1. CONFERENCE ON
THE BIOLOGY OF THE HUMAN DENTAL PULP
Classificationof pulpal pathosis
Samuel Seltzer, D.D.S.,’ Philadelphia, Pa.
TEMPLE USIVERSITY SCHOOL OF DENTISTRY
Clinical evidence which indicates the presence of severe pulpal pathosis dictates a
treatment policy of pulp extirpation and endodontic therapy. In the absence of such
evidence, therapeutic management by indirect pulp capping is the preferable regimen.
In such cases, efforts should be made to maintain pulp vitality, even though chronic
pulp intlammation may persist. The vitality of the pulp should be maintained as
long as possible in the absence of evidence that chronic pulp inflammation is harm-
ful to the well-being of the organism. The defensive capacity of the pulp is thereby
retained.
In the past, pulp diseases have been classified on a clinical basis by the use
of histologic terms. Traditionally, clinical and histopathologic nomenclature has
been intertwined, resulting in a mishmash of misleading terms and diag-
noses.2*~72,w 125For example, an “acute serous pulpitis” has been taken to mean
that the patient has pain (hence the adjective acute), that the pulp is inflamed
(pulpitis) and that the character of the inflammation is nonsuppurative (serous).
However, the term has also implied that, on a clinical basis, the pulp is overly
sensitive to cold and that it reacts more quickly to the electric pulp tester than
the pulp of a control tooth.
Other clinical diagnoses, sucl~ as hyperemia, a pathologic entity in which
blood vessels are dilated and filled with erythroeytes, have brought the concept
of therapy into the classification. With such a diagnosis, thermally sensitive teeth
react quickly to the electric pulp tester, but sWymptomsdisappear when a sedative
dressing is placed in the teeth ; presumably, the pathosis is reversed.
The more modern investigations of Mitchell and Tarplee, Matsumiya and
associates,“0 Seltzer and his collcagues,85~sB Ogilvie and Ingle,63 Pheulpin and
co-workers,o* Holz and co11eagues,35 Fiorc-Donno,25 Baumc,” Tyldeslcy and
Munlford,*36 and Hes.+ have demonstrated the futility of attempting to mix
clinical and histopathologic classifications. Instead, the status of the pulp has
been classified on the basis of clinical symptoms plus the results of certain test
*Professor and Chairman, Department of Endodontics.
269

2. 270 Seltzer Oral Surg.
August, 1972
proCedures.27v32,S%85 Such classifications lead only to a suggestion of treatment
procedures. A calculated guess concerning the histologic status of the pulp can
be made, but it is only a guess. To prove whether the guess was correct, either
the tooth must be extracted or the pulp must be extirpated and processed for
histologic examination. Histologic studies of extirpated pulps leave a great deal
to the imagination because of the distortion, twisting, and ripping of pulp tissue
which necessarily occur during removal of the pulp with a barbed broach.
In most classifications of pulp pathosis, it is implied that the pulp reacts in
the same manner to all irritants. As will be shown, such is not the case.
Cognizance must be taken of etiologic factors when any classification of pulp
diseases is attempted.
A discussion of classification of pulpal pathosis must, therefore, be based on
(1) etiology (history), (2) histopathology (laboratory findings), and (3) symp-
toms (clinical findings).
ETIOLOGY
Changes in the dental pulp, like changes in other connective tissues, may be
inflammatory or degenerative. Aside from physiologic aging-the normal “wear
and tear” of bodily tissues-such changes are induced by disease processes, such
as caries and periodontitis. A significant number of changes are also initiated
by various dental manipulative and restorative procedures (dentistogenic) .
Before discussing classifications of pulp diseases, it is desirable to examine,
briefly, the causes and results of alterations in the dental pulp.
Changes in pulp may be due to aging, dental tissue manipulations (dentisto-
genie), disease processes (caries, periodontal disease), and trauma.
Changes due to aging
Aging of human tissues is genetically controlled. It has often been said,
jocularly, that living to a ripe old age involves selection of the proper parents.
Many theories of the causes of aging have been advanced. According to Shocks7
and to Curtis,Zo among these are the following: (1) The wear-and-tear theory,
which simply postulates that the organism wears out with use. Each cell is
endowed with specific amounts of vital substances, such as enzymes. When these
substances are used up, they are not replaced. Eventually, death of the cells and
the organism ensues. (2) Mathematical theories have been postulated in which
an empirical mortality curve fits into a formulated equation. (3) The cellular
interaction theory is based on the dependence of every part of the body on every
other part. For example, all endocrine glands are interdependent for proper
functioning, Individual cells in any organ are dependent on, and influenced by,
their neighboring cells. (4) The collagen theory postulates that collagen fibers
form continuously at a slow rate. The collagen is eliminated slowly or not at all.
As more and more collagen is elaborated, the cells of the tissues are gradually
choked off. Tissue function is hampered, and eventually cell death ensues. (5) In
the waste product theory, the metabolic waste products are not readily excreted
from the cells or intercellular fluids. Slowly, function is interfered with and
eventually the organism is poisoned. (6) In the endocrine theory, endocrine

3. Classification of pulpal pathosis 271
functions slowly decrease as the individual gets older. Cell metabolism is
gradually affected adversely. (‘7) The calcium theory suggests that aging is
caused by a defect in calcium metabolism. According to Selye and Prioreschi,86
large doses of vitamin D or parathyroid hormone in rats cause mineralization
of many soft tissues. Such changes resemble those seen in the tissues of the aged.
Injury of a tissue results in its calcification (calciphylaxis) , rendering the tissue
nonfunctional. (8) In the somatic mutation theory, it is postulated that the
somatic cells of the body develop spontaneous mutations. As more and more cells
mutate, eventually an appreciable number of cells are mutants. Since all cell
mutations are deleterious, eventually the organs become inefficient and senescent.
(9) The autoimmune theory suggests that autoimmune reactions develop with
aging. Such reactions develop when some of the cells of the body synthesize
proteins which differ immunologically from the other bodily proteins. The results
are immune and anaphylactic reactions within the body. (10) Circulatory
deficiencies increase with age. The consequences are deficient oxidation of cells,
eventuating in cell death and replacement by collagen. With increase in collagen
deposition, more capillaries are choked off, resulting in more anoxia. Mutations
may also be induced in the endothelial cells of the capillary, leading to break-
down of part of the capillary and further deficiency in circulation.
Many of these theories can be applied to concepts concerning retrogressive
and age changes in the dental pulp. Among the age changes which have been
reported to occur in the pulp are the following : (1) reduction in size and volume
of the pulp due to continued dentin deposition, (2) decrease in cellular compo-
nents, (3) increase in number and thickness of collagen fibers, (4) decrease in
number and quality of blood vessels and nerves, and (5) increase in pulp stones
and dystrophic mineralizations. Each of these changes will be discussed briefly.
Reduction in size and volume of pulp. With aging, the pulp chambers of all
teeth gradually become smaller because of continuous dentin deposition. As a
result of this deposition, there is a tendency toward eventual pulp obliteration.
The pattern for the dentin deposition varies somewhat among the different
groups of teeth. In molars, dentin is deposited mainly on the floor of the pulp
chamber, with lesser deposition on the occlusal and lateral walls.s5y =, goIn upper
anterior teeth, the greatest dentin deposition occurs on the lingual wall of the
pulp chamber as a result of masticating forces,B7-6Dwith subsequent deposition
in the incisal tip and walls of the pulp chamber. By the age of 71 years or more,
the pulp canal becomes almost obliterated. The additionally formed secondary
dentin is highly irregular, with fewer dentinal tubules.
Decrease in cellular components. The odontoblasts appear to undergo de-
generative changes with advancing age. Electronmicroscopic examinations reveal
more vacuoles in older odontoblasts. Gradually, the odontoblasts atrophy and
disappear over some or all areas of the dental pulp.997 X17The primary dentinal
tubules are also affected. Increases in peritubular dentinI 3oor increased deposit
of apatite crysta1s1o2may occur, The dentinal tubules are ultimately occluded, a
condition called “sclerosis” of dentin.
Aging effects a reduction in the number of cells of the pulp,99 possibly .as a
consequence of reduced circulation. The regression of older rat pulpal fibroblasts

4. 272 Seltzer Oral Surg.
August, 1972
is characterized by their diminution in size and in the number of cytoplasmic
structures associated with fibrogenesis. Most of the intracellular organelles of the
older fibroblasts, such as the rough-surfaced endoplasmic reticulum and the
mitochondria, are smaller. The Golgi complex is rarely found.lz4 There is also a
significant decrease in the number of regenerable cells.71 With increasing
maturity, the pulpal fibroblasts exhibit a decreased oxygen uptake.26 However,
aging does not result in uniform alteration of the enzymes of the catabolic
cycles, either aerobic or anaerobic, of the fibroblasts of the bovine dental pul~.~”
Increase in number and thickness of collagen fibers. In histologic examination
of older pulps with the light microscope, there is a relative increase in the num-
ber of argyrophilic reticular fibers and in the number and thickness of collagen
fibers as compared to young pulps, IX7 This increase is apparent because of a
reduction in the volume of the pulp by the continuous deposition of secondary
dentin. The increase in the number of collagen fibrils is also actual, as has been
shown by electronmicroscopic examinations of the pulps of premolars and molars
of normal persons aged 13 and 14 years and of those aged 56 to 62 years.16 Such
examinations revealed that in the ground substance of the younger pulps there
was a scarce distribution of collagen fibrils about 750 A in diameter. Collagen
bundles were embedded in a denser ground substance. In the pulps of premolars
and molars of normal persons aged 56 to 62 years, there was a decided increase
in the number of collagen fibrils. Near the collagen fibrils, bundles of unstriated
small fibrils, about 150 A in diameter, were noted.
Decrease in number and quaZity of bZood vessels and nerves. Aging has an
adverse effect on the number and quality of blood vessels supplying the dental
p~lp.~ Blood vessels of aged pulps undergo arteriosclerotic changes, resulting in
a diminished blood supply to the cells of the coronal portions of the pulp~.~~s”
Comparisons of the pulpal blood vessels of noncarious teeth from younger
persons (less than 20 years of age) with those of older persons (40 to 70 years
of age) were made by Bernick. lo Typically, the pulpal arterioles from young
teeth consisted of endothelial layers abutting directly on a thin internal elastic
membrane. The media consisted of one or two layers of muscle cells, and the
adventitia contained collagenous and elastic fibers. PAS-stained sections showed
a deep red stain of the internal elastic membrane, whereas the media and
adventitia stained pink.
In contrast, the arterioles of the older pulps exhibited hyperplasia of the
intima with a resultant narrowing of the vessel lumen. The internal elastic
membrane was masked by the deposition of a PAS-positive material. In some
older pulps, there was also a hyperplasia of the elastic fibers together with
deposition of PAS-positive material. Dystrophic changes in the media and adven-
titia were also noted. In some instances, deposition of fine mineral deposits was
observed to have progressed to complete obliteration of both adventitia and
media.
The number of blood vessels supplying the coronal pulp tissue was extensive
in younger teeth. Such blood vessel numbers decreased in the older teeth,
regardless of whether or not the pulps exhibited mineralizations.

5. Volume 34
Number 2
Classificatio~n of pulpal pathosis 273
Few studies have been made of the age changes of the nerves of human teeth.
Armenio and associates2 and Bernickg have indicated that retrogressive changes
do occur, probably as a result of progressive mineralization of the radicular
nerve sheath and nerve itself. As a consequence, there is a reduction in the nerve
branches in the coronal portion of the aged pu1p.O Vacek and PlaEkova106 have
noted that, under caries, the pulp nerve fibers become coarsened and irregular
and argyrophilic varicosities are formed.
Imrease in pulp stones und dystrophic mineralization. Ground substance
alterations in the dental pulp apparently occur on aging. Such alterations result
in a decreased reactivity and predominance of highly aggregated, less soluble
macromo1ecules.115 Such changes may contribute to cellular degenerations and
increased dystrophic mineralizations.
Senescence of the dental pulp is increased by caries and periodontal disease;
dystrophic mineralizations apparently increase markedly as a result of aging
and disease processes.s~7Q,12QAtrophic changes of the pulps of fifty-four intact
teeth from a sample of 1,000 persons, ranging in age from 61 to 100 years, were
noted by Zakson.l14 Concurrently, dystrophic mineralizations were markedly
increased. Such findings of increased mineralizations as a result of aging were
confirmatory of earlier ones by Thomas,lo3 HilJ3* Euler,Q4 Shroff *O and more
recently by Saunders ,78 Such mineralizations suggest that circulatory distur-
bances may be the initiating factor.
Dentistogenic changes
Operative manipulations, such as cavity and crown preparations, the insertion
of restorations, crown and inlay impressions, and cementations cause changes in
dentin and pulp. 12gThe severity of the reactions varies with the depth of prepara-
tion 93, 953 104 use of coolants,22,Q7,9*, 111,112
deniin,O”
d egree of pressure exerted on the
rotational speed of the bur,83pI11 and other factors.4QT5o The reactions
are further influenced by the application of various medicaments to the dentin
or pulp (as in pulp-capping and pulpotomy procedures) and by the chemical and
physical properties of restorative materials. 40,Q6gIQ7Inasmuch as biologic varia-
tions occur among different persons, a direct cause-and-effect relationship cannot
always be quantitated. Following operative procedures, such changes as the
production of dead tracts and/or an increase in peritubular dentin, occur in the
primary dentin. Reparative dentin is subsequently elaborated under the involved
dentinal tubules, unless the pulp tissue is so severely damaged that it is rendered
necrotic. A calciotraumatic response, visible in histologic sections between
primary and reparative dentin, occurs as a result of the injury to the odonto-
blasts. The injured odontoblasts of rats’ teeth have been examined under the
electron microscope. Such electronmicroscopic observations have indicated that
the odontoblasts undergo a series of alterations after being cut at 150,000 r.p.m.
under a water coo1ant.83 The membranes of the endoplasmic reticulum become
fragmented, and the mitochondria degenerate.
Such changes occur after a half-hour and appear to be the result of protein
denaturation induced by desiccation, 118plQ3:13xheat, and vibration, although the

6. 274 Seltzer Oral Slug.
August, 1972
role of heat appears to be controversial. 22,llGl 133Two days later, Zach and asso-
ciates113found that the odontoblasts were pyknotic and some were displaced into
the dentinal tubules.
In human teeth, the immediate response of the odontoblasts is dependent on
the severity of the injury. Such changes as a shift of the cytoplasm from the cell
body into the odontoblastic process and an increase in cytoplasmic vacuoles and
lipid granules occur.95 In severe injuries, the cells are damaged irreversibly.
Should the odontoblast eventually degenerate, it would appear that other
cells in the pulp, probably undifferentiated mesenchymal or reserve cells, assume
the function of elaborating reparative dentin.83, Q1,II39126s131,134
An acute inflammatory response in the vicinity of the odontoblastic layer
follows severe injury of the odontoblasts. According to Langeland, but disputed
by Brtinnstriim,118 this response is initiated by displacement of the affected
odontoblasts and erythrocytes into the involved dentinal tubules. Chemical
mediators, liberated from the injured cells, are responsible for the initiation of
the inflammation. The capillaries in the odontoblastic layer, ordinarily obscure
or not seen in histologic sections, become visible as a result of dilatation. The
lumina of these vessels became packed with erythrocytes. The ensuing edema
causes compression of the odontoblasts and separation of these cells from the
dentin, resulting in disruption of t,he pulpodentinal membrane.131 In more severe
injuries, especially those resulting from chemicals, margination of polymorpho-
nuclear leukocytes along the capillary walls can be observed. Presently, these
leukocytes migrate through the vessel walls and infiltrate the odontoblastic layer
and the subjacent cell-free zone. Approximately one week later, the predominant
cell population consists of lymphocytes and macrophages. Plasma cells may
be found occasionally, but not usually. Under ideal circumstances, the granula-
tion tissue is gradually resorbed and repair is completed. The only remaining
evidence of the injury is the presence of reparative dentin. In effect, the
reparative dentin represents a mineralized scar. Despite the elaboration of
reparative dentin, the chronic inflammation may persist for months or years.
In many instances, scattered chronic inflammatory cells have been found in the
pulp many years after the operative injury has occurred.84, 85In the absence of
granulation tissue, the presence of such inflammatory remnants has been desig-
na.ted as a “‘transitional” stage.
Following severe injury, the pulp does not recover. Such severe injuries are
usually chemically induced, especially when the chemicals are placed near or
directly on the pulp following mechanical pulp exposure. Should an abscess
develop, the pulp does not usually heal. W* Instead, chronic inflammation per-
sists, eventually ending in total pulp necrosis. The terminal result in the produc-
tion of a periapical lesion.
Fig. 1 depicts the dynamic pulp changes which may follow operative
manipulations.
Changes due to disease processes
Caries. Dental caries is a slow, intermittent, insidious, microbial disease which
gradually causes demineralization of the enamel and dentin as well as proteolytic

7. Volume 34
Number 2
Classificatiov~ of pulpal patkosis 275
Mild or absence
of reaction
I
Recovery < ywith a restoration-Chronic partial
pulpitis
I
+
Chronic total
pulpitis
Chronic apical
periodontitis
Fig. 1. Pulp reactions to mechanical, thermal, and chemical irritants.
digestion of the collagen matrix of the dentin. As a result, various chemical
changes of the dentin take place. Magnesium and carbonate content are reduced,3a
whereas fluorine content is increased. 37 There are various quantitative changes
in the amino acid composition of the dentin ; some are increased, whereas others
are reduced. In addition, there is a large increase in the content of carbohydrate
material, the formation of a brown pigment, an increased resistance to break-
down by collagenase, and a loss or diminution of fluorescence in ultraviolet
light.23 The primary dentinal response is an increase in peritubular dentin, also
called “sclerosis” of the dentin. 3oSuch sclerotic dentin acts as a barrier to the
further penetration of bacterial metabolites, isotopes or dyes.5 With large-scale
carious breakdown of dentin, the dentinal tubules may either become completely
occluded by mineral deposits, remain empty, or become invaded by bac-
teria 33, 99,130
Pulp response to dental caries begins almost with the inception of the carious
lesion in the enamel. BrlnnstrGm and Lind14 and Langeland found scattered
chronic inflammatory cells in the pulp under the initial carious lesion (transi-
tional stage). The inflammatory response is directly initiated either by the
injurious metabolites of the microorganisms involved in the carious process or
by antigens of these microorganisms which activate destructive immunologic
processes.
When dentin becomes cariously involved, cells of the pulp manufacture
reparative dentin which is deposited under the involved dentinal tubules. The
quantity of reparative dentin elaborated appears to be equal to the amount of
dentin lost due to caries.54 The original odontoblasts degenerate. Reparative
dentin is generally lined with an odontoblastic layer only one or two cells in

8. 276 Seltzer Oral Surg.
August, 1972
depth. Therefore, the cells responsible for reparative dentin elaboration appear
to be derived from the reserve cells in the pulp. Despite its function of occluding
the cariously involved dentinal tubules, reparative dentin is nonetheless perme-
able to medicaments and isotopes.50
In deep-seated lesions, when the carious process has involved the reparative
dentin, chronic inflammation of t,he pulp is evident.73 When the pulp is finally
invaded by microorganisms, an abscess forms opposite the exposed dentinal
tubules. According to Massler,j4 the responsible microorganisms generally are
pyogenic streptococci, pyogenic staphylococci, and anaerobic gas-forming bacilli.
The remainder of the coronal portion of the pulp has by now become converted
to granulomatous tissue. The radicular portion of the pulp may remain intact
for a long period of time, and yet the blood vessels may appear dilated.
Zerlotti’s*15 examinations of sixty-eight pulps from cariously involved, painful
teeth revealed that even when the entire coronal pulp tissue was inflamed, the
radicular tissues were unaffected. However, even though vital radicular tissue
may persist for a long time, the apical periodontal ligament may exhibit chronic
inflammation. Thus, under the irritation of dental caries, the classic dynamic
change from acute to chronic inflammation, as results from operative procedures,
is not evident. Contrasted to the rapid, acute inflammation induced by operative
procedures, the slow, intermittent carious process elicits a slowly developing,
chronic inflammatory response in the pulp, which never has the identical features
of the acute inflammation seen following operative manipulations. Instead,
macrophages and lymphocytes predominate originally. In the late stages, both
acute and chronic inflammation is visible in cariously involved pulps. Poly-
morphonuclear leukocytes are attracted to the regions beneath the cariously
involved dentinal tubules. These leukocytes increase in number as the carious
process approaches the pulp tissue (Fig. 2).
Histochemical studies115 have indicated that during the acute phases of
caries-induced pulpitis, tissue components break down. Argyrophilic and col-
lagen fibers become fragmented and disrupted. Protein-carbohydrate complexes
become markedly degraded. Concurrently, tissue synthesis occurs in the chron-
ically inflamed areas. Reaggregation and rearrangement of argyrophilic fibrils
and metachromatic ground substance predominate. The fibroblasts are probably
responsible for the synthesis of the matrix, since they demonstrate a high con-
tent of RNA, as well as granule-containing glycoproteins, acid mucopolysaccha-
rides, sialic acid, and proteins bearing free e-amino groups of lysine-hydroxyly-
sine.
Breakdown of the pulp results in the formation of an abscess directly be-
neath the region of the invading microorganisms, perhaps mediated by the
release of lysosomal hydrolases from the polymorphonuclear leukocytes.lol In
the remainder of the coronal pulp tissue, the chronic inflammatory infiltrate with
its rich content of macrophages, lymphocytes, and plasma cells may indicate
the presence of an antibody-mediated hypersensitivity reaction. Excessive anti-
gens available in high concentrations from the microorganisms involved in the
carious process may cause synthesis of immunoglobulins. The immune antigen-
antibody precipitates thus formed may, in the presence of complement, become

9. Volume 34
Number 2
Classification of pulpal pathosis 277
Untreated caries
1Pulp
1Intact pulp with scattered chronic inflammatory cells
[transitional stage)
Exposure 1
Acute partial pulpitis t-- Chronic partial pulpitis
Drainage
>
--me-----mm----
Blockage
! Chronic total pulpitis I
Acute apical <- 1 I-
Pulp-periapical
periodontitis Drainage, Chronic apical periodontitis 11
tissue complex
.--------------4
Fig. 8. Pulp reactions to dental caries.
chemotactic for polymorphonuclear leukocytes. lo8plo9Phagocytosis of these immune
precipitatePo5 may then result in cell degradation with release of lysosomes into
the pulp tissue. The liberation of proteasesGowould then result in the formation
of a pulp abscess. The rich granulation tissue barrier below the abscess prevents
further spread of inflammation into the radicular pulp tissue. Gradually, with
repeated episodes of polymorphonuclear leukocyte-mediated reactions of the
Arthus type, the immune response reaches into the radicular tissue and eventu-
ally into the periapical tissues, where a typical granulomatous lesion develops.
Periodontal disease. Although some controversy exists,57 periodontitis ap-
pears to have a degenerative effect on the dental pul~.~~, T6184$85A number of
investigators have demonstrated that the periodontal ligament and the pulp
are supplied by the same vessels.17*l*l 21,42Thus, it appears reasonable that in-
flammatory and degenerative lesions of the periodontal ligament affect the
blood supply of the pulp. Histochemical studies have demonstrated the pres-
ence of increased amounts of enzymes, such as alkaline and acid phosphatases,
5-nucleotidase, glucose-6-phosphatase, and ATPase, in the pulps of periodontally
involved teeth as compared to those of normal teeth. Such increased concentra-
tions of enzymes were found especially in the endothelium of the blood vessels.11s
Circulatory disturbances result in atrophy of pulp cells, fibrosis of pulp tissue,
dystrophic mineralizations within the blood vessels, nerves, and collagen fibers
of the dental pulp, as well as inflammatory changes. Should lateral or acces-
sory canals become exposed as a sequel to periodontal inflammation and bone
resorption, there is interference with the blood supply to portions of the pulp.
Microorganisms may then gain access to the pulp tissue ; there they localize and
multiply. The result is the development of a chronic pulpitis, ending in pulp
necrosis.
Should the periodontal lesion cause epithelial proliferation and bone resorp-
tion near the root apex, an apical pulpitis may be induced. Resorption of bone

10. 278 Seltzer Oral Surg.
August, 1972
and apical periodontal inflammation may also simulate periapical lesions caused by
pulp disease. There is also some evidence that root planing may cause permea-
bility changes of the dentinal tubules, resulting in easier passage of irritants
between the oral environment and the pulp.“l
Trauma
Accidental trauma. Traumatic insults to the crowns of teeth, with or without
root fractures, may cause pulp degenerations due to rupture of blood vessels
supplying the pulp. Hard-tissue formation is stimulated; dentin or cementum-
like depositions occur within the pulp tissue, possibly with eventual obliteration
of the pulp and necrosis of the remaining pulp fragments.3l l1 Such traumatic
incidents frequently end with pulp necrosis and root canal infection.4* 13jI9129y53p58
In root-fractured teeth, healing may occur, with connective tissue or min-
eralized tissue interposed between the segments, or granulation tissue may
form and persist between the fragments1
Trauma from occlusion. Trauma from occlusion has frequently been indicted
as a cause of pulp inflammation or degeneration, but such findings have not
been documented experimentally. 45 However, it is conceivable that long-acting
occlusal trauma could eventually lead to pulp damage resulting from compres-
sion of the pulp vasculature. Degenerated pulp tissue might then become infected
through anachoresis or through the pumping of microorganisms into the pulpal
circulation from the gingival crevice. lzo However, those possibilities are con-
jectural.
HISTOPATHOLOGY
As has been shown, pulp pathosis may be of degenerative or inflammatory
etiology. Histopathologically, therefore, abnormal pulp conditions may be elassi-
fied under the headings pulposis (atrophy or degeneration of pulp), pulpitis,
(inflammation of pulp), or necrosis (death of pulp).
Pulposis results from normal aging, caries, trauma, periodontal disease, op-
erative procedures and, systemic factors. Histologically, pulposis is characterized
by the reduction in the quantity and size of pulp cells (including odontoblasts,
fibroblasts, undifferentiated mesenchymal cells), increase in pulp stones, dys-
trophic mineralization of fibers, vascular and neural elements, increased Sol-
lagen deposition, increased peritubular and reparative dentin formation in the
coronal and radicular parts of the tooth, and decreased blood and nerve supply.
Pulpitis may be acute or chronic, partial or total.
Acute pulpitis
In acute pulpitis, the inflammatory changes are usually induced by oper-
ative procedures on the dentin but may result from mechanical pulp exposure
or pulpotomy procedures. The acute pulp inflammation is characterized by
inflammatory changes in the odontoblastic layer, directly under the involved
dentinal tubules. The inflammation generally does not extend into the deep
pulp tissue. Edema causes disruption of the odontoblastic layer and a reduc-
tion in the number of odontoblasts. Dilated capillaries, filled with erythrocytes,

11. Volume 34
Number 2
Cla.ssification of pulpal pathosis 279
are evident. Polymorphonuclear leukocytes (neutrophils and eosinophils) are
seen both in the capillaries and extravascularly.
Acute inflammations, mixed with chronic ones, are also seen in the pulps
of carious teeth directly under heavily infected reparative dentin or under
exposures.
Chronic pulpitis
Chronic pulpitis, resulting from mild to moderate irritating operative
manipulations, is usually seen in the subodontoblastic layer under the involved
dentinal tubules. The cell-rich and cell-free zones are invaded by macrophages,
lymphocytes, and, occasionally, plasma cells. These cells are also found, after
more severe chemical injuries, in the deeper pulp tissues. Abundant dilated capil-
laries, new fibroblasts, and reticular and collagen fibers are also present. In the
older lesions, abundant quantities of reparative dentin are elaborated, pre-
sumably by undifferentiated reserve cells. The odontoblastic layer lining this
reparative dentin usually consists of a single layer of flattened, fibroblastic
appearing cells. The radicular pulp tissue usually is intact but contains widely
dilated blood vessels.
Under dental caries, chronically inflamed pulps are usually densely infiltrated
with lymphocytes and plasma cells. Under deep carious dentinal lesions, pulp
abscesses develop under the heavily infected or necrotic dentinal tubules. Poly-
morphonuclear leukocytes are abundantly present around the liquefaction ne-
crosis. Granulation tissue may involve the remainder of the coronal pulp tis-
sue, but the radicular tissue may remain resistant. However, periapical changes,
such as dilated blood vessels, edema, alveolar bone resorption, and scattered
chronic inflammatory cells, may be noted.
Huge quantities of amorphous reparative dentin, lined with fibroblast-like
cells, are found under the involved dentinal tubules.
Necrosis
In severe pulpitis of operative origin and under deep-seated caries, portions
of the coronal pulp undergo liquefaction necrosis (abscess). Such a reaction
usually leads eventually to total pulp necrosis. Histologically, partial pulp ne-
crosis exhibits a liquefied zone, surrounded by live, dead, and dying polymorpho-
nuclear leukocytes. Portions of, or the remainder of, the coronal pulp tissue are
converted to granulation tissue rich in macrophages, lymphocytes, and plasma
cells. It is tempting to consider the presence of lymphocytes and plasma cells
as a sign of localized antigen-antibody reaction. In time, the radicular pulp
tissue succumbs, and granulation tissue is found in the apical portion of the
root canal and also in the periodontal ligament.
In pulposis, a coagulation type of necrosis may be found. The pulp cells
are shrunken, and the nuclei are pyknotic or karyorrhectic. Collagen fibers
persist, but they may be heavily mineralized. Nerves and blood vessels are also
sites for dystrophic mineralizations. Pulp stones are abundant, and the dentinal
walls, both coronally and radicularly, are covered with large amounts of repar-
ative, amorphous dentin, tending toward obliteration of pulp and space.

12. 280 Seltzer Oral Surg.
August, 1972
Transitional stage
The pulp of primary dentin under initial carious attack, and occasionally
of periodontally involved teeth, exhibits scattered chronic inflammatory cells,
macrophages, and lymphocytes in the region of the tubules beneath the carious
enamel and dentin. The number of such cells gradually increases as the caries
progresses, but chronic inflammation does not develop until the reparative dentin
becomes involved.
A transitional stage is also to be found in the pulp under the heavy deposits
of reparative dentin elaborated following operative procedures and restorations.
Such findings are indicative of pulp recovery from the irritation, but scattered
inflammatory cells may persist in the pulp for years, following the insertion
of the restoration. Such pulps also exhibit signs of pulposis, presaging poor
recovery from subsequently applied irritants.
In summation, the following represents the entire spectrum of histopath-
ologic diagnosis of pulp pathosis :
1. Atrophic pulp
2. Transitional stage
3. Acute partial pulpitis
4. Chronic partial pulpitis
A. with liquefaction necrosis
5. Chronic total pulpitis
6. Total pulp necrosis
SYMPTOMATOLOGY
There is no clinical sign or symptom which designates the histopathologic
status of the pulp with certainty. The use of electric, thermal, percussion, and
palpation tests helps to establish an empiric diagnosis, but none of the tests
are completely reliable. Other clinical findings, such as referred pain, mobility,
and x-ray findings, are reliable for some forms of pulp pathosis but not for
others.
Classification based on pain
Pain is the most common symptom of a diseased pulp. In the absence of
pain, most pulp pathoses remain undetected in vivo. Pain is usually indicative
of tissue damage and, to some extent, usually connotes the extent of the dam-
age. However, the psychologic component of pain frequently gives a misleading
picture of the severity of the underlying disease process. Fear of dentists and
dental procedures frequently causes an exaggerated perception of pain, result-
ing in an incompatibility of symptoms and pulpal pathosis. Under those circum-
stances, the severity of pain cannot be correlated with the severity of tissue
change. 31, 61, "17, 110
Characteristics of pulpal pain. Various designations, such as sharp, dull, in-
termittent, continuous, throbbing, diffuse, etc., have been used to describe pulpal
pain. Our studies, as well as those of Tyldesley and Mumford, have failed to
uncover any correlation between specific pain characteristics and histopathologic
status of the pulp. On the other hand, Massler55 has claimed that a differentia-

13. Clussification of pulpal pathosis 281
tion can be made between dentinal pain, characterized as being of a sharp,
lancinating character, and pulpal pain, which has a dull, throbbing quality.
Probably, the distinction arises from the fact that in dentinal pain the pri-
mary stimulation is of the nerve endings in and around the odontoblastic layer,
composed of slowly conducting “c” fibers. On the other hand, in the more severe
types of pulp pathosis, the deeper pulp nerves are more likely to be stimulated.
The medullated fibers of the deeper pulp tissues are “a” fibers, which are
faster.
Intensity (severity) and duration of pain. Severity and duration of pain
appear to be partially related to the status of the pulp. Mild to moderate pain
is usually associated with less inflamed pulps. Severe pain and pain of long du-
ration appear to be reliable indicators of severe pulpitis and/or pulp necrosis,
but occasionally such symptoms are misleading. 5gSevere pain usually indicates
the presence of liquefaction necrosis. In the cariously involved teeth, pulp
abscesses are usually found under pulp exposures. In restored teeth, pulp
abscesses may develop over a long period of time. However, severely inflamed
pulps may be painless when drainage is not impeded.
Spontaneity of pain. The occurrence of spontaneous pain appears to be an
indication of severe pathosis of the deep pulpal tissues.121 Pain initiated by
stimuli, such as cold, heat, and sweets, which disappears within seconds, probably
indicates that nerve endings in the odontoblastic layer have been stimulated.
Persistence of such pain probabily indicates a more extensive inflammatory
involvement.
Thermally induced pain. Pain induced by thermal stimuli, such as heat and
cold, which persists after the removal of the stimulus is indicative of pulpitis
or pulp necrosis.52 There does not appear to be a correlation between the type
(acute or chronic) or severity (with or without liquefaction necrosis) of the
pulp pathosis and the type of thermal stimulus. 74Inflamed or necrotic pulp can
react to either, both, or neither of the two stimuli.
Sensitivity, of a short duration, to thermal stimuli is apparently increased
in pulposis induced by periodontal disease.85 When pain persists after removal
of the stimulus from periodontally involved teeth, pulpitis should be suspected.
Electrically induced pain. Although significance has been claimed by some
investigators77 pain elicited by the electric pulp tester is a poor indicator of
the status of the pulp. No correlation between the pain perception threshold
and the condition of the pulp has been discovered by Mumford,61l 621132Reyn-
olds,74 Lundy and Stanley,52 and Johnson and co11eagues.3Q,*OHowever, patho-
logically involved pulps appear to react with pain more or less quickly than
corresponding control teeth.84>85Even necrotic pulps occasionally evince painful
responses to the electric pulp tester.
History of prior pain, Recording of a previous history of pain correlates
well with the presence of destructive pulpal pathosis. More than 90 per cent
of patients in pain, when interrogated, reported that they had experienced pain
in the same tooth at some time prior to their present pain experience. In at
least 80 per cent of those patients, moderate to severe pulpitis and/or necrosis
of the pulp was found.84l 85

14. 282 Seltzer Oral Surg.
August, 1972
SUMMARY
In summation, pain, although not a completely reliable indicator of the status
of the pulp, can be used as a guide, together with other signs and symptoms.
Clinically, the pain may be classified as mild, moderate, or severe odontalgia.
The implications of such categorization are as follows: Mild to moderate odon-
talgia is usually associated with transitional stages, chronic partial pulpitis, or
atrophic pulps. Pain which arises spontaneously or which persists following
thermal stimulation, together with a history of previous pain, usually indicates
the presence of severe pulp damage, probably irreversible by therapeutic mea-
sures. Severe pain in cariously involved teeth usually indicates pulp expo-
suress or severe pulp pathosis, probably with liquefaction necrosis.44j 84s85Under
restorations, pain usually indicates the presence of an irreversible pulpitis or
pulp necrosis.
Classification for therapeutic purposes
A diagnosis of the extent of pulpal involvement in pulposis or pulpitis is
difficult; it is easier to determine from clinical findings that a pulp is necrotic.
Despite the difficulty in correlating clinical and histologic findings, the clinician
must make a diagnosis of the status of the pulp, inasmuch as correct diagnosis
dictates proper treatment. The diagnosis is a prediction, based on clinical judg-
ment, of the type of pulp treatment indicated and its probable outcome. Such
a prediction has led to the following designation of pulp diseases: reversible or
irreversible, treatable or nontreatable, pulps indicated for pulp capping or
conservative pharmacotherapy, or pulps indicated for extirpation or root canal
therapy. Gs27*7o,135Such designations are empiric and cannot be proved by pres-
ently available investigative modalities. 31The evaluation of symptoms can only
permit an educated guess as to whether or not the pulp can be treated and
saved. Correlations between clinical symptoms and histopathology are difficult
and fraught with error. Although severe symptoms of pain, swelling, etc. are
usually indicative of severe pulp damage, this correlation does not always hold
true.
The basic premise of all clinical classifications is that pulps exhibiting no
symptoms or mild to moderate symptoms (predominantly pain) are judged
to be amenable to therapy with a reasonable chance for recovery. When severe
symptoms are present, the pulp is usually judged to be beyond repair.
Our findings have led us to the conclusion that the most significant factor
in determining whether or not a pulp can be treated by drugs is the pres-
ence of an abscess. Such a determination may usually be made when there has
been a history of previous pain, there is no reaction to pulp tests, the results
of electric tests differ markedly from those of control teeth, pain is spontaneous,
severe, and long lasting, and thermal irritants or tests evoke severe pain which
persists after removal of the stimulus. Additional clinical findings, such as
tooth elongation, mobility, sensitivity to percussion and palpation, and the pres-
ence of swelling and/or a sinus tract are further evidences of severe pulp
pathoses which are nontreatable. Thus, the course of treatment is based on
clinical judgment, but there is no sure way to determine afterward whether

15. Volume 34
Number 2
Classification of pulpal pathosis 283
that judgment was correct. Even clinically successful pulp therapy, which ap-
parently has vindicated the judgment of the therapist, does not actually confirm
that judgment. Should symptoms be relieved and should the pulp remain rela-
tively free of symptoms and maintain its vitality, such therapy might be con-
sidered to have been successful in resolving pre-existing pulp inflammation.
However, there is no sure way of knowing what the condition of the pulp was
at the time of treatment. Conversely, should pain or swelling develop subsequent
to treatment, the treatment might have been unsuccessful or the diagnosis might
have been incorrect; the pulpitis was so severe that it could not be reversed.
Actually, there is no way of determining which alternative was the correct one.
The pulp may not have been inflamed initially, the inflammation might persist
without symptoms, or the pulp might have become necrotic without symptoms.
Inflammation may have been induced by the manipulative procedures or medica-
ments applied, or the pulp may have been subsequently irritated by the develop-
ment of new or recurrent caries, leaky restorations, or trauma. Thus, unsuc-
cessful pulp therapy which terminates in endodontic treatment or extraction
does not necessarily mean that the clinical judgment was incorrect.
Clinical judgment has, therefore, dictated pulp therapy. With respect to the
treatment of deep-seated carious lesions, two schools of thought have emerged.
One school believes that the cariously involved tooth always has a pulp inflam-
mation. In such cases, caries should be excavated completely, even if pulp ex-
posure results.4g’ lop,lz8 The other school believes that, rather than risk pulp
exposure by complete excavation of caries, “indirect pulp capping” is desirable.
Such a belief is baaed on findings that the deep layers of carious dentin are
sterile and the pulp is not infected or inflamed until almost or actually ex-
posed.55s73,*I, *8 There is sufficient evidence to support the contentions of both
groups.
In my view, the clinical evidence already enumerated, which indicates the
presence of severe pulpal pathosis, dictates a treatment policy of pulp extirpa-
tion and endodontic therapy. In the absence of such evidence, therapeutic man-
agement by indirect pulp capping is the preferable regimen. In such cases,
efforts should be made to maintain pulp vitality, even though chronic pulp
inflammation may persist. The vitality of the pulp should be maintained as long
as possible in the absence of evidence that chronic pulp inflammation is harm-
ful to the well-being of the organism. The defensive capacity of the pulp is
thereby retained.
REFERENCES
1. Andreasen, J. O., and Hj&+ing-Hansen, E.: Intra-alveolar Root Fractures : Radiographic
and Histologic Study of 50 Cases, J. Oral Surg. 25: 414, 1967.
2. Armenio, G., Terio, B., and Laforgia, P. D.: Aspetti Degeneration Senili Della Fibre
Nervose Della Polpa Dentale, Riv. Clm. Odontol. 11: 1, 1956.
3. Arwill, T.: Histopathologic Studies of Traumatized Teeth. Odontol. Tidskr. 70: 91, 1962.
4. Arwill, T., Henschen, B., and Sundwall-Hagland, I.: The Pulpal Reaction in Trauma-
tized Permanent Incisors in Children Aged 9-18, Odontol. Tidskr. 75: 130! 1967.
5. Barber, D., and Massler, M.: Permeability of Active and Arrested Carious Lesions to
Dyes and Radioactive Isotopes, J. Dent. Child. 31: 26, 1964.
6. Baume, L. J.: Diagnosis of Drseases of the Pulp, OFGALSn~o. 29: 102, 1970.
7. Baume, L. J., and Fiore-Donno, G.: Versuch emer Klassifmierung der Pulpaerkrankungen
nach Klinisch-symptomatologischen Gesichtspunkten, Zahnaerztl. Welt/Reform. 63:
709, 1962.

16. 284 Seltzer Oral Surg.
August, 1972
8. Bennett, C. G., Kelln, E. E., and Biddington, W. R.: Age Changes of the Vascular
Pattern of the Human Dental Pulp, Arch. Oral Biol. 10: 995, 1965.
9. Bernick, 8.: Age Changes in the Blood Supply to Human Teeth, J. Dent. Hes. 46: 544,
1967.
10. Bernick, S.: Effect of Aging on the Nerve Supply to Human Teeth, J. Dent. Res. 46:
694, 1967.
11. Blackwood, H. J.: Tissue Repair in Intra-alveolar Root Fractures, ORAL SURG.12: 360,
1959.
12. Bradford, E. W.: The Dentine, a Barrier to Caries, Br. Dent. J. 109: 387, 1960.
13. Brown, L. R., Jr., and Rudolph, C. E., Jr.: Isolation and Identification of Microorganisms
From Unexposed Canals of Pulp-Involved Teeth, ORALSTJRG.10: 1094, 1957.
14. BrLnnstrGm, M., and Lind, P. 0.: Pulpal Response to Early Dental Caries, J. Dent. Res.
44: 1045, 1965.
15. Buest, T. B.: Demonstration of Sclerosis of Dentin in Tooth Maturation and Caries,
Dent. Cosmos 76: 305, 1934.
16. Cahan, P. M.: Electron Microscopic Study of Human Dental Pulp (Abstr.), J. Dent.
Res. 49: 688, 1970.
17. Carranza! F. A., Itoiz, M. E., Cabrini, R. L., and Dotto, C. A.: A Study of Periodontal
Vascularization in Different Laboratorv Animals. J. Periodont. Res. 1: 120. 1966.
18. Castelli, W. A., and Dempster, W. T.: The Periodontal Vasculature and Its Responses
to Experimental Pressures, J. Am. Dent. Assoc. 70: 890, 1965.
19. Chirnside, I. M.: A Bacteriological and Histological Study of Traumatized Teeth, New
Zeal. Dent. J. 53: 254? 1957.
20. Curtis, H. J.: Biological Mechanisms of Aging, Springfield, Ill., 1966, Charles C Thomas
Publisher.
21. Cutright, D. E., and Bhaskar, 8. N.:
ORAL SURG.24: 442.1967.
A New Method of Demonstrating Microvasculature,
22. Dachi, 8. F., and Stigers, R. W.: Pulpal Effects of Water and Air Coolants Used in
High Speed Cavity Preparation? J. Am. Dent. Assoc. 76: 95, 1968.
23. Eastoe, J. E.: Chemical Organization of the Organic Matrix of Dentine. In Miles, A. E.
W. (editor) : Structural and Chemical Organization of Teeth, New York, 1967, Academic
Press, Inc., Vol. II, pp. 302-303.
24. Euler, H. : Halkeinlagerungen und Pulpagefasse, Paradentium 4: 102, 1952.
25. Fiore-Donno, F. : Comparisons Between Clinical and Histopathological Diagnosis of
Dental Pulp Diseases, Sehweiz Monatssehr. Zahnheilkd. 78: 1148, 1968.
26. Fisher, A. K., Belding, J. H., Opinsky, J. S., and Spinella, D. J.: The Influence of the
State of Tooth Development on the Oxygen Quotient of Normal Bovine Dental Pulp, J.
Dent. Res. 38: 208, 1959.
27. Fuchs, M., and Szymaniak, E.:
Czas. Stomatol. 21: 1321, 1968.
Clinical Classification of Diseases of the Dental Pulp,
28. Gardner, A. F.: Pathology of the Dental Pulp With Clinical Correlations, Pratt. Dent.
Monogr. May, 1963.
29. Hamp, E. G.: Isolation and Identification of Spirochetes Obtained From Unexposed Ca-
nals of Pulp-Involved Teeth, ORALSURG.10: 1100, 1957.
30. Hareourt, J. K.: Further Observations on the Peritubular Translucent Zone in Human
Dentine, Aust. Dent. J. 9: 387, 1964.
31. Hattyasy, D.: Possibilities of the Conservation of the Damaged Dental Pulp, Int. Dent.
J. 16: 63. 1966.
32. Hess, J.-C.: Current Concepts of Pulp Pathology and Therapy, Rev. Franc. Odontostom-
atol. 14: 61, 1967.
33. Hess, J.-C.: Endodontie, Paris, 1970, Libraire Maloine, S.A.
34. Hill, T. J. A.: A Textbook of Oral Pathology, ed. 4, Philadelphia, 1949, Lea & Febiger,
pp. 211-217.
35. Holz, J., Fiore-Donno, G., and Baume, L. J.: Contr8les biologiques des materiaux d’obtu-
ration : normalisation des methodes experimentales et des criteres d’evaluation, Schweiz.
Monatsschr. Zahnheilkd. 78: 307, 1968.
36. Johansen, E.:
,Tuly, 1962.
The Nature of the Carious Lesion, Dent. Clin. North Am., pp. 305-320,
37. Johansen, E., and Nordback, L. G.: Chemistry of Carious Lesions. III. The Fluoride
Content of Carious Dentin, Preprinted abstr. 143, Int. Ass. Dent. Res., 40th general
meeting, St. Louis. 1962. n. 39.
38. Johan&, E.: IJltrastr&&e of Dentin. In Miles, A. E. W. (editor) : Structural and
Chemical Organization of Teeth, New York. 1967. Academic Press. Inc.
39. Johnson, R.-H., Christensen, G.’ J., Stigers; R. W., and Laswell, k. R.: Pulpal Irritation
Due to the Phosphoric Acid Component of Silicate Cement, ORAL SURG.29: 447, 1970.
40. Johnson, R. H:, Daehi, S. F., and Haley, J. V.: Pulpal Hyperemia-A Correlation of
Clinical and Hmtologic Data From 706 Teeth, J. Am. Dent. Assoc. 81: 108, 1970.
41. Eindlova, M., and Ma&m, V.:
Acta Anat. (Basel) 37: 163, 1959.
Blood Circulation in the Rodent Teeth of the Rat,

17. Classification of pulpal pathosis 205
42. Kramer, I. R. H.: The Vascular Architecture of the Human Dental Pulp, Arch. Oral
Biol. 2: 177, 1960.
43. KrGncke, A.: Das Schmerzsymptom bei Erkrankungen der Pulpa, Osterr. Z. Stomatol.
65: 162, 1968.
44. Kiinze!, W.: Probleme der direkten Pulpaiiberkappung. IV. Mitteilung: Histologische
und khnische Betrachtungen zur HeilungsfLhigkeit des freigelegten entziindlich erkrank-
ten Zahnmarkes. Dtsch. Stomatol. 18: 503. 1968.
45. Landay, M. A.; Nazimov, II., and Seltzkr, 5.: The Effects of Excessive Occlusal Force
on the Pulp, J. Periodontol. 41: 3, 1970.
46. Langeland, K.: Tissue Changes m the Dental Pulp; an Experimental Histologic Study,
Odontol. Tidskr. 65: 306. 1957.
47. Langeland, K.: Tissue changes Incident to Cavity Preparation; an Evaluation of Some
Dental Engines, Acta Odontol. &and. 19: 397, 1961.
48. Langeland, K.: Criteria for Biologic Evaluation of Anterior Tooth Filling Materials,
Int. Dent. J. 17: 405, 1967.
49. Langeland, K., and’ Langeland, L. K.: Indirect Capping and the Treatment of Deep
Carious Lesions, Int. Dent. J. 18: 326, 1968.
50. Langeland, K., and Langeland, L. K.:
Am. Dent. Assoc. 76: 991. 1968.
Cutting Procedures With Minimized Trauma, J.
51. Lefkowitz, W.: The “V&ality” of the Calcified Dental Tissues. V. Protective Metamor-
phosis of the Dentin, J. Dent. Res. 21: 423, 1942.
52. Lund?, T., and Stanley, H. R.: Correlation of Pulpal Histopathology and Clinical Symp-
toms m Human Teeth Subjected to Experimental Irritation, ORAL SURG.27: 187, 1969.
53. MacDonald, J. B., Hare, G. C., and Wood, A. W. S.: The Bacteriologic Status of the
Pulp Chambers in Intact Teeth Found To Be Nonvital Following Trauma, ORAL STJFCG.
10: 318,1957.
54. Massler, M.: Preventive Endodontics: Vital Pulp Therapy, Dent. Clin. North Am., pp.
663-673, November, 1967.
55. Massler, M.: Pulpal Reactions to Dental Caries, Int. Dent. J. 17: 441, 1967.
56. Matsumiya, S., Suzuki, A., and Takuma, 8.:
1962, The Tokvo Dental College Press.
Atlas of Clinical Oral Pathology, Tokyo,
57. Maz&, B., anb. Massler, M. : -Influence of Periodontal Disease on the Dental Pulp, ORAL
SURG.~~: 592.1964.
58. Mazzarella, d.-AI,- Hedman, W. J., Jr., and Brown, L. R., Jr.: Classification of Micro-
organisms From the Pulp Canal of Nonvital Teeth, Research report, Project NM 008 015.
10.01, U.S. Naval Dental School, National Naval Medical Center, Bethesda, Md., Aug.
1, 1955.
59. Mitchell, D., and Tarplee, R.: Painful Pulpitis, ORAL SURG.13: 1360, 1960.
60. Movat, H. Z., Uriuhara, T., Macmorine, D. L.., and Burke, J. S.: A Permeability Factor
Released From Leucocytes After Phagocytosls of Immune Complexes and Its Possible
Role in the Arthus Reaction, Life Sci. 3: 1025, 1964.
61. Mumford, J. M.: Relationship Between the Pain-Perception Threshold of Human Teeth
and Their Histological Condition of the Pulp (Abstr.), J. Dent. Res. 44: 1167, 1965.
62. Mumford, J. M.: Pain Perception Threshold and Adaptation of Normal Human Teeth,
Arch. Oral Biol. 10: 957, 1965.
62A. Obersztyn, A.: Healing of Pinpoint Exposure of Rat Incisor Pulp Under Various
Capping Agents, J. Dent. Res. 45: 1130, 1966.
63. Ogilvie, A. L., and Ingle, J. I.: An Atlas of Pulpal and Periapical Biology, Philadelphia,
1965, Lea & Febiger.
64. Pheulpi?, J.-L., Fiore-Donno, G., and Baume, L.-J.: Les inflammations pulpaires: Leurs
diagnostics clinique et histopathologique, Schweiz. Monatsschr. Zahnheilkd. 77: 701, 1967.
65. Philippas, G. G.: Effects of Function on Healthy Teeth: The Evidence of Ancient
Athenian Remains, J. Am. Dent. Assoc. 45: 443, 1952.
66. Philippas, G. G.: Influence of Occlusal Wear and Age on Formation of Dentin and Size
of Pulp Chamber, J. Dent. Res. 40: 1186, 1961.
67. Philippas, G. G., and Applebaum, E.:
Dent. Res. 45: 778, 1966.
Age Factor in Secondary Dentin Formation, J.
68. Philippas, G. G., and Applebaum, E.:
Incisor, J. Dent. Res. 46: 1002, 1967.
Age Changes in the Permanent Upper Lateral
69. Philippas, G. G., and Applebaum, E.:
Teeth, J. Dent. Res. 47: 411. 1968.
Age Changes in the Permanent Upper Canine
70. Pilz, ‘w.: Clinical Diagnosis of Pulpitis With the Pathohistological or Symptomatological
Approach, Dtsch. Stomatol. 19: 120, 1969.
71. Pinzon, R. D., Toto, P. D., and O’Malley, J. J.:
Various Ages, J. Dent. Res. 45: 934, 1966.
Kinetics of Rat Molar Pulp Cells at
72. Rebel, H. H.: Grundlagen und Probleme der Klinische Heilkunde Miinchen, 1954, Carl
Hanser Verlag.
73. Reeves? R., and Stanley, H. R.: The Relationship of Bacterial Penetration and Pulpal
Pathosls in Carious Teeth, ORALSURG.22: 59, 1966.

18. 286 Seltzer Oral Surg.
August, 1972
74. Reynolds, R. L.: The Determination of Pulp Vitality by Means of Thermal and Electrical
Stimuli. ORALSURG.~~: 231.1966.
75. Rubach; W. C., and Mitchell, D. F.: Periodontal Disease, Accessory Canals and Pulp
Pathosis, J. Periodontol. 36: 34, 1965.
76. Rubach, W. C., and Mitchell, D. F.: Periodontal Disease, Age and Pulp Status, ORAL
SURG.19: 482. 1965.
77. Rubin. L. R.; On the Controversv of Classification of Caries and Pulnitis. Stomatoleiia
(Mosk.) 46: 90, 1967.
I A , D
78. Saunders, R. L. de C. H.: Vascular Supply of the Dental Tissues, Including Lymphatics,
In Miles, A. E. TV. (editor) : Structural and Chemical Oraanization of Teeth. New
York, 1967, Academic Press, Inc., vol. l., p. 235.
79. Sayegh, F. S., and Reed, A. J.: Calcification in the Dental Pulp, ORAL SURG.25: 8i3,
1968.
80. Schour, I.: Noyes’ Oral Histology and Embryology, ed. 8, Philadelphia, 1953, Lea &
Febiger, pp. 143-145.
81. Schroeder, A.: Indirect Capping and Treatment of Deep Carious Lesions, Int. Dent. J.
18: 381, i968.
_- -
82. Schwabe, C.: Age Dependent Changes of Certain Peptide Hydrolases and Dehydrogenases
in Bovine Dental Pulp, J. Dent. Res. 48: 951, 1969.
83. Searls, J. C.: Light and Electronmicroscopic Evaluation of Changes Induced in Odon-
toblasts of the Rat Incisor by the High-Speed Drill, J. Dent. Res. 46: 1344, 1967.
84. Seltzer. S.. Bender. I. B.. and Ziontz. M.: The Dvnamics of Pulp Inflammation: Corre-
lations’ Between Diagnostic Data and Actual Histologic Findings in the Pulp, ORAL
SURG.16: 846, 969,1963.
85. Seltzer, 8.. Bender, I. B.. and Ziontz. M.: The Interrelationship of Pulp and Periodontal
Disease, OVAL Sm&16: i474,1963. '
86. Selye, H., and Prioreschi, P. : Stress Theory of Aging. In Shock, N. W. (editor) : Aging,
Some Social and Biological Aspects, Washington, 1960, American Association for the
Advancement of Science, pp. 261-272.
87. Shock, N. W.: Aging, Some Social and Biological Aspects, Publ. No. 65, Washington,
1960, American Association for the Advancement of Science.
88. Shovelton, D. S.: A Study of Deep Carious Dentine, Int. Dent. J. 18: 392, 1968.
89. Shroff, E. R. : Pathology of the Dental Pul Aust. Dent. J. 59: 59, 1955.
90. Sicher, H.: Orban’s Oral Histology and a#mbryology, ed. 5, St. Louis, 1962, The C. V.
Mosby Company, pp. 121-127, 139-140.
91. Stallard, R. E.: Periodontal Disease and Its Relationship to Pulpal Pathology, Para-
dontol. Acad. Rev. 2: 80, 1968.
92. Stanley, H. R., Jr:, and Swerdlow, H.: Biological Effects of Various Cutting Methods
in Cavity Preparation: The Part Pressure Plays in Pulpal Response, J. Am. Dent. Assoc.
61: 450, 1960.
93. Stanley, H. R., Jr.: Traumatic Capacity of High Speed and Ultrasonic Dental Instru-
mentation, J. Am. Dent. Assoc. 63: 749, 1961.
94. Stenhan. R. M.: Correlation of Clinical Tests With Microscooic Patholoov of the Dental
Pu<p, J.‘Dent. Res. 16: 267, 1937.
I n*
95. Stewart, J. M.: The Immediate Response of Odontoblasts to Injury, Odontol. Tidskr. 73:
417, 1965.
i -,
96. Suarez, C. L., Stanley, H. R., and Gilmore, H. W.: Histopathologic Response of the
Human Dental Pulp to Restorative Resins, J. Am. Dent. Assoc. 80: 792, 1970.
97. Swerdlow, H., and Stanley, H., Jr.: Reaction of Human Dental Pulp to Cavity Prepara-
tion. I. Effect of Water Spray at 20,000 r.p.m., J. Am. Dent. Assoc. 56: 317, 1958.
98. Swerdlow, H., and Stanley, H., Jr.: Reaction of Human Dental Pulp to Cavity Prepara-
tion. II. At 150,900 r.p.m. With Air-Water Spray, J. Prosthet. Dent. 9: 121, 1959.
99. Symons, N. B. B.: The Microanatomy and Histochemistry of Dentinogenesis. In Miles,
A. E. W. (editor) : Structural and Chemical Organization of Teeth, New York, 1967,
Academic Press, Inc., vol. 1, pp. 317-318.
100. Symons, N. B. B.: Electron Microscopic Study of the Tubules in Human Carious Dentine,
Arch. Oral Biol. 15: 239, 1970.
101. Taichman, N. 8.: Mediation of Inflammation by the Polymorphonuclear Leukocyte as a
Sequela of Immune Reactions, J. Periodontol. 41: 228, 1970.
102. Takuma, 8.: Ultrastructure of Dentinogenesis. In Miles, A. E. W. (editor) : Structural
and Chemical Organization of Teeth, New York, 1967, Academic Press, Inc., vol. 1,
D. 364.
103. Thomas, B. 0. A.: Gerodontology: Study in Changes in Oral Tissues Associated With
Aging, J. Am. Dent. Assoc. 38: 207, 1946.
104. Tylman, S., Spence, J. M., Weiss, M. B., and Massler, M.: Pulpal Damage Under Extra-
coronal and Intracoronal Preparations (Abstr.), J. Dent. Res. 37: 984, 1958.
105. Uriuhara, T., and Movat, H. Z.: Allergic Inflammation. IV. The Vascular Changes
During the Development and Progression of the Direct, Active and Passive Arthus
Reaction, Lab. Invest. 13: 1057, 1964.
106. von Vacek, Z. D., and PaEkova, A.: Die Innervation der Zahne, Acta Anat. 36: 59, 1959.

19. Volume 34
Number 2
Classification of pulpal pathosis 287
107.
108.
109.
110.
111.
112.
113.
114.
115.
116.
117.
118.
119.
120.
121.
122.
123.
124.
125.
126.
127.
128.
129.
130.
131.
132.
133.
134.
135.
136.
Waechter, R. : Caries Profunda, Dtsch. Zahnaerztl. Z. 21: 601, 1966.
Ward, P. A., Cochrane, C. G., and Miiller-Eberhard, H. J.: The Role of Serum Comple-
ment in Chemotaxis of Leukocytes In Vitro, J. Exp. Med. 122: 327, 1965.
Ward, P. A., Cochrane, C. G., and Miiller-Eberhard, H. J.: Further Studies on the
Chemotactic Factor of Complement and Its Formation In Vivo, Immunology 11: 141,
1966.
Weiss, M. B.: Relationship of Pain to Pulp Damage, ORAL SURG. 12: 358, 1959.
Weiss, M. B.. Massler, M., and Spence, J.: Operative Effects on Adult Dental Pulp, Dent.
Prog.‘4: 6, i959. ’ ’ - ’ -
-.
Woods, R. M., and Dilts, W. E.: Temperature Changes Associated With Various Dental
Cutting Procedures, J. Can. Dent. Assoc. 35: 311, 1969.
Zach, L., Topal, R., and Cohen, G.: Pulpal Repair Following Operative Procedures,
ORAL SURG. 28: 587. 1969.
Zakson, M. L. : Age’ Specific Changes of Teeth in Aged and Senile Persons, Stomatologiia
(Mosk.) 48: 4:29, 1969.
Zerlotti, E.: Histochemical Changes in the Connective Tissue of the Dental Pulp During
Inflammation. ORAL SURG. 27: 664. 1969.
Bhaskar, 5. k., and Lilly, C. E.: Intrapulpal Temperature During Cavity Preparation,
J. Dent. Res. 44: 644, 1965.
Bhussry, B. R.: Modification of the Dental Pulp Organ During Development and Aging.
In Finn, S. B. (editor) : Biology of the Dental Pulp Organ, Birmingham, 1968, University
of Alabama Press, pp. 146-165.
BrLnnstrGm, M.: The Effect of Dentin Desiccation and Aspirated Odontoblasts on the
Pulp, J. Prosthet. Dent. 20: 165, 1968.
Brzezinska, B. : Histochemical Investigations of Certain Enzymes in the Dental Pulp in
the Course of Periodontal Disease, Czas. Stomatol. 22: 85, 1969. (From Oral Res. Abstr.
5: 207 (No. 1265), 1970.)
Grossman, L. I.: Origin of Microorganisms in Traumatized, Pulpless, Sound Teeth,
J. Dent. Res. 46: 551. 1967.
Guthrie, T. J., McDonald, R. E., and Mitchell, D. F.: Dental Pulp Hemogram, J. Dent.
Res. 44: 678, 1965.
Hall, D. C. : Pulpal Calcifications-A Pathological Process? In Symons, N. B. B. (editor) :
Dentine and Pulp: Their Structure and Reactions. Baltimore. 1968. Williams & Wilkins
Company, pp. 266-274.
I I I
Hamilton, A. I., and Kramer, I. R. H.: Cavity Preparation With and Without Water
Spray, Br. Dent. J. 123: 281, 1967.
Han, S. 5.: The Fine Structure of Cells and Intercellular Substances of the Dental Pulp.
In Finn, 8. B. (editor) : Biology of the Dental Pulp Organ, Birmingham, 1968, University
of Alabama Press, pp. 103-139.
Harndt, R.: Diseases of the Pulp and Their Diagnosis, Dtsch. Zahnaerztl. Z. 24: 389,
1969.
Harrop, T. J., and Mackay, B.: Electron Microscopic Observations on Healing in Dental
Pulp in the Rat, Arch. Oral Biol. 13: 365, 1968.
Hess, J. C. : Iatrogenic Pulp Disease, Rev. Fr. Odontostomatol. 16: 635, 1969.
Kriincke, A.: Treatment of Deep Carious Lesions, Int. Dent. J. 20: 238, 1970.
Langeland, K., and Langeland, L. K.: Pulp Reaction to Crown Preparation, Impression,
Temporary-Crown Fixation, and Permanent Cementation, J. Prosthet. Dent. 15: 129,
1965.
Llory, H., and Frank, R. M.: Ultrastructure de la dentine carike, Actual. Odont-Stomatol.,
NO. 88, pp. 507-522, December, 1969.
Marsland, E. A., and Shovelton, D. 8.: Repair in the Human Dental Pulp Following
Cavity Preparation, Arch. Oral Biol. 15: 411, 1970.
Mumford, J. M. : Thermal and Electrical Stimulation of Teeth in the Diagnosis of
Pulpal and Periapical Disease, Proc. R. Sot. Med. 60: 197, 1967.
Schuchard, A., and Watkins, C. E.: Thermal and Histologic Response to High-Speed and
Ultrahigh-Speed Cutting in Tooth Structure, J. Am. Dent. Assoc. 71: 1451, 1965.
Sveen, 0. B., and Hawes, R. R.: Differentiation of New Odontoblasts and Dentine Bridge
Formation in Rat Molar Teeth After Tooth Grinding, Arch. Oral Biol. 13: 1399, 1968.
Szymaniak, E., and Pankiewicz, H.: Current Views on the Clinical Diagnosis of Pulp
Inflammations, Czas. Stomatol. 21: 381, 1968.
Tyldesley, W. R., and Mumford, J. M.: Dental Pain and the Histological Condition of
t.he Pulp, Dent. Pratt. Dent. Rec. 20: 333, 1970.
Address correspondence to :
Dr. Samuel Seltzer
Department of Endodontology
Temple University School of Dentistry
3223 North Broad St.
Philadelphia, Pa. 19140