Dentin dysplasia: Review of the literature

and a proposed subclassification based on

radiographic findings
M. Kevin 0 Carroll, BDS, iUSD,a William K. Duncan, DDS, iUEd,b and
Teresa M. Perkins, DMD, MS,” Jackson, Miss.

SCHOOL OF DENTISTRY, UNIVERSITY OF MISSISSIPPI MEDICAL CENTER

The literature is reviewed to determine the radiographic appearances of the reported cases of dentin
dysplasia. The sometimes confusing nomenclature is rationalized. Four distinct forms of dentin dysplasia
type I and one form of dentin dysplasia type II are identified. There seems to be no need to identify more
than two distinct types of this relatively rare inherited defect of human dentin, but a proposed
subclassification of type I dentin dysplasia could make identification of the two types easier.
(ORAL SURC ORAL MED ORAL PATHOL 1991;72:119-25)

D entin dysplasia (DD) is the term currently fa-

vored for the condition reported in 1939 by Rushton’
as “dentinal dysplasia.” It appearsthat variations had
been previously reported, first by Ballschmiede2 in
1920 as “rootless teeth,” by Weiss3 in 1927 as an
“unusual caseof pulpstones,” and by Hitchin in 1936
as “pulp stones in every tooth.”
Shields et aL5 proposed a classification for herita-
ble human dentin defects in which they divided DD
into type I (DDl) and type II (DD2). Witkop6 arrived
at a similar distinction but used the term “radicular
dentin dysplasia” for DDl and “coronal dentin
dysplasia” for DD2. Attempting to fit earlier and later
reported casesinto this classification appears to have
caused some confusion.7-9The purpose of this article
is to reduce this confusion by categorizing the de-
scriptions of the reported casesthat appear to repre-
sent DD.
LITERATURE REVIEW
Many reports of DD 1 have appeared,‘0-20whereas
only a few reports of DD2 exist.21-25The titles of the
majority of reports do not classify the anomaly.26M42
Shields et al.5 and Richardson and Fantin reported
BAssociate Professor of Oral and Maxillofacial Radiology, Depart-
ment of Diagnostic Sciences.
bAssociate Professor and Chairman, Department of Pediatric
Dentistry.
CAssistant Professor, Department of Pediatric Dentistry.
7/16/26069
their DD2 casesas “anomalous dysplasia of dentin.”
Rao et a1.44described two casesthat they identified as
pulpal dysplasia, one of which radiographically re-
sembles DD2. Wald and Diner45 and Diner and
Chou4’j used the term “dysplasia of the dental pulp.”
Burkes et a1.23used the terms “dentin dysplasia II”
and “pulpal dysplasia” synonymously.
Nakata et a1.47reported a new type that they
described as interradicular DD, which was associated
with amelogenesisimperfecta. DD has also been re-
ported in association with calcinosis universalis, tu-
moral calcinosis,49-5’rheumatoid arthritis and hyper-
vitaminosis D,52 and sclerotic bone and skeletal
anomalies.53In the foreign-language literature, nu-
merous descriptions of DD have appeared.54-64The
quality of radiographic reproduction rendered most of
those reports less than useful in our endeavor. In ad-
dition to those referenced, others have been indexed
but were not verifiable by the authors. At least 190
caseshave been reported to date.
Shields et al.s characterized DDl as involving pri-
mary and permanent teeth that are clinically normal
in shape, size, and consistency. Radiographically, the
primary teeth showedtotal pulpal obliteration whereas
the permanent teeth showed preeruptive pulpal oblit-
eration, resulting in a crescent-shapedpulpal remnant
parallel to the cementoenamel junction. Numerous
periapical radiolucent areas in noncarious teeth were
essentially diagnostic of the disorder.
Shields et a1.5described the histologic findings in
DD 1 as showing a normal layer of mantle dentin and
119
120 0 Carroll, Duncan, and Perkins ORhi. SURG ORAl MED ORAL PATH01
July 1991

Fig. 1. Full mouth radiographic survey of patient reported by Ciola et al.’ Canines show enlargement of
pulp canal to accommodatelarge pulp stone. Root is bulged in area of canal enlargement. (From Ciola B,
Bahn SL, Goviea GL. ORAL SURG ORAL MED ORAL PATHOL 1978;45:317-22.1

Fig. 2. Panoramic radiograph of patient reported by Diamond.’ Canines and premolars exhibit pulp stones
in enlarged root canals with corresponding root bulges. (From Diamond 0. J Dent Child 1989;56:310-2.)

most of the remainder of the coronal dentin as normal.
In the area of dysplastic dentin the dentinal tubules
were blocked and shunted from their normal course
by numerous denticles. The periapical radiolucencies
are described as either granulomas’2, 30,37,39,40*53or
cysts* in histologic reports.
DD2 was characterized by Shields et alaSas involv-
ing primary teeth that may have a brown or bluish
amber coloration similar to that seen in hereditary
opalescent dentin and permanent teeth that may be
clinically normal in all respects,or may have a slight
ambercoloration. Radiographically, theprimaryteeth
showed total pulpal obliteration as in DDl, but the
permanent teeth had a normal root size and shape
*References 10, 11, 14, 15, 19, 32, 36, 39, 40.
with a thistle-tube pulp configuration and pulp stones
in every pulp chamber.
Histologic sections from one of the primary teeth in
one of their patients revealed a thin layer of normal
coronal dentin with a suddentransition to a very dense
amorphous dentin with few tubules. Melnick et a1.22
reported no normal dentin, describing it as disorga-
nized throughout on both light and electron micros-
COPY*
Shields et a1.,5in attempting to relate their newly
discovered DD2 to previously reported casesof den-
tin defects, found the literature often confusing. This
confusion may have been compounded by the inter-
pretation of the term “thistle-tube-shaped pulp
chamber,” which was part of their description of the
radiographic features of DD2. Ciola et a1.7(Fig. 1)
and Diamond9 (Fig. 2) interpreted the term to corre-
Volume12 Dentin dysplasia I 21
Number 1

Fig. 3. A, Diagram illustrating proposedDDla. Pulp is completely obliterated. Little or no root formation
is present. B, Diagram illustrating proposed DDl b. Pulpal remnant is minimal at cementoenameljunction.
Roots are very short with no visible canals. C, Diagram illustrating proposed DDlc. Two crescent-shaped
pulpal remnants and roots of intermediate length are present. No canals are visible. D, Diagram illustrating
proposed DDld. Pulp chambers are visible near cementoenameljunction. Canals are widened to accommo-
date pulp stones. Root bulge is seen in anterior teeth. Canals are visible in roots of normal length.

spond to the enlargement of the pulp canal in the
coronal third of the root to accommodate the large
pulp stones found in that location in many single-
rooted teeth. However, Shields et al. and Witkop6 in-
dicated that the roots in DD2 are normal and that the
abnormalities are coronal.
A review of the literature to date shows that
whereas the description of DD2 given by Shields et
a1.5is consistent with most other reports, that of DDl
is probably too limited. Steidler et a1.40pointed out
that the level of the interface between normal and ab-
normal dentin in DDl was variable. They suggested
dividing DDl into two subgroups, one in which the
affected teeth have a thin mantle of normal dentin and
diminutive roots, and the other in which there is a
thicker mantle of normal dentin and roots of interme-
diate length. They suggested that the teeth with
diminutive roots tended to have almost obliterated
pulp chambers, whereas those with roots of interme-
diate length had demilunar pulp chambers, becauseof
the more apical demarcation of the dysplastic defect.
Scala and Watts17 suggested a similar division.
Sauk et a1.,35in a scanning electron microscopic
study, postulated that DD is a defect in the epithelial
component of the developing tooth germ in which the
invagination of the root sheath occurs too soon and,
in a sequence of futile attempts to correct itself,
results in a stunted root form with an unusual whorl-
like pattern of dentin obliterating the pulp chambers.
Bixler65 and Wesley et al.1° disagreed with that
suggestion; the latter offer as an alternative hypoth-
esisan error in the continual induction of odontoblasts
after the interaction with the ameloblastic layer.
Witkop66 suggested that the dysplasia results from
epithelial cells from the sheath of Hertwig breaking
off and migrating into the dental papilla, where they
induce odontoblast differentiation and dentin forma-
tion. Melnick et a1.i3suggestedthat the abnormal root
morphology is caused by abnormal differentiation
and/or function of the odontoblasts.
Clearly, the precise nature of the defect has yet to
be determined. However, it seemsto us that there is
sufficient evidence to regard DD 1 as having four pre-
sentations, depending on the age of the individual
teeth at the time they are affected.
DISCUSSION
Dentin dysplasia type I
In reviewing the literature, we can identify four
broad categories of variation in the radiographic ap-
122 0 Carroll, Duncan, and Perkins
Fig. 4. Development of pulp stone at dental papilla as
shown by Diamond.9 Proposed DDld.
pearance of DD 1. In the first (Fig. 3, A), represented
in the reports of Logan et a1.,29Per1 and Farman,”
Morris and Augsburger,53 Baka’een et a1.,i6Luffing-
ham and Noble,42 Witcher et a1.,5’ and Duncan et
al 2othere is complete obliteration of the pulp and
usually little or no root development. This form
appears to develop before the sheath of Hertwig has
begun the processof root development and is the most
severe form of DD 1, This form appears to have the
greatest prevalence of periapical pathosis and tooth
exfoliation or extraction. For this variation we pro-
pose the term dentin dysplasia type la, or DDla.
In the second category, DDlb (Fig. 3, B), repre-
sented in the reports of Hoggins and Marsland, Lo-
gan et al., 29Miller,33 McFarlane and Cina,36 Morris
and Augsburger, 53Tidwell and Cunningham,37 Mel-
nick et a1.,i3 Petrone and Noble,14 Steidler et a1.,40
Luffingham and Noble, 42Scala and Watts l7 Witcher
et a1.,5’ Brenneise et al., I8 Van Dis and Allen I9 and
Duncan et al.,20there is a horizontal, crescent-shaped,
radiolucent line along the cementoenamel junction
that correspondsto Hoggins and Marsland’s line4* of
demarcation between the normal coronal and abnor-
mal radicular dentin. There is usually a short conical
root or roots a few millimeters in length. This form
appears to occur slightly later in the development of
the tooth than does DDla and results in less than
complete obliteration of the pulp, and somerudimen-
tary root structure, as if the sheath of Hcrtwig was
able, in a severely limited way, to form a tooth apex.
In the third category, DDlc (Fig. 3, C), represented
in the reports of Rushton,” 26Logan et a1.,29Graham
OK\L SLIRG OR \t ~t.0 ORAI. P.ATH~L
July 1991
Fig. 5. Interradicular DD as reported by Nakata et aL4’
Possible variation of proposed DDld.
et a1.,30Brookreson and Miller,32 Wesley et al.,”
Ciola et a1.,7Tidwell and Cunningham,37 and Van Dis
and Allen,” two crescent-shaped, horizontal lines,
concavetoward each other, are at the cementoenamel
junction and the root is about half the normal length.
This form of the dysplasia appears to occur suffi-
ciently late in the development of the individual tooth
to allow for significant root growth to take place, al-
beit abnormally. Usually there is no evidenceof a pulp
canal in the root.
In the fourth category, DDld (Fig. 3, D), repre-
sented in the reports of Weiss,3Hitchin Rushton,
Stafne and Gibilisco,28 Graham et a1.,30Elzay and
Robinson,3’ Petersson,34Hunter et al., 49Ciola et a1.,7
Coke et a1.,i2 Rankow and Miller,39 Nakata et a1.,47
Diamond,’ and Van Dis and Allen,i9 there is some
evidence of a pulp chamber at the level of the cemen-
toenamel junction. The roots are of normal length but
may be bulbous in the coronal third, where a large
pulp stone has developed within the root canal. This
form appears to arise latest in the life of the tooth be-
causethe pulp chamber is usually not obliterated, and
is the least severeform in that normal completion of
root formation occurs. In many instances the pulp
appears to be intact around the stone. In others it is
seen to be intact above and below the stone, which
seemsto be continuous with the dentin mesially and
distally.
In the first three categories the incidence of peri-
apical radiolucent areasis variable. In the fourth, only
a few instances have been reported. Rushton has
suggestedthat the root sheath, deprived of its expec-
Volume 72 Dentin dysplasia 123
Number 1

tation of defining a root of normal length, adopts the

alternative activity of cyst formation. If the root de-
velops to a normal length, then in most instances one
might not expect cyst formation. However, in the
dysplastic state some fragments of the sheath might
break off and result in the development of cysts.
Diamond9 showed a tooth in which the pulp stone
could be seendeveloping in the dental papilla while it
was in the coronal third of the root, although he de-
scribed it as DD2. The appearance of the pulp is rep-
resented diagrammatically in Fig. 4. Nakata et a1.47
showed a similar appearance for interradicular DD
(Fig. 5). If continued pulpal obliteration and root de-
velopment from the stage illustrated in Figs. 4 and 5
were to have occurred earlier in the life of the tooth
and with a greater degree of dysplasia, that is,
increased pulpal obliteration and decreased root
length, then it is conceivable that the resultant tooth
form might be that which is illustrated in Fig. 3, C,
rather than that in Fig. 3, D, rendering it possible to Fig. 6. DD2: Pulp chamber narrows suddenly at base
see those entities as a developmental continuum. (thistle-tube shape) into very narrow canal. Pulp stone is in
These four broad categories overlap somewhat in chamber rather than canal. No root bulge is present.
that one can sometimesseesomeroot development as
in Fig. 3, B, with the pulp obliteration of Fig. 3, A, and
some evidence of pulp canals as in Fig. 3, D, with the Rosenberg Gertzman et a1.68in 1983 reported a con-
double crescents of Fig. 3, C, increasing the possibil- dition of interrupted root development that they
ity of a continuum. called a new form of DD. It appears to us that Ciola
Therefore it seemsthat DDl can occur at different et a1.7have described two or more forms of DD 1 in the
stagesof tooth development and that the earlier it oc- same patient. Whereas the case of Eastman et a1.67
curs, the more severeis the pulpal obliteration and the appears different from DDl and DD2, being focal
stunting of the roots. rather than generalized, reports of other similar cases
are probably neededto seewhether another type des-
Dentin dysplasia type II
ignation is warranted. They described their case as
The radiographic appearance of DD2 is of a focal odontoblastic dysplasia. The caseof Rosenberg
normal-sized tooth but with extension of the pulp Gertzman et a1.68is also different from the others in
chamber into the root, development of a pulp stone(s) radiographic appearance, and they indicate that fur-
in the pulp chamber, and a sudden constriction at the ther investigation is necessaryto understand it more
base of the chamber into a very narrow canal as in- fully.
dicated diagrammatically in Fig. 6 (the thistle-tube Witkop,66 in attempting to update our understand-
shape), representedin the reports of Borkenhagen and ing of the differences between DDl and DD2, sug-
Elfenbaum, 52 Grimer,*’ Richardson and Fantin, geststhat becauseof new histologic information, DD2
Rao et a1.,44Shields et a1.,5Giansanti and Allen,*’ may really be a form of dentinogenesis imperfecta
Wald and Diner, 45 Diner and Chou,46 Melnick et type II. However, he recognizes that a revision of the
al.,** Burkes et al., 23Rosenberg and Phelan,24Steid- classification of inherited dentin defects is impracti-
ler et a1.,40Wetzel and Weckler, 63Hoff et a1.,64and cal because it would cause more problems than it
Jasmin and Clergeau-Guerithault.25 In some cases, would solve. Our proposedsubclassification would not
presumably those of relatively recent onset, the con- alter the existing one and might make it easier to dis-
striction may not be so sudden nor the canal so nar- tinguish between DDl and DD2 on the basis of the
row. In some the pulp stone is barely visible or occu- radiographic appearance of the permanent teeth.
pies only the coronal half of the chamber. The roots
SUMMARY AND CONCLUSIONS
are not bulbous, and periapical radiolucencies have
been reported only by Wald and Diner45 and Steidler DD can be divided into two types as proposed by
et a1.40 Shields et a1.5This typing can be done reliably on the
Eastman et a1.67in 1977 and Ciola et al.’ in 1978 basis of the radiographic appearance of the perma-
described two different conditions for which they nent teeth. (The primary teeth have a radiographic
suggested the name “dentin dysplasia type III.” appearance similar to each other in both types.)
124 0 Carroll, Duncan, and Perkins
The permanent teeth in DDl can have any of four
fairly distinct radiographic appearances:
Complete obliteration of pulp chambers and no
root development with many periapical radiolu-
cent areas
Horizontal, crescent-shaped,radiolucent pulpal
remnants and a few millimeters of root develop-
ment with many periapical radiolucent areas
Two horizontal, crescent-shaped, radiolucent
lines and significant but incomplete root devel-
opment, with or without periapical radiolucent
areas
Visible pulp chambers and oval pulp stones in
the coronal third of the root canal, with bulging
of the root around the stone and few if any pe-
riapical radiolucent areas
The permanent teeth in DD2 have normal root de-
velopment with a thistle-tube-shaped pulp chamber
extending into the root and containing pulp calcifica-
tion in the chamber rather than in the canal, and a
sudden constriction where the chamber becomesthe
root canal, which is very narrow.
The distinction between DDl and DD2 appears to
be significant enough to designate them as distinct
forms of the disease. Although the distinctions be-
tween the forms of DDl are useful clinically in terms
of treatment options, it does not appear to us that a
separate type designation is necessary.Therefore we
offer the described subclassification as a means of
stimulating discussion on the nature of this disorder
of odontogenesis.We recognize that it is basedon ra-
diographic features and in view of histopathologic and
genetic findings may need refinement to be accepted
in the diagnostic community.
The possible existence of additional forms of the
disorder as reported by Eastman et a1.,67Ciola et a1.,7
and Rosenberg Gertzman et a1.68may lead to further
modifications as DD is better understood.
We express sincere gratitude to Debbra Hunter for typ-
ing the manuscript and to Dr. Joseph S. Giansanti for his
encouragement and critical review.
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Reprint requests:
M. Kevin 0 Carroll, BDS, MSD
School of Dentistry
University of Mississippi Medical Center
2500 N. State St.
Jackson, MS 39216