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Hereditary opalescent dentine
HEREDITARY THOMAS
R.
ALLEY,
OPALESCENT
D.D.S.,*
AND
LESTER
PHILADELPHIA,
DENTINE
W.
BURKET,
D.D.S., M.D.,‘”
PA.
T
HIS article presents two patients with hereditary opalescent dentine in which the family history can be traced for several generations. The diagnosis and treatment of this condition are easily within the scope of the general practitioner. It has been variously termed hereditary hypoplasia of the dentine,’ transparent enameJ2 odontogenesis imperfecta, odontochronognosis, hereditary pigThe name hereditary opalescent mentatioq4 and hereditary opalescent dentine. dentine is to be preferred since it describes both the condition and its hereditary nature. This anomaly was claimed to be extremely rare by Hopewell-Smith6; however, more and more cases are being reported, perhaps because of a greater inFinn4 divides hereditary anomalies terest in thorough diagnostic procedures. of tooth color into “brown hypoplasia of the enamel ” and “opalescent dentine. ” Brown or yellow hypoplasia of the enamel is an entirely different condition and should not be confused with hereditary opalescent dentine. In the enamel hypoplasias the enamel is the affected tissue, while in hereditary opalescent dentine it is the dentine that is affected. In hereditary opalescent dentine, the enamel is normal in structure but is devoid of pigmentation and has a slightly abnormal refractive index.7 Hereditary opalescent dentine is a non-sex-linked Mendelian dominant characteristic. If one parent is affected, 50 per cent of the siblings should show the characteristic.* Occasionally a generation may be skipped. This is one of the few anomalies in which both the permanent and the deciduous teeth are involved. Since the enamel is essentially normal this condition may be considered a mesenchymal dysplasia. The roots of these teeth also show abnormalities. The unerupted crowns and pulp chambers appear normal in the roentgenogram. Following eruption, there is a rapid calcification of the pulp chambers and root canals, and a darkening in the color of the clinical crown. Once the teeth begin to erupt, the difference in size between the crowns and the roots becomes apparent in the roentgenogram, and they resemble deciduous teeth. Some examples of hereditary opalescent dentine are found in patients with osteogenesis imperfecta; however, either condition may occur alone. Mittelman” reported a 6-year-old child who had experienced numerous fractures of the lower extremities, and whose teeth had the typical amberlike homogeneous translucency of hereditary opalescent dentine. Roentgen-ray studies of the child revealed that the crowns and roots of the erupted teeth were disproportionate in size, and that the pulp chambers were partially calcified. Winter and Maiocco’O *Instructor **Professor
in Oral Medicine, in Oral Medicine,
School of Dentistry, School of Dentistry, Z?8
University University
of Pennsylvania. of Pennsylvania.
HEREDITARY
OPALESCENT
DENTINE
329
reported several examples of osteogenesis imperfecta and hereditary opalescent reported on fifteen members of three generations of a family dentinc. RobertP Numerous other cases who were affected with hereditary opalescent dentine. have been recorded by Roberts and Schour,5 Wilson and Steinbrecher,12 and Noyes.13 Clinical Features.-The characteristic clinical findings consist of a peculiar opalescent purplish-brown or gray color of the teeth, a rapid attrition of the crowns, and a marked reduction in carious lesions. Finn,* Hodge,3 Roberts and Schour,5 and others have reported that these teeth have a low caries susceptiThis belief was also borne out in the patients examined by us. Roberts bility. and Schour5 state that the opalescence observed is a postformative and posteruptive phenomenon. Noyes13 believes that the abnormal color observed is due to atypical dentine formation and to obliteration of the pulp. The history will often reveal the familial nature of the condition. Roentgenographic studies will demonstrate roots which are small in relation to the crown and often pointed at the apex. There is a reduction in size or obliteration of the pulp chambers and canals, and a tendency to abscess formation in teeth without severe carions lesions. 7 The teeth are reported to be extremely brittle when extraction is attempted.14 Hodge and associates I6 stated that the dentine in these cases shows a microhardness of 65 to 70 as compared with the normal of 120 to 125. The water content is about 15.5 as compared with the normal of 13.2. There is about 10 per cent less inorganic matter but the mineral ratio is correct. The x-ray absorption value is 0.74 as opposed to the normal of 0.94. The enamel is normal as to mineral content, relative proportions of calcium and phosphorus, and water content. Histologic Structure.-The enamel, cementum, and periodontal membrane show no microscopic abnormalities, but there are many changes noted in the dentine. The dentoename1 junction is straight rather than scalloped as it is in normal teeth.15 This probably accounts for the weak attachment of the enamel to the dentine and the tendency for the enamel to chip, leaving exposed dentine. The mantle dentine shows a fairly normal number and arrangement of tubuli. Roberts and Schour5 report that the remainder of the dentine shows a smaller number of irregularly arranged tubuli with the number decreasing toward the They also state that there is considerable branching of these tubuli, PUlP. accentuated incremental stratification of the matrix, and poor calcification. This decreased hardness of the dentine, together with the poorly attached enamel, is undoubtedly responsible for the rapid wear of these teeth. Wilson and Steinbrecher? reported finding giant dentinal canals containing blood and surmised that the discoloration of the dentine was due to this abnormal blood supply. BuntingI reports hypoplastic defects in the dentine giving rise to interglobular spaces which are filled with a proteinlike substance. The pulp chambers and canals are progressively eliminated by the deposition of adventitious dentine. Calcification of the pulp chambers is often complete at 15 years of age.7
330
THOMAS
R.
ALLEY
AX‘1,
LESTER
W.
BURKET
Case Report The patients reported are a 23-year-old white woman and her 4$$-year-old daughter. The mother was first seen at the School of Dentistry, University of Pennsylvania, in 1940, when she reported for examination and possible treatment of her “brown teeth.” She has been followed continuously since t,hat time. The mother’s teeth had been a brown-purple color ever since their eruption. She reported that the color had darkened after eruption. Her deciduous teeth were also affected. She stated that her daughber’s teeth were affected and that the condition had been running in her family for at least six generations. There was no history of blue sclera or unusual fractures of the bones.
FFFMMMM
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M
F
,M
M
M
I &MMMMM I
Chart
I.--Shows
the indicates
affected individuals the patient described
in in
the patiect’s this paper,
family, and No.
indicated 2. her
by a circle. daughter.
No.
1
Roentgenograms taken at the age of 12 showed the pulp chambers of the erupted teeth nearly filled in with secondary dentine. The unerupted third molars appeared normal. There was considerable disproportion between the size of the crowns and roots. Few teeth showed carious lesions. (Fig. 1. ) Examination of the mother’s mouth revealed a normal mucous membrane and tongue. The color and mucosal tone were excellent. The papillae and coating of the tongue were normal. The patient gave a history of frequent and severe herpetic eruptions, but no lesions were noted at this time. All of the 23 permanent teeth present had the peculiar purple-gray opalescent appearance which is characteristic of this condition. The color phenomenon was more pronounced in the anterior teeth. There were several areas where pieces of enamel had fractured off exposing the red-brown dentine. All of the teeth showed considerable wear. This wear had resulted in a bite closure of several millimeters. There were two amalgam restorations present and one minimal carious lesion. The patient had a severe malocclusion with an overjet of 3/4 inch. The mandibular anterior teeth were bunched and several were in torsoversion. (Fig. 2.) Roentgenologic examination revealed that the pulp chambers of all teeth were calcified. Only six teeth had root canals which were not completely calcified. There was considerable disproportion between the crown and root size giving the impression of deciduous teeth. There was an area of osteosclerosis in the region formerly occupied by the mandibular right first molar. (Figs. 3 and 4.)
HEREDITARY
OPALESCENT
DENTINE
331
332
THOMAS
H.
ALLEY
.\SD
IXSTER
W.
BURKET
Treatment.-In view of the malocclusion, number of missing teeth, and poor root support, extraction and replacement by immediate complete upper and lower dentures were recommended.
Fig.
%.-Anterior
teeth
of
Fig. Fig. 9.-Roentgenogram pulp chambers and canals Fig. I.-Roentgenogram (leciduous teeth.
oatient
showinp
3.
ueculiar
of wear.
color
phenomenon,
malocclusion,
Fig. of
mandibular and disproportion of maxillary
and
areas
4.
right premolar region showing between crown and root size. central incisors showing similarity
calcification to
appearance
of of
On Nov. 17, 1950, the maxillary right premolars and mandibular right It was necessary to remove second molar were removed under local anesthesia. these teeth surgically since they were so soft that the forceps literally bit through them. It was necessary to free each tooth totally from its surrounding tissues with bone chisels and surgical burrs as elevators would only break away pieces of the tooth structure. The patient was given 300,000 units of crystalline penicillin intramuscularly following removal of these and subsequent teeth. Following these extractions, the patient had an attack of acute herpetic stoma-
HEREDITARY
OPAIJCSCEST
333
DENTISE
titis. She was started on high vitamin B complex therapy and the lesions reThe remaining posterior teeth were surgically removed gressed ten days later. at two subsequent sittings. In March, 1951, impressions were taken and immediate complete maxillary and mandibular dentures were constructed. The bite was opened 4 mm., and On an alveolectomy was planned to correct partially the maxillary protrusion. April 25, 1951, the remaining anterior teeth were surgically removed, alveolectomy performed, and the dentures inserted. The patient was extremely pleased with her improved had become very conscious of her dental deformity.
Fig.
5.-Four-and-one-half-year-old
extreme
daughter wear of
of previous the deciduous
patient showing dentition.
appearance
peculiar
as she
color
and
Histologic Sstudy.-A mandibular premolar extracted from this patient was decalcified and sectioned. The pulp chamber was completely obliterated by adventitious dentine, but a portion of the pulp canal was still present. The dentoenamel junction was not scalloped. The odontoblastic layer had degenerated. There were large areas of interglobular dentine. The dentinal tubuli were irregularly arranged and resembled secondary dentine. The 41/-year-old daughter of the previous patient appeared to be a normally developed child with some suggestion of oriental features. There was no evidence of blue scleras, and no history of fractures. All the deciduous teeth were present and in normal occlusion. They exhibited the same abnormal translucency as those of her mother, but were of a darker brown. They showed signs of extreme wear and were free from caries. (Fig. 5.)
Summary The patients reported demonstrate hereditary opalescent dentine not associated with osteogenesis imperfecta. This condition is not as rare as the literature would lead one to suspect. The anomaly is easily recognized by the
334
THOMAS
H. ALLEY
AXD
LESTER
W.
BURKET
peculiar opalescent purple-brown color of the teeth, few carious lesions, extreme attrition, and by the characteristic roentgenologic findings of calcified pulp chambers and malproportion of root and crown size. When these patients are encountered, there are two methods of treatment, i.e., the placing of jacket crowns on the teeth, or extraction and replacement by complete dentures. The latter method is usually indicated because of the usual poor root support, a tendency to abscess formation without severe caries, and especially for economic reasons. The patients should be warned of the hereditary nature of this condition.
References ;: 3. 2 7”. 8: 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
Matilda, Moody,
S. : Hereditary Hypoplasia of the Dentine, J. Am. Dent. A. 16: 866, 1929. Hereditary Tendencies in Tooth Formation, J. Am. Dent. A. 21: 1774, E.: 1934. Hodge, H., et al.: Hereditary Opalescent Dentine, J. Am. Dent. A. 26: 1633, 1939. Opalescent Dentin, J. Am. Dent. A. 25: 1240, 1938. Finn, S.: Hereditary Roberts, E., and Schour, I.: Hereditary Opalescent Dentin, Am. J. Orthodontics and Oral Surg. (Oral Surg. Sect.) 25: 267, 1939. Dentinogenesis Imperfecta, Dental Cosmos 63: 425,192l. Hopewell-Smith, A.: Oral Medicine, Philadelphia, 1946, J. B. Lippincott Company. Burket, L. W.: Hereditary Opalescent Dentine; Am. J. Orthodontics and Roberts, E., and &hour, I.: Oral Burg. (Oral Surg. Sect.) 25: 267, 1939. Mittelman, J. S.: Osteogenesis Imperfecta, ORAL SIJRG., ORAL MED., AND ORAL PATH. 3: 1562, 1950. Osteogenesis Imperfecta and Odontogenesis ImWinter, G. R., and Maiocco, P. I).: perfecta, ORAL SURG.,ORAL MED.., AND ORAL PATH.~: 782,1949. Roberts, W. R.: Hereditary Dentinogenesis Imperfecta, Brit. D. J. 87: 6-10, 1949. Wilson, G. W., and Steinbrecher, M.: Hereditary Hypoplasia of the Dentine, J. Am. Dent. A. 16: 866, 1929. Noyes, F. B.: Hereditary Anomaly in the Structure of Dentine, J. D. Res. 15: 154, 1935. Clark, F. H., and Clark, C. S.: Absence of Toot.h Enamel, J. Hereditary 24: 425, 1933. Boyle, P. E.: Kronfeld’s Histopathology of the Teeth and Their Surrounding Structures, Philadelphia, 1949, Lea & Febiger, p. 21. Hodge, H. C., et al.: Hereditary Opalescent Dentin. III. Histological, Chemical and Physical Studies, J. D. Res. 19: 521, 1940. A Roentgen-Ray Absorption Study of Hereditary Opalescent Dentin, McCauley, H. B.: J. D. Res. 21: 112, 1942. Bunting, R.: Oral Pathology, Philadelphia, 1929, Lea & Febiger, p. 118.
R.
ALLEY,
OPALESCENT
D.D.S.,*
AND
LESTER
PHILADELPHIA,
DENTINE
W.
BURKET,
D.D.S., M.D.,‘”
PA.
T
HIS article presents two patients with hereditary opalescent dentine in which the family history can be traced for several generations. The diagnosis and treatment of this condition are easily within the scope of the general practitioner. It has been variously termed hereditary hypoplasia of the dentine,’ transparent enameJ2 odontogenesis imperfecta, odontochronognosis, hereditary pigThe name hereditary opalescent mentatioq4 and hereditary opalescent dentine. dentine is to be preferred since it describes both the condition and its hereditary nature. This anomaly was claimed to be extremely rare by Hopewell-Smith6; however, more and more cases are being reported, perhaps because of a greater inFinn4 divides hereditary anomalies terest in thorough diagnostic procedures. of tooth color into “brown hypoplasia of the enamel ” and “opalescent dentine. ” Brown or yellow hypoplasia of the enamel is an entirely different condition and should not be confused with hereditary opalescent dentine. In the enamel hypoplasias the enamel is the affected tissue, while in hereditary opalescent dentine it is the dentine that is affected. In hereditary opalescent dentine, the enamel is normal in structure but is devoid of pigmentation and has a slightly abnormal refractive index.7 Hereditary opalescent dentine is a non-sex-linked Mendelian dominant characteristic. If one parent is affected, 50 per cent of the siblings should show the characteristic.* Occasionally a generation may be skipped. This is one of the few anomalies in which both the permanent and the deciduous teeth are involved. Since the enamel is essentially normal this condition may be considered a mesenchymal dysplasia. The roots of these teeth also show abnormalities. The unerupted crowns and pulp chambers appear normal in the roentgenogram. Following eruption, there is a rapid calcification of the pulp chambers and root canals, and a darkening in the color of the clinical crown. Once the teeth begin to erupt, the difference in size between the crowns and the roots becomes apparent in the roentgenogram, and they resemble deciduous teeth. Some examples of hereditary opalescent dentine are found in patients with osteogenesis imperfecta; however, either condition may occur alone. Mittelman” reported a 6-year-old child who had experienced numerous fractures of the lower extremities, and whose teeth had the typical amberlike homogeneous translucency of hereditary opalescent dentine. Roentgen-ray studies of the child revealed that the crowns and roots of the erupted teeth were disproportionate in size, and that the pulp chambers were partially calcified. Winter and Maiocco’O *Instructor **Professor
in Oral Medicine, in Oral Medicine,
School of Dentistry, School of Dentistry, Z?8
University University
of Pennsylvania. of Pennsylvania.
HEREDITARY
OPALESCENT
DENTINE
329
reported several examples of osteogenesis imperfecta and hereditary opalescent reported on fifteen members of three generations of a family dentinc. RobertP Numerous other cases who were affected with hereditary opalescent dentine. have been recorded by Roberts and Schour,5 Wilson and Steinbrecher,12 and Noyes.13 Clinical Features.-The characteristic clinical findings consist of a peculiar opalescent purplish-brown or gray color of the teeth, a rapid attrition of the crowns, and a marked reduction in carious lesions. Finn,* Hodge,3 Roberts and Schour,5 and others have reported that these teeth have a low caries susceptiThis belief was also borne out in the patients examined by us. Roberts bility. and Schour5 state that the opalescence observed is a postformative and posteruptive phenomenon. Noyes13 believes that the abnormal color observed is due to atypical dentine formation and to obliteration of the pulp. The history will often reveal the familial nature of the condition. Roentgenographic studies will demonstrate roots which are small in relation to the crown and often pointed at the apex. There is a reduction in size or obliteration of the pulp chambers and canals, and a tendency to abscess formation in teeth without severe carions lesions. 7 The teeth are reported to be extremely brittle when extraction is attempted.14 Hodge and associates I6 stated that the dentine in these cases shows a microhardness of 65 to 70 as compared with the normal of 120 to 125. The water content is about 15.5 as compared with the normal of 13.2. There is about 10 per cent less inorganic matter but the mineral ratio is correct. The x-ray absorption value is 0.74 as opposed to the normal of 0.94. The enamel is normal as to mineral content, relative proportions of calcium and phosphorus, and water content. Histologic Structure.-The enamel, cementum, and periodontal membrane show no microscopic abnormalities, but there are many changes noted in the dentine. The dentoename1 junction is straight rather than scalloped as it is in normal teeth.15 This probably accounts for the weak attachment of the enamel to the dentine and the tendency for the enamel to chip, leaving exposed dentine. The mantle dentine shows a fairly normal number and arrangement of tubuli. Roberts and Schour5 report that the remainder of the dentine shows a smaller number of irregularly arranged tubuli with the number decreasing toward the They also state that there is considerable branching of these tubuli, PUlP. accentuated incremental stratification of the matrix, and poor calcification. This decreased hardness of the dentine, together with the poorly attached enamel, is undoubtedly responsible for the rapid wear of these teeth. Wilson and Steinbrecher? reported finding giant dentinal canals containing blood and surmised that the discoloration of the dentine was due to this abnormal blood supply. BuntingI reports hypoplastic defects in the dentine giving rise to interglobular spaces which are filled with a proteinlike substance. The pulp chambers and canals are progressively eliminated by the deposition of adventitious dentine. Calcification of the pulp chambers is often complete at 15 years of age.7
330
THOMAS
R.
ALLEY
AX‘1,
LESTER
W.
BURKET
Case Report The patients reported are a 23-year-old white woman and her 4$$-year-old daughter. The mother was first seen at the School of Dentistry, University of Pennsylvania, in 1940, when she reported for examination and possible treatment of her “brown teeth.” She has been followed continuously since t,hat time. The mother’s teeth had been a brown-purple color ever since their eruption. She reported that the color had darkened after eruption. Her deciduous teeth were also affected. She stated that her daughber’s teeth were affected and that the condition had been running in her family for at least six generations. There was no history of blue sclera or unusual fractures of the bones.
FFFMMMM
FMFM
I
@
M
F
,M
M
M
I &MMMMM I
Chart
I.--Shows
the indicates
affected individuals the patient described
in in
the patiect’s this paper,
family, and No.
indicated 2. her
by a circle. daughter.
No.
1
Roentgenograms taken at the age of 12 showed the pulp chambers of the erupted teeth nearly filled in with secondary dentine. The unerupted third molars appeared normal. There was considerable disproportion between the size of the crowns and roots. Few teeth showed carious lesions. (Fig. 1. ) Examination of the mother’s mouth revealed a normal mucous membrane and tongue. The color and mucosal tone were excellent. The papillae and coating of the tongue were normal. The patient gave a history of frequent and severe herpetic eruptions, but no lesions were noted at this time. All of the 23 permanent teeth present had the peculiar purple-gray opalescent appearance which is characteristic of this condition. The color phenomenon was more pronounced in the anterior teeth. There were several areas where pieces of enamel had fractured off exposing the red-brown dentine. All of the teeth showed considerable wear. This wear had resulted in a bite closure of several millimeters. There were two amalgam restorations present and one minimal carious lesion. The patient had a severe malocclusion with an overjet of 3/4 inch. The mandibular anterior teeth were bunched and several were in torsoversion. (Fig. 2.) Roentgenologic examination revealed that the pulp chambers of all teeth were calcified. Only six teeth had root canals which were not completely calcified. There was considerable disproportion between the crown and root size giving the impression of deciduous teeth. There was an area of osteosclerosis in the region formerly occupied by the mandibular right first molar. (Figs. 3 and 4.)
HEREDITARY
OPALESCENT
DENTINE
331
332
THOMAS
H.
ALLEY
.\SD
IXSTER
W.
BURKET
Treatment.-In view of the malocclusion, number of missing teeth, and poor root support, extraction and replacement by immediate complete upper and lower dentures were recommended.
Fig.
%.-Anterior
teeth
of
Fig. Fig. 9.-Roentgenogram pulp chambers and canals Fig. I.-Roentgenogram (leciduous teeth.
oatient
showinp
3.
ueculiar
of wear.
color
phenomenon,
malocclusion,
Fig. of
mandibular and disproportion of maxillary
and
areas
4.
right premolar region showing between crown and root size. central incisors showing similarity
calcification to
appearance
of of
On Nov. 17, 1950, the maxillary right premolars and mandibular right It was necessary to remove second molar were removed under local anesthesia. these teeth surgically since they were so soft that the forceps literally bit through them. It was necessary to free each tooth totally from its surrounding tissues with bone chisels and surgical burrs as elevators would only break away pieces of the tooth structure. The patient was given 300,000 units of crystalline penicillin intramuscularly following removal of these and subsequent teeth. Following these extractions, the patient had an attack of acute herpetic stoma-
HEREDITARY
OPAIJCSCEST
333
DENTISE
titis. She was started on high vitamin B complex therapy and the lesions reThe remaining posterior teeth were surgically removed gressed ten days later. at two subsequent sittings. In March, 1951, impressions were taken and immediate complete maxillary and mandibular dentures were constructed. The bite was opened 4 mm., and On an alveolectomy was planned to correct partially the maxillary protrusion. April 25, 1951, the remaining anterior teeth were surgically removed, alveolectomy performed, and the dentures inserted. The patient was extremely pleased with her improved had become very conscious of her dental deformity.
Fig.
5.-Four-and-one-half-year-old
extreme
daughter wear of
of previous the deciduous
patient showing dentition.
appearance
peculiar
as she
color
and
Histologic Sstudy.-A mandibular premolar extracted from this patient was decalcified and sectioned. The pulp chamber was completely obliterated by adventitious dentine, but a portion of the pulp canal was still present. The dentoenamel junction was not scalloped. The odontoblastic layer had degenerated. There were large areas of interglobular dentine. The dentinal tubuli were irregularly arranged and resembled secondary dentine. The 41/-year-old daughter of the previous patient appeared to be a normally developed child with some suggestion of oriental features. There was no evidence of blue scleras, and no history of fractures. All the deciduous teeth were present and in normal occlusion. They exhibited the same abnormal translucency as those of her mother, but were of a darker brown. They showed signs of extreme wear and were free from caries. (Fig. 5.)
Summary The patients reported demonstrate hereditary opalescent dentine not associated with osteogenesis imperfecta. This condition is not as rare as the literature would lead one to suspect. The anomaly is easily recognized by the
334
THOMAS
H. ALLEY
AXD
LESTER
W.
BURKET
peculiar opalescent purple-brown color of the teeth, few carious lesions, extreme attrition, and by the characteristic roentgenologic findings of calcified pulp chambers and malproportion of root and crown size. When these patients are encountered, there are two methods of treatment, i.e., the placing of jacket crowns on the teeth, or extraction and replacement by complete dentures. The latter method is usually indicated because of the usual poor root support, a tendency to abscess formation without severe caries, and especially for economic reasons. The patients should be warned of the hereditary nature of this condition.
References ;: 3. 2 7”. 8: 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
Matilda, Moody,
S. : Hereditary Hypoplasia of the Dentine, J. Am. Dent. A. 16: 866, 1929. Hereditary Tendencies in Tooth Formation, J. Am. Dent. A. 21: 1774, E.: 1934. Hodge, H., et al.: Hereditary Opalescent Dentine, J. Am. Dent. A. 26: 1633, 1939. Opalescent Dentin, J. Am. Dent. A. 25: 1240, 1938. Finn, S.: Hereditary Roberts, E., and Schour, I.: Hereditary Opalescent Dentin, Am. J. Orthodontics and Oral Surg. (Oral Surg. Sect.) 25: 267, 1939. Dentinogenesis Imperfecta, Dental Cosmos 63: 425,192l. Hopewell-Smith, A.: Oral Medicine, Philadelphia, 1946, J. B. Lippincott Company. Burket, L. W.: Hereditary Opalescent Dentine; Am. J. Orthodontics and Roberts, E., and &hour, I.: Oral Burg. (Oral Surg. Sect.) 25: 267, 1939. Mittelman, J. S.: Osteogenesis Imperfecta, ORAL SIJRG., ORAL MED., AND ORAL PATH. 3: 1562, 1950. Osteogenesis Imperfecta and Odontogenesis ImWinter, G. R., and Maiocco, P. I).: perfecta, ORAL SURG.,ORAL MED.., AND ORAL PATH.~: 782,1949. Roberts, W. R.: Hereditary Dentinogenesis Imperfecta, Brit. D. J. 87: 6-10, 1949. Wilson, G. W., and Steinbrecher, M.: Hereditary Hypoplasia of the Dentine, J. Am. Dent. A. 16: 866, 1929. Noyes, F. B.: Hereditary Anomaly in the Structure of Dentine, J. D. Res. 15: 154, 1935. Clark, F. H., and Clark, C. S.: Absence of Toot.h Enamel, J. Hereditary 24: 425, 1933. Boyle, P. E.: Kronfeld’s Histopathology of the Teeth and Their Surrounding Structures, Philadelphia, 1949, Lea & Febiger, p. 21. Hodge, H. C., et al.: Hereditary Opalescent Dentin. III. Histological, Chemical and Physical Studies, J. D. Res. 19: 521, 1940. A Roentgen-Ray Absorption Study of Hereditary Opalescent Dentin, McCauley, H. B.: J. D. Res. 21: 112, 1942. Bunting, R.: Oral Pathology, Philadelphia, 1929, Lea & Febiger, p. 118.