approximately
200 million fillings, 35 million single crowns, and 10
rnillion bridges were performed. In addition, there
were 50 million extractions. Almost everything per-
formed in the first 3 categories is caries-related. It is
also relevant that 17,390,000 endodontic treatments
vvere carried out that year. Furthermore, in the endo-
dontic clinic ofthe University of Connecticut Health
Center, approximately 90% of all endodontic ther-
apy is carried out in teeth that were restoratively
treated previously. Which part of the pulpal break-
down is caries-related (recurrent caries), of iatro-
genic nature, or due to the cumulative effect of all
irritants can only be speculated. The reasons for the
50 million extractions are not given in the ADA sur-
vey; it is ndt known whether the teeth were treated
earlier or if the reason for the extraction is caries or
periodontal disease. It can be assumed that before an
individual has reached 40 years of age most extrac-
tions are due to caries, whereas after 40 the extrac-
tions are mostly due to periodontal disease or a com-
bination of both. Particularly in the geriatric popula-
tion, root caries has taken on major proportions and
presents a difficult treatment problem. Thus, caries
continues to represent a practical and socio-medical
problem of great economic importance. In this re-
gard the pulpal sequelae of dentin caries are of par-
ticular interest because prevention of pulpal damage
149
La n ge l a n d
considerably reduces the need for extensive restora-
tions, and endodontic therapy and its sequelae.
There is disagreement in the literature regarding
how early the pulpal response to caries can be detect-
ed (2-6). This is due to lack of acknowledgement of
the proficiency of the available histologic method-
ology. Enamel and dentin caries may be siinul-
taneously demonstrated in ground sections. How-
ever, the technique of producing ground sections to-
tally destroys the pulp and will not allow any
observations of soft tissue and its cells. On the other
hand, demineralization of mature teeth ~ for the pro-
duction of paraffin or Em sections - leads to elimin-
ation ofthe enamel. Thus, enamel caries and pulpal
reaction cannot be demonstrated simultaneously in
the same section (7,8). However, it was earfier point-
ed out that the presence of a few infiammatory cells
in the pulp of clinically intact teeth could be due to
clinically undetected caries or doubtful conditions
subjacent to a discolored occlusal fissure (9, 10).
Ma t e r i a l a n d me t he d s
The material upon which this article is based has ap-
peared in a number of earlier investigations. Readers
interested in the details of clinical and histopatholo-
gic methodology and how these may clarify aspects
of distinct disagreement are referred to those publi-
cations. The investigations deal with: reactions to in-
itial caries (7) and to increasingly extensive caries
(11); caries in combination with attrition (12); re-
actions to the effect of carious dentin in
experimental cavities of intact dentin (13) (with the
intent of developing a reproducible model for the
evaluation of restorative procedures and materials);
reactions to the eflect of medicaments ranging from
silver nitrate and camphorated monoclorophenol to
penicillin and corticosteroids, and reactions to re-
storative procedures and materials in carious cavities
(1420); and reactions to indirect capping in the
treatment of deep carious lesions (21). Further inves-
tigations deal with: the microbiologic aspects of den-
tin caries and their pulpal sequelae (22); the diagnos-
tic criteria for the treatment of caries-
induced pupitis (23); the light and electron micro-
scopic study of teeth with carious exposures (24);
periodontal disease and root caries in the geriatric
populadon (25); pulp biopsies in teeth with peri-
apical radiolucencies related to caries (26); and the
breakdown ofthe remaining pulp and its periapical
sequelae involving endodontic therapy (27-29).
These studies encompass more than 2,000 teeth. The
patients represent a cross-section of the population
from children all the way through to the geriatric
population.
In order to obtain sections of reproducible quality,
methods and criteria as used and described in the
quoted references are essential (7, 8, 10-18, 22, 24,
26).
Obs e r va t i o n s
In teeth with only early indications of clinical caries
such as a discoloration of an occlusal fissure or of an
approximate surface, a minor accumulation of in-
fiammatory cells could be observed where the dentin
tubules involved with caries terminated in the pulp.
Clinically, a sharp probe did not catch, and radio-
grams did not reveal any interproximal caries. Upon
extraction there could be discoloration ofthe proxi-
mal surfaces, but no macroscopically observable loss
of enamel. However, in typical selected histologic sec-
tions taken from the area of a discolored fissure or
discolored interproximal surface, micro-organisms
were only present in the superficial end of the in-
volved dentinal tubules.
It should be noted that very minute (if any)
changes had occurred in the predentin at this stage
of development, and there could be a slightly reduced
odontoblast layer where the involved dentinal tu-
bules terminated in the pulp. Bacterial stains (e.g..
Brown & Brenn) demonstrated the presence of bac-
teria in the peripheral end of the dentinal tubules,
and also in their side branches. It is evident that de-
mineralization of the tubule walls had not taken
place, but it was not necessary for the penetration of
the bacteria, the diameter of which does not exceed
that ofthe side branches ofthe tubules (Fig. 1). Both
Brown & Brenn and PAS/Alcian Blue demonstrated
distinctive stain changes confined to the content of
the tubules pulpal to the bacteria. Tubules in the
same area that were not invaded by bacteria did not
show these typical color changes. Neither the remain-
ing matrix ofthe peri tubular nor intertubular dentin
was involved in this color change.
Caries progress occurred by increases in depth and
in width. Bacteria advanced towards the pulp while
widening the surface area and undermining the en-
amel. In general, the severity ofthe pulpal response
also increased with a significant increase in the num-
ber of infiammatory cells.
In addition, a marked increase in dystrophic calci-
fication occurred in the pulp chamber, in the root
canal, and on the canal walls. The calcification could
become so extensive that it took up a major part of
the pulp chamber, narrowed the root canals, and
made the walls extremely irregular (Fig. 2). This
makes endodontic therapy if necessary afterwards
- more difficult and may, as an end result, jeopardize
or worsen prognosis.
Recording the severity ofthe pulpal response was
totally dependent on the direction and location of
the sections and their relation to the carious area as
demonstrated in a molar with deep caries: 596 sec-
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T i s s u e r e s p o n s e t e d e n t a l c a r i e s
Fig. J- Tooth with discolored occlusal ri.s.sure, but no attachment of a sharp probe, and thus diagnosed a.s no clinical caries.
A. Histologieally, presence of bacteria in some dentinal tubules (horizontal arrows) and where these tubules terminate in the pulp,
a concentration of cells in the odontoblast layiM" (oblique arrows, orig. mag. x 32).
B. Organic debris and bacterial plaque in the occlusal lissure (vertical arrow in A, orig. mag. x250).
C. Bacteria in debris in oeelusal fissure in B (orig. mag. x 1000). -i i l r
D. Bacteria in the peripheral end of the adjacent dentinal tubules and their side branches. Note tlie dearly discernible cliains oi
bacteria in side branehes (orig. mag. x 1000).
E. From area ofleft arrow in A: small concentration ofehronic inllammatory eells (orig. mag. x 250).
151
Fig. 2. Maiidibular fust molar, medium to deep caries. No previous uoi- present pain.
A. Section, through center of pulp ehamber and the root canal of distal root, ofT center of mesial root. Ofthe 3.5 mm across the
pulp chamber of this seetion, 2.7 mm is occupied by calcifications (between horizontal arrows). No orifice, and only part ofthe root
canal ofthe mesial root, but an area of resorption outside the main canal (vertical arrow). Circumferential apposition on the canal
walls causes narrowness and irregularity of canal (horizontal lower arrows, orig. mag. x 8).
B. From area of middle horizontal arrow in A: free ealcification surrounded by ehronic inflammatorv cells and fibroblasts (orie mac
x250). \ b- b-
C. From dense cell concentration in A: small and large lymphoeytes, plasma eells, macrophages, and fibroblasts (orig. mag. x 630).
D. Amorphous dystrophie calcification from pulp chamber: left top arrow in A, free in pulp ehamber (orig. mag. x 63).
E. Calcification attached to the pulp chamber floor in A. Distance to pulp chamber eeiling 0.1 mm (orig. mag. x 63).
Clinical consideraliom. Although ealeifications occur frequently, even in the \m\p of impaeted teeth, they are pathologic entities. They
occur by deposition of calcium salts in dead and dying tissue. The capability of pulp tissue to respond to injury is reduced by the
same volume as the calcifications. When endodontic therapy finally becomes necessary, they render the canal irregular and twisted,
eausing difficulties in establishing optimal working length and obtaining the smooth clean canal wall required for adequate obturation!
152
T i s s u e r e s p o n s e t e d e n t a l c a r i e s
Fig. 3- Photomoniagc from one tooth where caries penetration involves approximately 3/4 of the dentin thickness (but not the
irritation dentin) may explain the discrepancy among authors in regard to onset and extent of inllammatory response to canes.
A. The farthest penetration of bacteria into the dentinal tubules is indicated by horizontal arrows. The dividing area between prmiaiy
dentin and irritation dentin (the "calciolraumatic line") is indicated by vertical arrows, pointing upwards. In the subjacent pulp, a
concentration of cells is seen exclusively in the right part.
B. Healthy non-inflamed pulp tissue typical of approximately 200 sections cut in lhc left part of this pulp. , . .
C. Inflammatory reaction remote from the odontoblast layer, typical of approximately 200 sections cut in the area pomtc-d out wit
oblique arrow. Note: no inflammatory cells can be seen between the odontoblast layer on top and the concentration ol cells centra y.
D. From area of the vertical downward arrow in right part of A. Dense concentration of primarily chronic mllammatory c
throughout the odontoblast layer adjacent to the termination of the involved dentinal tubules. 1 t in
Clinical considerations. If seetions had been cut exclusively in the area of B, the diagnosis would have been deep caries, out o
inflammation. If they had been cut in the area of C, the diagnosis would have been deep earies, but no 5'''"'^'^f'"."'^7;''!f"- ,^
inflammation and the termination of the involved dentinal tubules. Only sections including the area in L wouia gi\e uit us,
answer, that an inflammation is caused by deep caries. Thus, different and contradictory results may be arrived at depenaing upon
direction and number of sections, unless seetions are cut throughout the entire pulp chamber.
153
Langeland
154
Fig. 4. Mandibular flrst molar. Deep caries treated with indirect pulp capping, permanently leaving soft leathery dentin under the
restoration. The remaining "leathery" carious dentin was treated with 10% AgNOj, the carious lesion covered with a thick mix of zinc
oxide eugenol, and the tooth restored with oxyphosphate cement and amalgam. The observation period was 32 months. The patient had
no previous nor present pain.
A. Cavity floor, irritation dentin and adjacent pulp. Extensive layer of solid irritation dentin, but total lack of formation in area under coronal pulp (horizontal
arrows) where there are AgNO3 particles and pulp tissue remnants. Dense concentration of cells in coronal part of pulp chamber, a. Empty space (artifact)
due to liquefaction necrosis in vivo, and washing out of liquefied tissue during histologic processing. Density of cells tapers oil'to normal with increasing distance
from carious lesion (orig. mag. x 16).
B. From irregular irritation dentin. Note AgNO3 particles in crosscut dentinal tubules and in adjacent odontoblast layer with di.sintegrating ncutropliilic
leukocytes (orig. mag. x 1000).
C. From area of dense irritation dentin: AgNO;i in dentinal tubules on both sides of calciotraumatic line (vertical arrow in A), and in soft tissue inclusions of
the irritation dentin.
D. Mostly neutropbilie leukocytes along empty spaee a in A. These are the cells responsible for the condition described in A.
E. AgNO] particles in pulp and concentrated in cells along vessels (orig. mag. x 1000).
Clinical consideralions. Although precipitation of calcium salts occurs in dentinal tuhulcs during the carious process, tubules remain open to penetration, and
even a thick layer of irritation dentin docs not ]5rotect the pulp against irritation and destruction. Absence of pain does not indicate absence of inllammation
and destruction. Contrary to Fusayama and Jordan ct al., no carious dentin may be left under a restoration.
T i s s u e r e s p o n s e t o d e n t a i c a r i e s
Fig. 5. Premolar ol young individual demonstrating the cumulative elfecl of caries restored with a composite lilliii". The patient had
severe pam, whieh disappeared upon restoration of the cavity and then reappeared after several tnonths
A. Pulp horns seem solidly filled with irritation dentin, which generally is thought to protect the pulp from injury Note onenines in the dentin (arrows) (orig.
mag. x25). r r j j ^ 8
B. Less than I mm away, pulp tissue remaining in buccal pulp horn, and lemaining pulp tissue in palatal pulp horn (arrows) (orig. mag. x 25).
C. from spaces pointed out with arrows in A. These spaces contain soft tissue with neutrophilic leukocytes as evidence of communication with the pulp tissue
S centrally. Smce the half-hie of neutrophilic leukoeytes is only 7 h, this is fmal evidence of movement ofthe disintegration products ofthe dentinal tubules -
I bacterial to.xins, monomer, catalysts, tissue lluid, and odontoblast processes - from the periphery, and a chemotactic movement of neutrophilic leukocytes
5 from the pulp tissue into the space where irritation products occur.
I D. From the coronal pulp. Large numbersofneutrophilic leukoeytes, lymphocytes, and plasma cells. The inflammatory response-particularly the neutrophilie
leukocytes, which have to be renewed constantly - emphasizes the fact that the pulp has not been protected against the irritants penetrating from the surface,
and that the irritation is continuous.
Clinical comideratiom. The cuniulative effect of caries and iatrogenesis eaused by a eomposite material can, in the long run, cause total pulp destruetion, leading
to the necessity of endodontic therapy and its sequelae. Prevention of pulpal damage (an endodontic objective) by early and correct treatment prevents this
costly proeedure.
i . :-; " ' " . . , . ; ; / . .. 155
Langeland
Fig. 6. A. Specimen taken from "leathery" dentin after removal of surface debtis and surface carious dentin. Dentinal tubule full of
dead or dying bacteria (orig. mag. x 20,000).
B. For gDniparisori^^specirrien JakenJ'rom^dceper part^jf leathery dejitin of mandibular finst molar from another patient; sensitive to
heat, cold, and electric stimulation, but not sensitive to pereussion or palpation. These bacteria have attached three-unit membranes,
and electrolucent granules in the cytoplasm indicate live baeteria (orig. mag. x 10,000).
Clinical consideralions. All leathery dentin must be removed to fulfill the simplest requirement for healing: remove all pathogenic^?
bacteria.
156
Tissue respense to dental caries
"le. /.
i. The man
.The mandibular second molar, first lfiolar, and second premolar of a 1 7-yeai-old male had extensive carious lesions with no history of paiii. The teeth were
sted with cold, heat, electric, percussion, and palpation stimuli, which caused responses similar to those in non-involved tcclh in opposite arch. All soft
rious dentin was excavated. Culture of dentin spiculcs taken from hard cavity floor following exca\-ation identified Slrej)lococciis mulam (types C, D), S.
Fig. 7.
teste
car
sanguis, and S. mitis. Histologic examination iiU'oK'ed eleetron microscopy of leathery dentin (see Fig. 6).
B.-G. Paraflin sections taken from mandibular second molar in A.
B. Cavity floor and adjacent coronal pulp. The ealciotraumatic line appears between primary and irritation dentin (\ ertical arrows). Odontoblast layer is
reduced, horizontal arrow points to an artifact, a fold ofthe section (orig. niag. x 25).
C. From cavity floor. Bacteria in dentinal tubules of hard dentin after removal of all soft carious dentin. Brown c& Brenn stain (orig. mag. x 1000).
D. Primary dentin, calciotraumatic line, irritation dentin with fewer dentinal tubules than in primary dentin and reduced odontoblast layer (orig. mag.
x250).
E. Chronic inflammatory cells, including degratuilated mast cells (orig. mag. x 8t}0).
F. Numerous calcifications in coronal pulp tissue (orig. mag. x 63).
G. Calcifications take up considerable part of pulp hmien (orig. mag. x 250).
Clinical consideralions. Large carious lesions can occur in the absence of pain. Unknowingly, in many cases of deep caries, the clinician will restore teeth with
varying atnounts of bacteria remaining under the cavity. This will contribute to pulpal disintegration in the fultue. Although occurring frequently, calcifi-
cations are pathologie entities, resulting at a minimum in less pulp tissue to respond to injury.
m
La n ge l a n d
A. Mandibular second premolar and second molar of a 19-year-old male with extensive carious lesions, but no history of pain. Sensitive to cold drinks. Second
premolar was hypersensitive to cold test, responded normally to heat, electric stimulus, and palpation. Radiographically, there was a slightly ex]:)anded
periodontal space. All soft carious dentin was excavated down to hard dentin without perforation. Culture of dentin spieules from hard cavity lloor identified:
Streptococcus mutans (types C, D), 11.8%; S. sanguis, 8.8%; S. mitis, 79.4%.
B-G. Paraffin sections taken from second premolar in A. Sections A and C are approximately 0.3 mm apart.
B. Gives impression of arrested penetration in irritation dentin (Brown & Brenn, orig. mag. x 25). C demonstrates baeterial penetration into the pulp.
C. Bacteria in dentinal tubules and in the adjacent pulp in necrotic (n) area (Brown & lirenn, orig. mag. x 1250).
D. Section adjacent to that in C. Area of penetration of bacteria. Disintegrating neutrophilic leukocytes in necrotic (n) area (hematoxylin and eosin, orig.
mag. X 1250).
E. Large numbers of neutrophilic leukoeytes with a few chronie inflammatory cells intermixed in zone bordering the necrotic zone (orig. mag. x 1000).
F. From area deeper in pulp. Chronic inflammatory cells, several with granulated cytoplasm, mast cells (orig. mag. x 1000).
G. From root pulp. No inflammation (orig. mag. x 1000).
Clinical considerations. Despite inspection of a cavity floor under rubber dam and with the use of a sharp probe a bacterial perforation to the pulp may remain
undetected. The clinician would be entitled to (and would) restore this tooth, a treatment whieh would fail after an unpredictable time period. Note: always
record this on the patient's treatment record, and inform the patient ahout this possibility in cases of deep caries.
158
T i s s u e r e s p e n s e to d e n t a i c a r i e s
Fig. 9. EM. Speeimen from area of penetration of bacteria to the pulp similar to that in Figs. 8 and 16.
A. Dendn border (top), adjaeent debris and bacteria of neerotie pulp tissue (n and arrows), part of neutrophilie leukocyte (nl), and
remnants of bacteria and their membranes (orig. mag. x6300).
B. Neutrophilic leukoeyte with pyknotie nucleus at opening of dentinal tubule with debris (orig. mag. x 2500).
Clinical considerations. The attraction of neutrophilic leukocytes to the area of bacterial penetration to the pulp leads to its ultimate
destruction. Following the engulfment of bacteria the leukocytes disintegrate, afier which the engulfed baeteria - dead or alive - are
reintrodueed to the pulp, and the enzymes ofthe leukoeytes produee a liquefaction necrosis. If not removed a vicious circle is started
and the liquefaction necrosis will expand.
459
La n go l a n d
Fig. 10. 7; -
Twcnty-year-old male. Filling broke 2 years before. No spontaneous paiu, but slight thill ache 2 3 miu o
No reaction to cold or sweet. The tooth was negative to tests with cold, electric, and heat, but p'^'^ii>"' I'l 1
A. Mesial earious cavity reaehing pulp h o " ~ " ' "' '^ ' - -:
111 stimulation with chcvviug pressure and hot food.
c to percussion stimulation.
lorn, recurrent or eontinuing caries under remaining jjart of filling. Periajjical radiolucency both roots,
anal orifiee (Brown & Brenn, orig. mag. x 1000). B. Necrosis and bacteria in mesial root
irom main canal (orig. mag. x 200).
C. Chronie inflammatory cells mid-root main canal (orig. mag. x 1250).
H. Unaltered non-inllained pulp tissue in apical third of main canal (orig. mag. x 1250).
Clinical considerations. Although there is necrosis in the entire coronal pulp chamber down to the orifice ofthe root canals and a periapical radioluccncy, there
is 9 mm of vital tissue remaining in the root canal and no inflammation at all iti the ajjieal thir'^ .,r.i. .,..1., T* CK....I^ K.. :n n.. .,^<.i (U... .!..... ......
baeteria in the remaining vital part ofthe pulp.
ne oritice ot tnc root canals and a pcnapicat raaiotuccncy, ttiere
lird ofthe pulp. It should be speeifically noted that there are no
160
Tissuo respenso to dontal caries
Fig. 11. Maxillary premolar of 20-year-old patient. The patient had no history of pain, tuir present pain. The tooth was diagnosed
radiographically during general examination.
A, B. Hematoxylin and eosin stained sections detnonstrating root with attached periapieal lesion, and the main canal.
A. Including the apical foramen, remnants of neerotie pulp tissue in the main canal, vital tissue in foramen (horizontal arrow).
B. Total cut of the main canal, artifact in foraminal area.
C. Section stained aeeording to Brown & Brenn. Periapical lesion partly torn away during eutting. Lateral canal with necrotic
remnants 3/4 into canal, organized vital inflamed pulp tLsstie conneetiiig with periodontal lesion of pulpal origin, 3 mm from apex
(vertical arrow). Apieal ramifleations with neerotie remnants 0.8 and 0.3 mm from apex (horizontal arrows).
D. Root canal wall with baeteria adjacent to dentin (orig. mag. x 1000).
E. Root canal wall. Bacteria in dentinal tubules adjacent to canal with necrotic content (orig. mag. x 1000).
F. Lateral canal pointed out by arrow iti C. Necrosis in pulpal part of canal, concentration of neutrophilic leukocytes, and then vital
pulp tissue connecting with periodontal lesion of pulpal origin (orig. mag. x 1000).
161
La n ge l a n d
Fig. 12. Specimen taken from root eanal wall of tooth with similar condition to that described in Fig. 11. Presence of necrosis ofthe
root pulp was diagnosed clinically. EM section confirms the presence of baeteria in the dentinal tubules of the root eanal wall in
predentin (pd) and mineralized dentin (md). Some of the bacteria are dead: electrodense body and/or separated membrane
(horizontal arrows). Some are alive: electrolucent body and attached membrane (vertical arrows) (orig. mag. x 3150).
Clinical consideralions. From the point of view of a practical clinical approaeh there are two prineipally different preconditions: 1) in
the presence of a vital root pulp there are no bacteria in the root canal (Figs. 1-12). 2) In the presence of necrosis in the root canal
and the lateral canal, there are baeteria in the dentinal tubules ofthe root canal wall (Fig. 11). In the first type, represented by '
Figs. 1-10, sinee no baeteria are present in the root canal, all of them can be treated equally from a biologic point of view if
endodontic therapy becomes necessary. A one-visit technique is permissible, if otherwise desirable and feasible. In the second type, i
represented by Figs. 11 and 12, a one-visit technique is not aeeeptable. The problem is removing or neutralizing the bacteria that ]
may have established themselves in the dentinal tubules of the root canal wall. Inability to remove the bacteria adds to endodontic j
failures. j
162
T i s s u o r e s p o n s e t o d o n t a l c a r i o s
l ! ' '
Fie 13 A. Mandibular right second molar. Patient's chief complaint was pain and a history of pain. Tooth did not respond to pulp
tests, but was tender to percussion. Radiograph shows a deep earious lesion approaching the pulp ehamber. Wefl-defined penapicat
radiolueencies surrounded by selerotie bone are present around the mesial and distal roots.
BH. Pulp tissue extirpated from the chamber and mesiolingual canal of second molar in A.
B. Upper segment, coronal pulp; lower segment, root pulp (hematoxylin and eosin; original magnification x 20).
X 1250).
F. Intact and degranulated mast cells (hemato.xylin and eosin; orig. mag. x 1250).
i f h i i f l t ll d i h l l ( hma t x G. Concentration ofehronic inflammatory cells deep in ihe coronal pulp (hematoxylin and eosin; orig. mag.
H' . NO inflammation present in the apical part ofthe root pulp (hematoxylin and eosin; orig. mag. x 1250).
Clinical considerations. This case exemplifies the condition in teeth with partial or eomplete periapical lesions and necrosis oi tne coronai
pulp. Vital and often non-inflamed pulp tissue still remains in the root canal.
163
La n go l a n d
Fig. 14. Mandibular first molar of 49-ycar-old female. No pain. Clinically caries-free. Caleulus, periodontal disease, and bone loss
from 2/3 to 3/4 of root.
A. Note narrowness of pulp ehamber seen throughout all serial sections (orig. mag. x 8.5).
B. Bacterial plaque and adjacent dentinal tubules with bacteria (oblique arrows in A) (orig. mag. x 400).
C. Farthest penetration of baeteria in dentinal tubules (vertieal arrow in A) (orig. mag. x400).
D. Where dentinal tubules invaded by baeteria terminate in the pulp (horizontal arrow in A), a small but dense accumulation of
lymphoeytes and macrophages (a: artifact; pulp tissue torn away from dentin during processing) (orig. mag. x400).
164
T i s s u e r e s p o n s o t o d e n t a l c a r i e s
Fig. 15. Periodontal disease and pocket involving 2/3 3/4 of root. Radiogram demonstrated a periapical lesion, confirnicd histologieally.
A. Apieal part of root with attached periapical lesion.
B. Mid-root placjue adjacent dentinal tubules with bacteria (Brown & Brenn, orig. mag. x400).
C. Pulpal necrosis and bacteria where tubules in B end in pulp.
D. Pulp tissue apical to neerotie area, and dense concentration of neutrophilic leukocytes (orig. mag. x800).
E. From periapical lesion. Dense concentration of lymphocytes, macrophages, plasma cells, and fibroblasts. No nerves transversing
the lesion in this section.
Clinical considerations. When bacteria ]3enetrate to the ])ulp of a root eanal that is greatly reduced in volume and establish necrosis,
the circulation to the coronal pulp terminates, neerosis is established in the pulp coronal to the bacterial invasion, and the disintegration
products seep back or arc delivered by adjaeent functioning veins to the periapieal tissue and eausc a periapical lesion.
165
La n ge i a n d
tions were taken through the carious lesion. In about
200 sections there was no inflammatory response at
all, and in another 200 sections there was a concen-
tration of inflammatory cells centrally in the pulp
with no apparent correlation to the termination of
the carious tubules. However, in the remaining sec-
tions there was a direct correlation between the den-
tinal tubules involved in caries and the severe inflam-
mation at their pulpal termination (Fig. 3).
When caries was left untreated, it expanded in
width and depth, and first involved the peritubular
dentin and then the intertubular matrix. The bulk
ofthe lesion was wedge-shaped, with the base ofthe
wedge towards the surface. Peripherally, more or less
the entire dentin mass was infiltrated by bacteria, al-
though this mass still remained in situ for a long time.
An important aspect of caries related to the pulpal
degeneration was the irritation dentin, the irregular
dentin that is laid down and confined to the area
where the tubules involved with bacteria terminate
in the pulp. This dentin was irregular and unpredict-
able in amount, just as the dentinal tubules penetrat-
ing were irregular in their run. Wherever odonto-
blasts had disintegrated their dentinal tubules ter-
minated, but did not necessarily occlude. Pulp tissue
frequently remained as cellular fmger-like inclusions.
The variability and unpredictability of this con-
dition was expressed by the fact that in some places
no irritation dentin had been formed, whereas in the
near vicinity - within a millimeter - there were large
amounts of irritation dentin, only covered by pulp
fibroblasts lying spindle-shaped at a 90 angle to that
ofthe end ofthe dentinal tubules.
This condition is exemplified in cases of "indirect
pulp capping" (originally suggested by Fauchard) by
leaving carious dentin contacting the pulp rather
than removing it all "of fear of exposing the nerve
and make the treatment worse than the disease" (30).
The surface carious dentin was removed, 10% silver
nitrate was applied to the leathery dentin (assumed
by some not to be infected), which was then covered
with a thick mixture of zinc oxide and eugenol, and
the tooth was restored with zinc oxyphosphate ce-
ment and amalgam. The observation period was 32
months. A thick layer of irritation dentin was present
under the major part ofthe cavity, but interrupted in
some areas where no irritation dentin had been laid
down, and where an area of necrosis was established.
There was evidence of bacterial and silver nitrate
particle penetration in the dentinal tubules, in in-
clusions ofthe irritation dentin, and in the adjacent
pulp, particularly along vessels (Fig. 4).
Further evidence for the openness and per-
meability of such tubules was demonstrated in cases
of untreated deep caries. In one example, irritation
dentin filled the entire pulp horn of a premolar.
Examination of this irritation dentin in the single sec-
tion revealed inclusions of soft tissue, as lakes sur-
rounded by dentin. In this case of long-standing car-
ies, vital tissue was present in these inclusions. As ulti-
mate evidence of penetrability, neutrophilic
leukocytes were present in these inclusions (Fig. 5).
In the study of the relationship between bacterial
penetration and the hardness ofthe dentin, anaerobic
and aerobic culturing on mitis salivarius agar iden-
tified Streptococcus mutans (types G, D), S. mitis, S.
sanguineous, S. faecalis, and S. hovis in various combi-
nations in all cases in the leathery dentin. In about
one-third ofthe teeth streptococci were also cultured
from the final culture taken from the hard cavity floor
beneath the leathery dentin.
When these teeth were examined histologieally,
EM sections from the outer portion of the leathery
dentin demonstrated that massive amounts of bac-
teria were also involved with intertubular dentin, but
were confined to dentinal tubules in the deeper areas
ofthe leathery dentin (Fig. 6). Two typical examples
will be described - a mandibular second molar (Fig.
7) and a mandibular second premolar (Fig. 8) nei-
ther of which involved a clinically observable perfor-
ation. In both examples, subculturing of dentin chips
from the hard cavity surface showed bacterial
growth. No spontaneous pain occurred despite deep
and extensive cavities that were verified radiograph-
ically (Figs. 7, 8). However, the 2 cases were histolo-
gieally different: in the molar, bacteria had not per-
forated to the pulp, while in the premolar they had,
but there was no clinically observable perforation in
any of the cases. A light-microscopic section of the
molar demonstrated the presence of bacteria in den-
tinal tubules under the hard cavity floor following the
meticulous removal of all soft carious dentin. In the
underlying pulp, pathologic changes were evident by
the presence of neutrophilic leukocytes and chronic
inflammatory cells in addition to extensive calcifi-
cation (Fig. 7). In the second example (the mandibu-
lar second premolar; Fig. 8), where the patient had
no spontaneous pain either, but had sensitivity to
cold, and the excavation similarly did not result in
clinically observable perforation, the histologic
examination demonstrated the perforation by bac-
teria to the pulp. In the area of bacterial perforation
there was a minor area of necrosis localized to the
penetration of the bacteria (Fig. 8). It should be
noted, however, that despite the necrosis, the pres-
ence of bacteria in the pulp horn, and a severe inflam-
mation in the entire coronal pulp, there was non-in-
flamed tissue in the root canal (Fig. 8). The necrotic
area was surrounded by a dense accumulation of neu-
trophilic leukocytes, and the adjacent pulp showed
acellular tissue remnants indicating partial liquefac-
tion. Away from the center ofthe breakdown, there
was a typical chronic inflammatory response with
large numbers of plasma cells, small and large
166
T i s s u e r e s p o n s e to d o n t a l c a r i o s
lymphocytes, macrophages, fibroblasts, mast cells,
and foam cells. At this stage the entire root pulp could
still remain totally free of inflammatory cells (Fig.
8G). The only pathologic condition was dystrophic
calcification centrally in the root pulp and calcifi-
cation on the canal walls. The necrosis was verified
in EM studies where specimens from the area of pen-
etration of bacteria demonstrated live and dead bac-
teria with tissue debris, and neutrophilic leukocytes
with pyknotie nuclei (Fig. 9).
The next clinically discernible stage of develop-
ment was when the entire coronal pulp tissue was
involved in the necrosis. Except for expansion in vol-
ume ofthe pulpal disintegration, the important prin-
cipal difference was the presence of a radio-
graphically visible periapical lesion in the presence of
a vital root pulp. Not only was the root pulp vital,
but for a long time it was only partially inflamed.
Calcification {[ree in the pulp and on the canal walls)
and resorption remained as the only evidence of path-
ology in the root pulp (Fig. 10).
The last stage in caries-related pulpal destruction
was when necrosis and bacteria entered the root ca-
nal. At this time the clinically important difference
was that bacteria could have gone retrogradely into
the tubules of the root canal wafl. This condition
could (and in this case did) happen in the total ab-
sence of pain, similar to the earlier stages. Vital pulp
tissue with nerves and vessels remained in the most
apical part of the main canal. In addition, where a
lateral canal was present in an area where necrosis
was established in the main canal, there was necrotic
tissue in the adjacent part of the lateral canal, fol-
lowed by a transition zone of necrosis/neutrophilic
leukocytes, and then vital and inflamed tissue con-
nected to the periodontal lesion of pulpal origin (Fig.
11). Most importantly, it was verified in EM sections
taken from the root canal wall adjacent to a necrotic
pulp that live and dead bacteria had established
themselves in the adjacent dentinal tubules (Fig. 12).
This is what makes a difference in therapy. Since the
bacteria involved are anaerobes or facultative an-
aerobes, a good prognosis is dependent upon their
elimination.
The fact that vital pulp tissue remained in the root
canal in the presence of a periapical lesion was con-
firmed by taking pulp biopsies by simple extirpation
ofthe pulp in cases where there was a periapical radi-
olucency (Fig. 13) (25). Smears from the coronal
pulp demonstrated bacteria, disintegrating blood,
and inflammatory cells. The extirpations demon-
strated continuous pulp tissue at lengths up to 10 mm.
Acute inflammatory cells were present in the most
coronal part, chronic inflammatory cells in the adjac-
ent area, and finally in the apical area, there was vi-
tal, and in most cases, non-inflamed tissue (Fig. 13).
This cellular interrelationship was maintained as ne-
crosis moved in the apical direction, but the necrosis
and bacteria were also confined to the root canal in
clinically advanced cases, even in the presence of
swelling.
Root caries and its sequelae has achieved increas-
ing importance with the increase ofthe geriatric pop-
ulation. The problems are related to the continuous
retraction of gingiva and the periodontal ligament,
gingival root resorption, and erosion. As the root and
the cementum become exposed, this creates a new
environment for oral bacteria. Before caries is estab-
lished, however, resorption can result in lacunae co-
ming in through the cementum into the dentin. De-
pending upon the response of the individual in our
studies, reattachment could occur providing oral hy-
giene improved dramatically. If not, the result was
root caries, either in previous resorption lacunae or
directly on the cementum surface.
There was no apparent histologic difference be-
tween coronal and root caries. Bacteria were present
in the dentinal tubules following the penetration or
elimination of cementum by resorption/erosion.
Where the carious dentinal tubules terminated in the
pulp there was initially a minor inflammation (Fig.
14). With increasing involvement a minor area of ne-
crosis was established with the presence of bacteria.
There were, however, 2 additional problems; 1) the
much shorter distance from the surface ofthe root to
the pulp, and 2) pulp and root canal calcification
considerably reduced the amount of pulp tissue cap-
able of reacting to injury. Thus, in case of root caries
under these circumstances, the midroot necrosis may
cut off the circulation to the coronal pulp and cause
a severe reaction in the remaining pulp and a lesion
in the periapical tissues (Fig. 15).
Di s c u s s i o n
Because of the limitations of our histologic method-
ology it is quite speculative to correlate pulpal inflam-
mation and enamel caries (2, 3,6). However, meticu-
lous methodology does allow a direct correlation to
be demonstrated between superficial dentin caries
and pulpal inflammation (Fig. 1) (9, 10).
The etiology of pulpal inflammation in superficial
caries should be considered the result of metabolites
and breakdown products of bacteria, disintegration
products of odontoblast processes and of the tissue
fluid in the dentinal tubules. This condition is indicat-
ed by the color changes in the involved dentinal tu-
bules in front ofthe bacteria. At this stage, the pulpal
inflammation is clinically reversible provided the
pioneer bacteria, which are located in the hard den-
tin, are removed.
This is in disagreement with Fusayama (31), who
made the statement: "When caries penetrates dentin,
softening is always deepest, discoloration is next and
167
La n go i a n d
bacterial invasion is last". Fusayama's use of Knopp
hardness testing is not a valid method to measure the
hardness of fine structures such as dentinal tubules,
where the first changes occur (Fig. 1). Further evi-
dence contrary to his statement was demonstrated in
the cases of deep caries, where bacteria were found in
the dentinal tubules pulpal to the cavity floor follow-
ing the meticulous removal of all soft carious dentin
(Figs. 7, 8).
T'here is disagreement among investigators re-
garding the severity of pulpal involvement at various
depths of the carious process. It has been observed
that there was no significant pulpal disturbance when
the remaining dentin thickness, including irritation
dentin, was 1.1 mm (32), or even at an average of
0.31 mm (5). Similar observations are also made in
individual cases in our material; however, as the re-
sponse is usually seen in 5 |a. paraffin sections or in
ultrathin EM sections, we can only estimate what the
total reaction will be, unless the third dimension of
the reaction is investigated by taking and evaluating
serial sections throughout the entire pulp. Since this
would be an insurmountable task in a study involving
a large enough number of teeth to be representative
of all aspects of caries, the next most realistic indicator
ofthe extent ofthe inflammation is to find the section
demonstrating the most severe reaction among all the
serial sections. If an insufficient number of sections
have been cut, or if none ofthe sections have involved
the reaction area, then contradictory results may be
obtained in the same specimen, as demonstrated in
Fig. 3, where no reaction, an apparently non-related
reaction, and a severe reaction were demonstrated in
sections taken from the same pulp.
It has been suggested that stereologic and morpho-
metric methods be used to deal with this problem
(33-38). Unfortunately, however, such methods de-
pend upon random sectioning (34, 35), which is ac-
ceptable for a tissue with repetitive structures such as
liver or kidney, but which may not be accurate for
pulp tissue, as demonstrated in Fig. 3. The accuracy
will still depend on the original cut going through the
area ofthe most severe reaction. Also, the morphome-
tric measurements are dependent on this procedure.
Sections outside that area would represent a false
negative. Taking as an example the most sophisti-
cated equipment for this purpose, the Quantimet
900, Nicholsen (39) states: "Agreement among the
pathologists and with the Quantimet is good for ex-
treme cases. The pathologists do not agree on ran-
kings of intermediate dogs and their median ranking
does not correlate well with the Quantimet".
Thus, when dealing with such superbly precise
equipment one should keep in mind basic principles
for the use of statistics in biology as expressed by
Sheps: "A number may be precise but inaccurate
while a description may be vague but accurate" (40).
It seems that a good deal ofthe disagreements regard-
ing pulpal reactions are related to the many variables
in methodology rather than in factual differences in
reactions.
Another important aspect of pulpal destruction is
pathologic calcification. Following calcification of
tissue less pulpal tissue remains to respond to injury.
Although calcification occurs in the dental pulp of
clinically intact teeth, and even in the pulp of impac-
ted teeth (41), and is therefore recorded as normal
by some, the calcifications increase in numbers and
amounts during the carious process. Thus, regardless
of the fact that they may be considered normal by
frequency, there is no doubt that biologically they
represent precipitation of calcium salts in dead and
dying tissue and thus represent pathologic entities
(Fig. 2) (42-44).
T'here is a distinct disagreement regarding the
function ofthe dentin changes due to caries. Gener-
ally, it is thought that the calciotraumatic line and
the dentin formed in pulpal direction - alternatively
called secondary, tertiary, reparative, protective, and
irritation dentin (45) - together prevent penetration
of irritants to the pulp.
Two opposing trains of thought are derived from
German/Austrian literature from the start ofthe 20th
century. The discussion is still going on: one group
uses protective dentin - the old German term Schutz-
dentin; the opposing group uses irritation dentin - the
old German term Reizdenlin. The first term represents
the opinion that the dentin formed under the impact
of caries protects the pulp against destruction. The
second term represents the observation that the den-
tin is formed due to irritation, regardless of what the
irritant is (in this case caries). Analyzing these terms,
it seems evident that this dentin is not protective, ex-
cept possibly in one aspect: where it is laid down there
will be a longer distance for the bacteria to travel in
order to arrive in the pulp itself. In addition, protecti-
veness is related to narrowing ofthe dentinal tubules,
which may occur by deposition of calcium salts,
either hydroxyapatite or whitlockite. Grosscut of
such tubules may give the impression that some of
them are obliterated. However, the area remains
open, as demonstrated by in vivo penetration of bac-
teria, stains, silver nitrate, or radiographic markers,
and the presence of neutrophilic leukocytes is firm
evidence of penetration (Figs. 1, 3-5, 710). Since it
is an established fact that leukocytes have a half-life
of 7 h (46), their presence in the inclusions in the
irritation dentin is evidence that irritation products
-bacterial disintegration products, metabolites, and
toxins - continuously move from the surface of the
carious lesion into this inclusion, chemotactically at-
tracting the neutrophilic leukocytes into movement
from the vessels ofthe pulp. ;
The presence of neutrophilic leukocytes adjacent!
166
T i s s u e r e s p o n s o t o d e n t a l c a r i e s
to the predentin is further evidence of the penetra-
bility ofthe carious dentin. Regardless ofthe irregu-
larity, many dentinal tubules remain open to pen-
etration (Figs. 1, 3-5). Thus, the old term "protective
dentin" does not seem to be appropriate. The under-
lying pulp is in a stage of inflammation and disinte-
gration.
Although inflammation is one of the protective
mechanisms ofthe pulp as elsewhere in the body, it
also has destructive aspects. When neutrophilic
leukocytes disintegrate, lysosomes release enzymes
that are capable of causing liquefaction necrosis of
the involved tissue (47). When this minor area of ne-
crosis is first established, bacteria will thrive under
these conditions, and at this stage the pulpal inflam-
mation may be irreversible (Figs. 4, 5, 8-11, 13-15).
The explanation for the development of periapical
lesions at this early stage is that the accumulated dis-
integration products of the coronal pulp, bacterial
disintegration products, and their toxins - not whole
bacteria - are transferred through veins to the peri-
apical tissue. Support for this statement may be found
in the experimentation by Barnes & Langeland (48),
where circulating antibodies were demonstrated as
a result of placing antigens (bovine serum albumin,
human gamma globulin, or sheep erythrocytes) into
the pulp chamber of monkeys, or where particles of
Kerr sealer were demonstrated in regional lymph no-
des after introduction confined to root canals of mon-
key teeth (49).
The appearance and disappearance of periapical
lesions has led to clinical misunderstanding regarding
the etiology ofthe lesion. In a study of 24 teeth with
apical radiolucencies, Jordan et al. (50) used disap-
pearance or reduction of the periapical lesion in 11
teeth as the basis for a clinical recommendation of
indirect capping procedures. This indicates a misun-
derstanding of the biologic sequence. The lesion is
there because of the disintegration products coming
from the partially necrotic pulp (Figs. 8, 9, 13-15).
When the major part of these disintegration products
are removed by excavation of most ofthe carious den-
tin in an indirect capping technique, the bulk ofthe
irritants have been eliminated, and therefore the irri-
tation products arriving in the periapical area have
been reduced. This may allow for a temporary heal-
ing of the lesion, but the pulpal disintegration con-
tinues and the lesion is re-established. There is pres-
ently no medicament or material that kills the bac-
teria of carious dentin and does not simultaneously
kill the pulpal cells. Therefore, the remaining pulp
disintegrates at an unpredictable rate, and (of par-
ticular interest for long-term clinical success) calcifi-
cation will occur, possibly worsening the prognosis
when endodontic therapy becomes necessary (Figs.
2, 7, 14, 15) (51).
The fact that pain may be absent is not evidence of
lack of pulpal destruction or inflammation. In a study
of 224 teeth there was severe inflammation with the
presence of numerous neutrophilic leukocytes and
partial necrosis in 81 teeth in the total absence of
pain, previous as well as present (22).
Thus, what necessitates a different clinical ap-
proach in the endodontic therapy of pulpal disease
and its sequelae is not, as was previously believed,
presence or absence of a periapical lesion, or a distinc-
tion between vital or necrotic teeth - it is the occur-
rence of necrotic pulp tissue in the root canal, giving
the bacteria the opportunity to enter the dentinal tu-
bules ofthe root dentin (Figs. 11, 12). It is important
to clinically distinguish how far the pulpal necrosis
goes in the apical direction. As has been demonstrat-
ed (24, 26), a periapical lesion may be present while
the entire root canal pulp is vital and not yet invaded
by bacteria (Figs. 10, 13). Practically, having estab-
lished the presence of a continuous root pulp tissue,
the therapy is that of a vital case (or pulp), even in
the presence of necrotic coronal pulp and a periapical
lesion. In such a tooth there is no biologic problem
with treatment in one sitting. However, if necrosis is
established in the root canal, success and long-term
prognosis will depend upon the elimination of the
bacteria from the dentinal tubules of the root canal
wall (Figs. 11, 12). This should be checked by cultu-
ring before the obturation of the canal, which pre-
cludes a one-visit technique.
The discussion in the literature about whether or
not nerves are present in the periapical lesion has
clinical relevance because ofthe lack of pain in many
instances of pulpal/periapical lesions. This lack of
pain is not correlated to absence of nerves, since their
presence has been demonstrated both in the remain-
ing apical pulp and in the periapical lesion, whether
this is a granuloma or a cyst (52).
In the United States in 1980, 11.8% ofthe popula-
tion was above the age of 65, and the percentage is
expected to increase to 20% by 2040. The population
over age 75 constituted 4.4% in 1980, and is expected
to rise to 7.6% by 2000, and to 11.5% in 2040 (53).
This will have a great impact on the need for dental
care, with a particular emphasis on the pulpal re-
sponse. The clinically important difference in pulpal
problems ofthe geriatric population is that a carious
lesion gingivally to midroot - which would only have
caused local inflammation in the coronal pulp - may
involve the entire circumference ofthe reduced vol-
ume of the root pulp. When necrosis occurs in the
root canal this may cut off the circulation to the cor- :
onal pulp, the contents of which will necrotize and
add to the destruction of the remaining radicular
pulp.
L a n g e l a n d f
Conciusions
1. The pulpal reactions caused by initial caries are
reversible following the removal of the infected
dentin.
2. Since many ofthe bacteria in dentin caries are
facultative anaerobes they should be removed
before restoration of the cavity.
3. The pulpal reactions in medium-deep caries are
reversible, except for irritation dentin and pulpal
calcification on the canal walls or free in the
lumen.
4. The severity ofthe recorded pulp reactions may
depend upon the location and direction of the
section.
5. Pain (or any type of sensitivity) is not a predict-
able indicator of the inflammatory stage of the
pulp.
6. In deep caries, bacteria may remain in dentinal
tubules of the hard cavity floor. Combined with
iatrogenesis, this may be the major reason for the
occurrence of pulpal disintegration under res-
toration.
7. The reason for indirect pulp capping failure is the
presence of bacteria and a possible minor area
of pulpal necrosis that is left in contact with the
capping medium. The success of any therapy de-
pends on the total removal of all disintegrated
tissue.
8. Indirect pulp capping is not an acceptable pro-
cedure.
9. Pulpal reactions persist under indirect pulp cap-
ping procedures.
10. The apparent clinical success of indirect pulp
capping, pulp capping, and pulpotomy is due to
the removal of the major portion of the disinte-
grated tissue.
11. Since no inert material is available - although all
disintegrated tissue has been removed - changes
of an inflammatory or degenerative nature will
slowly cause disintegration ofthe remaining pulp
tissue, including calcification, which will jeopar-
dize future endodontic therapy.
12. Inspection ofthe pulp after opening through the
dentin and washing out all disintegrated tissue
will give valuable information about the extent
of remaining vital pulp tissue.
13. Root caries must be treated early to prevent se-
vere pulpal destruction.
Acknowledgements-Vor their outstanding contribution
to their part ofthe experimental material covered in
this publication, I want to thank the following col-
leagues appearing in the list of references: Leena K.
Langeland, Leif Tronstad, Gabriel Tobon, Dale M.
Anderson, William E. Dowden, William R. Cotton,
George E. Clark, Louis M. Lin, Robert Block, Louis
I. Grossman, Kamran E. Safavi, Elizeu A. Pascon,
Glover W. Barnes, and Ricard E. Walton.
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171