Odontodysplasia Report
of two
cases
J. Lustmann, D.M.D.,” Jerusa.lem, Israel HEBREW
UNIVERSITY-HADASSAH
and
H. Klein,
review
of the
D.iW.D.,**
SCHOOL
OF
literature
and M. lJlma?zsky,
DENTAL
D.D.X.,***
MEDICINE
Odontodysplasia is a rare developmental anomaly affecting the tooth structures in both deciduous and permanent dentitions. The enamel is thin and uneven in thickness, and the detinal tissue surrounds very large pulp chambers. Denticles are present in the pulp organ. The maxilla is involved twice as frequently as the mandible. Most of the affected teeth are in the anterior segments; however, all other teeth can he affected. The cause is unknown. Because of the tendency of the affected teeth to develop abscesses, the most common treatment is extraction. Two additional cases are reported, and the literature is reviewed.
0
dontodysplasia is a rare developmental anomaly of hard dental tissues in which both enamel and dentin are involved. The condition affects both sexes and is often associated with the failure of teeth to erupt fully. In all published cases in which the deciduous teeth were involved, the permanent teeth in the corresponding segment were found to be similarly affected (Table I). In those cases in which the anomaly was detected only after the loss of the deciduous teeth, it has been suggested that the deciduous teeth must have been similarly affected.l-7 Although the anomaly is usually unilateral, casesof bilateral involvement have been described (Table I). The etiology is, as yet, undetermined. The first report on odontodysplasia was published in 1947, under the title of “arrested tooth devclopment.“b That report described x-ray findings only, with no details of the clinical and histologic picture. A second case report in 1953, under the same designation,” presented histologic and clinical findings. An additional case of special interest was published by Chaudhry and associates1 as “odontogenesis imperfecta.” This was the only case in which the anomaly was *Department **Department “**Department
of Oral Surgery. of Pedodontics. of Oral Pathology.
781
Oral May,
Fig. adjacent
1. Case
to first
1. Clinical right lower
appearance molar and
of left
the affected lower central
teeth. Suppurative swelling incisor areas (arrows).
Surg. 1975
present
present in both jaws, affecting fifteen permanent teeth in three dental segments. A number of cases have been &scribed under a variety of names, such as “odontogenic dysplasia”l0 and “unilateral dental malformation.“2 Zegarelli and associateszl introduced the term odontodysplasia, which has become the accepted term. In this article two additional casesof odontodysplasia are presented. CASE CASE
REPORTS 1
The patient was a 2-year-old girl who was referred to the Department of Oral Surgery of the Hadassab School of Dent,al Medicine in Jerusalem. She was referred 1)~ her physician because of a swelling that had affected the chin and right cheek for several months. On examination, the child was found to be normal, with no anomalies other than the swelling in the chin. She had not bad any of the common childhood diseases but had suffered from bouts of fever for which she received penicillin V-K and ampicillin. No adverse reactions were noted, and the child had never been hospitalized. She had one brother, aged 3 years, who was healthy. The swelling in the chin had appeared 35,4 months prior to her visit to the clinic. It was accompanied by pain, but the body temperature was normal. After treatment with penicillin V-K, the swelling decreased in size. However, when penicillin was discontinued, a second smelling appeared in the right cheek, which disappeared after further treatment with penicillin Y-K. Since then the child had been continuously receiving prophylactic closes of penicillin V-K, because the swelling on the chin had not completely disappeared, and she suffered from sensitivity and pain in the lower incisors on closing. It is of clinical value to mention that the child’s mother received 200 to 300 mg. of Largactil* and 6 to 10 mg. of Artanet daily during the first 2 months of pregnancy, because Other than this the mother had suffered no of psychotic reactions and hallucinations. illness during pregnancy. The child was born at full term, and there were no postnatal complications. According to the mother, superficial hemangiomas were present at birth in the right preauricular area and cheek, but they vanished, leaving no traces. “Chlorpromazin t Trihexyphenidyl
HCl. HCl.
Volume Number
Odontodysplasia
39 5
Fig. d. Case 1. First right lower molar affected hypoplastic nature of the enamel. A, Buccal view.
Fig. affected
Oral
3. Case 1. Full-mouth area are involved.
radiographs.
Both
by odontodysplasia, B, Oc,clusal view.
deciduous
teeth
783
demonstrating
and
permanent
marked
buds
in the
examination
According to the mother, the eruption of the deciduous teeth was normal and started at the age of 6 months. Examination revealed that, apart from the second deciduous right lower molar, which was in the process of eruption, the entire deciduous dentition was present and did not show caries. Except for the left lower deciduous molars, all the lower teeth were hypoplastic; in the left lateral deciduous incisor the pulp could be seen through the translucent lingual surface of the tooth, resembling the so-called pink tooth of Mummery. All the lower incisors were mobile and sensitive to percussion, and a suppurative swelling was present in the buccal suleus adjacent to the first right lower molar and left lower central incisor area. The maxillary teeth were normal (Figs. 1 and 2). Roentgenographic large
The roentgenographic pulpal cavities
findings and
picture was of great diagnostic wide-open apical foramina. The
value. dentinal
The hypoplastic layer was very
teeth thin
had and
704
Lu.stman?l,
Klein,
and Ulmansky
Oral May,
Surg. 1975
Fig. 4. Case 1. High magnification of an area of the dentin. The orientation of the dentinal tubules is completely irregular. (Hematoxylin and eosin stain. Magnification, x200.) Fig. 5. Case 1. Ground section of coronal aspect of incisor. The enamel is thin (arrow). The entire dentinal wall (D) is thinned. Almost half of the dentin thickness has a globular structure (63). (Magnification, x14.)
irregular and less radiopaque than that of normal teeth. The enamel could barely be seen; it was unevenly distributed over the coronary dentin and of unequal thickness. The tooth buds of the lower permanent incisors showed diminished calcification in comparison with the buds of the upper permanent incisors and had a ghostlike appearance. Tho premolar tooth buds on the right side were markedly less developed and less calcified than those on the left side. The tooth buds of both lower left molars appeared to be normal. The affected teeth presented a wider periodontal membrane than that of the unaffected teeth (Fig. 3). Treatment The patient was given 1 Gm. of ampicillin daily for 1 week, for treatment of the abscesses in the lower affected segments. The swelling vanished after treatment but recurred 2 weeks later. At this stage, the decision was made to extract the abscessed teeth, which was done under general anesthesia. Large quantities of granulation tissue and bone fragments were curetted from the periapical regions and were sent for histopathologic examination. Healing was quick and complete. Histologic
report
The histologic examination was made on the molar> which was sectioned longitudinally with a carborunclum disk and then split by means of a chisel. Half of the tooth was histologically sectioned after decalcification in order to preserve the soft tissues, while from the other half, which was previously examined with the help of the scanning electron
Volume Number
39 5
microscope,” grountl sections were prepnretl for the purpose of studying hart1 structures. The incisor was usecl for preparation of longitudinal ground sections only. Low-power magnification of the sections showed a very wicle pulp chamber and root canals surrounded 1)~ proportionally thin hard-tissue walls. In the coronal part, the outer surface of the enamel was irregular and seallopetl. The inner surface of the pretlentin was in many places irregular, ant1 in all the examine11 areas it was thickened and stainetl deeply with the hematoxylin and eosin stain. The tlcntinal tubules were irregular in size, shape, orientation, and distrilndon (Fig. 4). About half of the &din thickness had x globular structure (Fig. 5), which in many places protrude11 in a very irregular way into the pulp chamber; these round-shaped structures were also fount1 in the pulp organ, their size and shape being very similar to those of the dentin& wall. 1)enticles were often present in the pulp. CASE
2
A l’i-month-oh1 boy was brought by his mother to the 1)epartment of Petlodontics of the Haclassah School of I)ental Metlieine in Jerusalem. The mother was worried because of the very slow eruption of the maxillary right central xnd lateral incisors. The patient did not complain of pain in the affected area; nor was any swelling present. The mother rePorte11 that the maxillary left incisor am1 both mnntlilmlar incisors hat1 erupted at the age of 4y~ months. Eruption of the maxillary right central *~ntl lateral incisors hat1 startetl at 11 months of age, ant1 there seemed to be no continuation of eruption. The family history showed that the patient’s parents were not related to each other. Neither the parents nor their families sufEere(l from any dental anomalies. The patient’s mother had receivetl hormonal treatment tluring pregnancy because of previous multiple miscarriages. The report of the mother’s gynecologist revealed that the patient’s granllmother ant1 mother ant1 her three sisters sufferetl from familial bieornuate anI1 double uterus. In the second month of pregnancy thr patient’s mothclr re(*ctivcd prog&:rtivcs and continued with an injection of Proluton 1)epot.t once per week until dclivcsry. The child was ljorn nt full term without any complications during birth or in the postntrtal period. There was no report thnt the children of the mother’s sisters suffered from any tooth anom:tlies. Oral
examinations
Examination of the patient revealetl partial eruption of the maxillary right central incisor, lateral incisor, and cuspitl. The central anI1 lateral incisors showecl severe hypoplasia. The cuspicl revealed partial hypoplasia on the mesial sille of the crown. Except for these three affected teeth, all the others were normal. At the age of 32 months the boy returnesl for examination. His mother reported “sheclcling” of the right upper central incisor. Oral c~xaminntion rrvcde~l that thca right upper czentrnl incisor wns missing ; eontinuetl cbruption of the right upper later:\1 incGsor nntl full eruption of the right upl”r cxnincx wpr( &dent. Roentgenographic
findings
At the age of 17 months the severe hypoplastic teeth showetl large pulpal cavities withnormal crown and root formation. ‘1%~ dentinal layer of the crowns anal roots was extremely thin, anal the apices were wicle open. The tooth burls of the maxillary right permanent central rind lateral incisors and cuspid wcbre visildc only in thc,ir outline‘, with a thin layer of enamel, in comparison to the well-tlevelopetl tooth hurls of the left central itnIl lateral incisors (Fig. 6). The roentgenogram at t,he age of 32 months revealed the remaining root of the right out
*The scanning t Hydroxyprogesteron
electon
microscope caproate.
study
is untler
preparation.
786
Lustmann,
Fig.
Klein,
and Ulmansky
6. Case 2. Radiographs
Oral May,
of affected
Fig. 7. Case 2. Radiograph of affected area of the right upper central incisor after pathologic
area
at 17 months
Surg. 1975
of age.
at 32 months of age. Note fracture of the crown.
the persistent
root
upper central incisor and the open apex of the right upper lateral incisor and cuspid. The permanent tooth buds of the right central and lateral incisors showed severe developmental disturbances. The tooth buds of the left upper central and lateral incisors had developed normally (Fig. 7). Treatment tral
Treatment in the form of extraction and lateral incisors was proposed,
of but
the severely the parents
affected maxillary did not give their
deciduous consent.
cen-
DISCUSSION
Since the first publication of a case of odontodysplasia by McCall and Wald,8 forty-eight more cases have been published (Table I). In addition, Rushton’* mentioned nine other nonpublished cases; in only three were there radiographic and histologic findings, so that only those three could be included with some certainty as cases of odontodysplasia. One case which was among the unpublished cases of Rushton was later published.13 Our two cases bring the total of confirmed published cases to fifty-one.
Orro,ltod?J,Spltl.Sin
x
787
7
Fig.
8.
Involved
permanent
teeth reportedin
the
7
literature.
Of the forty-eight C~SCS in which the sex of the patient was stated, thirty-one were in fcmalcs and scvcntccn WCR in males; this suggeststhat females arc more prone to the condition than arc males. According to the accepted definition, odontodysplasia is a developmental anomaly affecting both deciduous and permanent dentitions. Table II shows that this condition is generally discovcrctl during t,hc eruptive periods of the deciduous and permanent teeth. It is interesting to stress that odontodysplasia is in many cases discovered because of the presence of abscessesin areas adjacent to the affected teeth. Of twenty-nine casesin which the clinical symptoms were described, fourteen were brought to notice because of abscessesand swellings ; in eleven cases,diagnosis of odontodysplasia. was subsequent to delay or lack of eruption in the affected segment; in one case, through routine x-ray examination ; in one case, because of spontaneous fracture of crowns ; and in another two, through malformed teeth (Table 1). In nearly all the casesin which the diagnosis was made because of the presence of abscesses, there was no decay and the infection reached the pulp, probably because of the thinness and malformation of the enamel and the dentin.’ L Odontodysplasia usually affects only one jaw. Only in one published case’ were both the maxilla and the mandible affrcted. The two jaws are not affected
Oral May,
I. Iteported casw of odontodysplasia up to the year 7973
Table
1947
1953
10 7yl2
hf F
1956
13
F
1059
5
M
9
M
Youniau and WereldW
1961
4%
F
Chaudhryi
1961
7
F
Abscess”
Sibly and Zimmermannlo
1962
S
M
Routine examination*
Bergman
Zegarelli
et
al.2
et al.11
1963
1963
X-3
7
F
7
F
9
F
14
M
x-1
1963
-
Worth and Poyton (Worthaa)
1963
3
M
Allen
1965
9
M
Goodridge (Rushtonla)
1965
7
F
32111
Rix
1965
8
M
/
1966
3%
F
1123456
3
F
zzziq
2%
M
edcba
4
F
(Rushtoniz)
Abrams and Groper14
et al.:1
1966
of eruption*
Lack
of eruption*
Mass
=I
Worthes
(Rushtonic)
Lack
Abnormal tooth development
-
Alexander
Surg. 1975
L!E labede
in mandible” -
112 11 123456
-
I1p
Abnormal t,ooth development* Abscess*
1 I
-3’
Abscess*
654321[ de
(
456
Abscess*
In cases in which information was available, pregnancy and delivery were normal. x-l = Tooth k exfoliated because of trauma at age of 4 years. z-d = Case No. 2 is not included because of lack of information. x-3 = Teeth 211 suspected. 2-4 = Teeth /d-and e in the affected area were normal. 2-5 = Two upper premolars and first molar. x-6 = Buds of teeth j35 not visible on roentgenograms. x-7 = Teeth /45 hypoplastic but without changes of the type seen in odontodysplasia. r-8 = Tooth q suspected. *Treatment
: Extractions.
Volume Number
39 5
I-Cont’d
Table
Author Bouyssou
et al.21
1966
11
F
Stafnels
1967
9
M
3q
Miller and Seymour4
1968
11%
F
3”1(
Hnnkey and Duckworth
1968
2%
M
Koblin
1969
3
F
9
F
10
F
and Schubelj
Pindborgsa
1970
Galeone
et al.27
Schulzens
1970
Rolling
et al.29
Reever
and
Kingsa
Rosenblumir
x-4
Witkopal Colby
1970 21’& F
1970 1971 1971
IO
F
I972
5
M
Leonard and McClure34
1972
9
M
Burch
1973
16
F
1973
I1
Gibbard x-7
et
al.16
1973
54321 I 123456 11123
dcba( edcha
mq XT
-
7%
Sappa
dcba 1 abcde
-
1972
and
pz3
1112
F
Gardner
F
2%
F
2yA
M
81/1
M
Lustmann X-R
and
et al.
1973
of eruption*
Lack
of eruption*
Abscess*
L.!&&!!
Abscess
4322(
Delayed
I
I
6
65432)
11234
of eruption
Cystic
enlargement*
Abscess* pi3
Spontaneous fracture of crowns -s-
3zlJ 11123
1 abcde
eruption
Abscess* IJack
zq
F
2
Lack
X-5
1 abcde
6
-*
-* -*
J
65
(123 1
a?‘2 F Pinkham Burke@
-
1 I 123 56
-
et al.16
Abscess*
p+
-
eruption*
1
1 abc e
3%
Petersss
zij 7654
4
1972
of eruption’*
Delayed
F
1971
and
pm
F
x-6
Hintz
Lack
2%
et al.32
Czukora
1 / 1234567
F
29& M
1971
Niegells
a labcde
L-A I&h
-*
2
F
4
F
8
F
2
F
TFizipx
Abscess”
1%
M
32J
Delayed
1 1234567
Lack
of eruption
F
Lack
of eruption
eruption
II. Number of casesdiscovered according to age
Table Age
nt discocery
Numlrrr
(yr.)
l-4 20
of cnscs
4-7 3
I
7-n
I
22
ll3
in the same proportion. Of fifty cases, the maxilla was inrolvctl in thirty-four and the mandible in only sixteen, a ratio roughly of 2 :l. Several reports suggest that the lesion is usually unilateral with no tendency to spread across the midline. I-lowcvcr, cxcrptions are occasionally found. Of a total of fifty-one cases.there were eleven in which the damage crossed the midline and affected both sides, and in the case reported by Chaudhry and associates1 three segments were affected in both jaws. In casesin which the damage crossed the midline in the maxilla (eight cases), only the central incisor on the opposite side was affected. In the mandible, when the damage crossed the midline (three cases), several teeth on both sideswere affected. The lesion appears to hc more common in the anterior segment, affecting incisors and canines in both jaws. This applies to two thirds of the affected teeth in both deciduous and permanent dentitions (Fig. 8). In almost cvcry case, the affected teeth were consecutive; in Niegel’s casc,l’ however, two teeth were missing, but they might have been removed during previous surgical interventions. In another case,“’ two teeth in the affected area were hypoplastic but othcraisc without changes of the type of odontodysplasia. In a third example, I7 teeth @and Fin the affected arca were normal. The cause of the anomaly has not yet bc~~nd&rmined. In order to understand this problem with any SL~CCCSS, one must understand the character of the anomaly. Odontodysplasia affects both the deciduous and permanent dentitions of the samearea. In several casesthere is a det,ailed report concerning the damage of both dcntitions, but cvcn when the anomaly WA diagnosed at an oldrr age, after the deciduous teeth had been lost, there is cvidcncc to indicate that the tleciduous teeth, too. wcrc affectctl. It would appear from this that the damage is continual, starting from thcl moment that the dcciduons tepth begin to dcvclop, roughly in the fourt,h month of pregnancy, until the permanent teeth are fully devclopcd, roughly at the age of 15 years (apart from t,hird molars). The damage to the two dcntitions cannot 1)~scparatcd, so that the causatirct Factor must be active in both the deciduous and permanent dentitions. Over thtl >-cars, various etiologic factors hart bcc>nsung&cd, SW.~~as local traLltlla,23
.A. !I. 11. 11’. 14
il~f(ydtion,Z,
3, !!, 12
loc;l]
iscfllclrli;~,:‘s
lK
irradiation
nv l’s I’, I’
metabolic and nutritional tlist,urbances or vitamin (leficiency,l’~ “9 I4 and hypcrpyrcsia.“~ *I, ’ g Irowcw, notic of these suggestions can bc maintained, since: (a) in no report hnvc the above-mentioned factors been proved and (1)) the agc7lt had to hccomc operative in about the fourth month of intrauterine life and ciIIIs(l scww and pcrmanc~nt damage to the drtual organ, or continue to act right through the period of dcvclopmc>nt,of the tlcciduous and permanent tlentitions. None of the above-mentioned agents fits these rcyuirements. Ischemia is also difficult to accept when we consider that WC arc discussing an area of the fan in whirh the blood supply is rich and in which therr arc so many collaterals.
Volume 39 Number 5
(ienctic factors have also been suggested,1, 3, 11,I* but this suggestion is difficult to accept, since, there is no instance of two affected mcmbcrs in the same family. Second, if the genetic factor were the cause, all the teeth should have been affected, as in the casesof amclogenesisand dcntinogenesis impcrfccta, wllcrcas in odontotlysplasia the damage is, for the most part, segmentary and asymmetrical. There arc two other ctiologic factors which should hc considered. Rushton” suggcstcd that a viral infection could pcrmancntlv damage the dental organ in the early stages of development. 1)amage to the developing embryo from viral int’cction during intrauterine life is known to occur. Thr virus may possibly remain latent within the cells of the dental organ for may gears and SO affect the primordium of the permanent teeth. This throrp is difficult to prove hecausc of the lack of detailed information in regard to the prenatal period and because of the difficulty in diagnosing many of the common viral infections. Finally, the role of local somatic mutations must be considcred.2, “‘7 I4 If the early stages of tooth formation are involved, both deciduous and permanent teeth of the affected segment will be defective, The two last-mentioned hypotheses fail to explain why the permanent molars, which develop from the distal extension of the dental lamina, should bc WIaffected in these cases,when the second deciduous molar is defective. This perhaps indicates that the tooth bud rather than the dental lamina is the affected element. KobliniSJ suggests that some local induction defect in the early stages of tooth development results in anomalous formation of dentin and enamel, terminating in this kind of anomaly. Extraction of abscessedteeth is the only treatment that has been given, since no restorations can bc made of either deciduous or pcrmancnt teeth. The main factor to be considered is that of timing. In small children, abscesseddeciduous trcth should bc extracted ant1 the other affected teeth should be preserved as long as possible in order to avoid damage to the developing jaws. In older children, the abscessedpermanent teeth should be extracted and all other affected teeth should be retained, if possible, until a permanent prosthesis can be inserted. Rome of the typical diagnostic signs of odontodysplasia arc bhinned walls of the teeth, witlc pulpal chambers, and delayed eruption. This information was obtained from examination of deciduous and permanent, teeth of young patients. l’inkham and Burkes’ described a patient with odontodysplasia whom they followed roentgenologically from the age of about 5 years np to about 14 years. In that cast all the pcrmancnt teeth of the left, ripper scgmcnt mere affected. They showed that the affected teeth did not lose their eruptive potential, but the ruptive rate was slower than that of other teeth. By the end of the follow-up period the thickness of the dentin was almost identical to that of the normal teeth. The existence of the almost normal dentin thickness permitted restorative treatment of those teeth with periapical pathosis. From their report, one may conclude that the extraction of the teeth with odontodysplasia is not the only treatment possible. If the permanent teeth erupt, it is worth while to protect them from fracture and infection by using preformed crowns without. any preparation. This proccdurc may preserve the vitality of
Oral May,
the ilffcrtd teeth, as well iis permit continuous formation stages those affectctl teeth may be treated bp any restorative
of dentin. proccdurc.
Surg. 1975
In later
REFERENCES
1. Chaudhry, Imperfecta: 2. Bergman, 16:
A.
P., Wittich, H. C., Stirkel, 1’. It., and Holland, M. R.: Report of a Case, ORAL RUKG. 14: 1099-1103, 1961. G., Lysell, L., and Pindborg, J. J.: Unilateral Dental Malformation,
48-60,
Odontogenesis ORAI,
SURG.
1963.
3. Alrxander, TV. N., Lilly, G. E., and Irby, TV. B.: Odontodysplasia, ORAL SURG. 22: 814-820, 1966. 4. Miller, W. A., and Seymour, R. H.: Odontodysplasia, Br. Dent. J. 125: 56-59, 1968. 5. Koblin, I., and Achubel, F.: Reitrag zur Odontodysplasie, Dtsch. Zahnaerztl. Z. 24: 219225,
1969.
6. Czukor,
J.: Lokalizalt dysplasias odontogenesin (Odontodysplasia), Fogorv. Rz. 65: 1511972. Pinkham, J. R., and Burkes, E. J., Jr.: Odontodysplasia, ORAL SURO. 36: 841-850, 1973. McCall, J. O., and Wald, 8. S.: Clinical Dental Roentgenology ed. 3, Philadelphia, 1952, TV. B. Saunders Comuanv. LID. 169-170. Suher, T., Jump, E. ‘B.,” and ’ I I Landis, R. I,.: Localized Arrested Tooth Development, 0~~1, SURo. 6: 1305-1314, 1953. Sibley, I,. C., and Zimmermann, E. R.: Odontogenic Dysplasia, ORAL SURG. 15: 1370-1373, 1962. Zegarelli, E. V., Ku&her, A. H., Applrbaum, E., and Archard, H. 0.: Odontodysplasia, ORAL SUKG. 16: 187-193, 1963. Rushton, M. A. : Odontodysplasia : “Ghost Teeth,” Br. Dent. J. 119: 109-113, 1965. Hxnkey, G. T., and Duckworth, R. : Odontodysplasia in the deciduous dentition, Dent. Practit. 19: 93-95, 1968. Report of Three Cases, 5. Dent. Child. Abmms, A. M., and Groper, J.: Odontodysplasia; 15.1.
7. 8. 9. 10. 11. 12. 13. 14.
33:
353-362,
15. Niegel, 16. Gihbard,
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S.: Die Odontodysplasie, Dtsch. P. D., Lee, K. W., and Winter,
Z. 27: 434-439, 1972. Zahnaerztl. G. B.: Odontodysplasia, Br. Dent.
J. 135:
525-532,
Report of a Case, J. Dent. Child. 38: 327-330, 1971. 17. Rosenblum, F. N. : Odontodysplasia: Odontodysplasia With Associ18. Burch, M. S., Besley, K. W., and Samuels, H. P.: Regional of a Case, ORAL SIJRG. 31: 44-48, 1973. ated Midline Mandibular Cyst : Report Eine pathogenetisehe Theorip dcr odontodysplastischen Reihenbildung, 19. Koblin, I.: abreleited aus dem Vewleich der hisher vrroffentlichten Falle. Dtsch. Zahnaerztl. Z. 24: 655-662, 20.
21. 22. 23. 24. 25. 26. 27. 28.
29. 30. 31. 32. 33. 34.
1969.
Schulze, C.: fiber einen Fall von Hypoplasie der Hartsubstanzen bei Zahnen im Bereich des rechten Oberkiefers. Dtsch. Zahnaerztl. Z. 11: 14-25. 1956. Blackman, S. : An At& of Dental and Oral Radiology; Bristol, 1959, John Wright & Sons, p. 86. Douniau, R., and Werelds, R. J.: etude d’un Cas Exceptionnel d’Hypoplasie Dentaire, Acta Stomatol. Belp. 58: 393-409. 1961. Worth, H. My: Principles and Practice of Oral Radiologic Interpretation, Chicago, 1969, Yearbook Medical Publishers, pp. 89-90. Rouyssou, M., Grazide, A., and Guilhem, A.: Sur une Nouvelle Dysembryoplasie Systematis&: Les “Dents Fantomes” (Ghost Teeth), Actual. Odontostomatol. 75: 307-327, 1966. Stafne, E. C.: Oral Roentgenographic Diagnosis, cd. 2, Philadelphia, 1967, TV. B. Saunders Company, pp. 38-39. Pindhorg, J. J. : Pathology of the Dental Hard Tissues, Copenhagen, 1970, Munksgxard, pp. 120-123. Galrone, R. J., Philips, J. F., and Pincock, 1). G.: Odontodysplasia, ORAI, SUR(:. 29: 879. 8,50, 1970. Sehulze, C. : Developmental abnormalities of the Teeth and Jaws. In Gorlin, R. J., and Goldman, H. M., editors: Thoma’s Oral Pathology, ed. 6, St. Louis, 1970, The C. V. Moshy Company, pp. 146-148. Rolling, I., Moller, T. J., and Philipsen, H. P.: Regional Odontodyplasia, Tandlaegebladet 74: 1324.1331, 1970. Reever, J. R., and King, TV. C.: Unilateral Maxillary Odontodysplasia, J. Dent. Child. 38: 23-28, 1971. Witkop, J. C., Jr.: Manifestations of Genetic Diseases in the Human Pulp, ORAL SURG. 32: 278-316, 1971. Colhy, R. A., Kerr, D. A., and Robinson, H. B. G.: Color Atlas of Oral Pathology, ed. 3, Philadelphia, 1971, J. B. Lippincott Company, p. 53. Hintz, C. R., and Peters, R. A.: Odontodysplasia, ORAL SURG. 34: 744-750, 1972. Leonard, M., and McClure, I.: Odontodysplasia: A Case Report, J. Dent. 1: 43-45, 1972.
Volume
39
Nurnl)er
5
Odontodysplmsia
33. Gardner, I). CT., and Rnpp, J. P.: Regional Odontodysplasia, 36. \Vewltls, R. J., and I)ouni:\u, R.: LC~S “Lknts Fantomes” 13rlg. 69: 375-427, lW.2. Reprint
Icquests
to :
Dr. J. IAustmann lkpxrtnwnt of Oral Surgery Helxrw University-Hadass:l11 ,Jerus:~lom lsrael
Scl~ool
of Dental
Medicine
OMI, (Ghost
793
SUKQ. 35: 351-365, 1973. Teeth), Actx Stomatol.