Amelogenesis imperfecta with taurodontism Jim Congleton, DEPARTMENT
D.D.S., OF ORAL
MS., DIAGNOSIS,
and E. Jeff Burkes, Jr., D.D.S., SCHOOL
OF DENTISTRY,
MS.,
UNIVERSITY
Chapel Hill, OF NORTH
N. C.
CAROLINA
Reports of families having a combination of amelogenesis imperfecta and taurodontism are limited. This study of members of three families shows that the combination is inherited as an autosomal dominant trait. In each of the patients examined, neither condition was seen without the other. The enamel was rough and dysplastic and varied in color from white to yellow. Radiographically, taurodontism was present in the deciduous and permanent dentitions. The pulp chambers of the incisor teeth were larger than is usually seen at all ages. All patients had normal-appearing hair, fingernails, and bones. The distinction between amelogenesis imperfecta with taurodontism and the tricho-dento-osseous syndrome is discussed.
A
melogenesis imperfecta with taurodontism is an unusual combination of defects that has been reported in a limited number of families. In many cases the description of the affected members has been incomplete, creating confusion as to whether this combination can occur alone or whether it must be accompanied by hair and bone abnormalities. In this report, three families with amelogenesis imperfecta and taurodontism will be described.
dysplastic enamel was present on the erupted permanent teeth. Three relatives were examined; each one exhibited amelogenesis imperfecta with taurodontism. Teeth of other family members could not be examined because they had been removed and no preextraction records were available. In none of the family members has tightly curled or kinky hair been seen or reported at birth or anytime during life. They vary from average to above average in height and show no frontal bossing or square jaw forms.
CASE REPORTS Family No. 1
Family
A 3-year-old white boy was referred to the University of North Carolina School of Dentistry. The parents were concerned that the child might have the same dental characteristics as his father. After further questioning, it was reported that several generations of the family had exhibited similar dental findings (Fig. 1). Initial examination of the child revealed that the oral soft tissues were within normal limits. A full complement of primary teeth was present, but the enamel was thin and had areas of discoloration (Fig. 2). There was interproximal spacing between the anterior teeth. Radiographic examination revealed a normal complement of developing permanent tooth buds. The enamel of all teeth showed a radiodensity similar to or slightly greater than that of dentin. All teeth had pulp chambers which were larger than normal. The first and second primary molars exhibited very large pulp chambers with the bifurcation of the roots in the apical third of the root structure. The patient had slightly wavy hair and no fingernail abnormalities. A regular trabecular and bone growth pattern was present on radiographs taken for cephalometric studies. The patient was followed for restorative and routine care at the dental school. At age 9 the first permanent molars exhibited taurodont pulp chambers radiographically. All the primary molars showed a decrease in the size of the pulp chambers, but they were still noted to be largerthan normal. Pitted, 540
No. 2
Two children were referred to the University of North Carolina School of Dentistry because of significant tooth abnormalities. The mother reported that her teeth had poor enamel and that the same dental trait could be traced to her great-grandmother (Fig. 3). The oldest child, a 9-year-old white boy, was first seen in 1971 in the late mixed-dentition stage. Interproximal spacing was noted between all teeth. The enamel on all teeth was rough and yellow. Radiographic examination revealed that the permanent maxillary lateral incisors and the mandibular second premolars were congenitally missing. The enamel on every tooth was thin and had the same radiodensity as the dentin. The second primary molars exhibited large pulp chambers, and the first permanent molars exhibited moderately enlarged pulp chambers, with the bifurcation starting in approximately the middlethird of the root. At age 12, radiographs showed that the roots of the second permanent molars had an extremely conical shape with a very short bifurcation. The second child, a L/-year-old girl, was seen with her mother. She was in the early mixed-dentition stage. The enamel on all teeth was rough and yellow. There was interproximal spacing between all teeth. Radiographic examination revealed that the enamel on all teeth had the approximate radiodensity of dentin. All first and second primary molars and first permanent molars had large pulp chambers and short roots, consistent with taumdontism. A full complement of 00304220/79/120540+05$00.5010
0
1979 The C. V. Mosby Co.
Amelogenesis imperfecta with taurodontism
Volume 48 Number 6
541
Pediirw #l
Fig. 1. Family No. 1. developing permanent teeth was present radiographically. At age 12, each of the second permanent molars exhibited one large conical root with no evidence of bifurcation formation. The permanent teeth were small; there was interproximal spacing between all teeth. The enamel on all permanent teeth was thin, very rough, and discolored. A younger brother was seen at the School of Dentistry at age 4. Intraoral examination revealed a full complement of primary teeth. The enamel was similar to that of the older brother and sister. Radiograpic examination revealed that the primary molars had very large pulp chambers with only a suggestion of bifurcation of the root. The permanent maxillary lateral incisors and the mandibular second premolars were not evident on the radiographs. All of these patients have had straight to slightly wavy hair since birth. Their growth has been within the average for their ages, and bone density on skull radiographs has been within normal limits. The family members examined showed no evidence of growth disturbance, bossing or unusual facial form, or fingernail abnormality. Family No. 3 A 2%-year-old white boy was referred to the University of North Carolina School of Dentistry for diagnosis of unusual tooth formation and pulp chamber configuration. The father was concerned that his first child might have the same conditon he remembered being affected with when he was a child and for which his teeth had been removed. Examination of the boy revealed rough yellow enamel on the teeth. There was no
interproximal contact between the teeth throughout the mouth. Radiographs showed large pulp chambers in all the primary incisors and taurodontism of the primary molars (Fig. 4). The child’s two paternal uncles, his grandfather, and his great-grandfather had had their teeth removed at an early age because of a similar condition. It was further determined from history and dental records that a female cousin had the same condition (Fig. 5). Taurodontism with amelogenesis imperfecta was demonstrated radiographically from preextraction records in the father of the proband (Figs. 6 and 7). There was no other known hereditary condition in the family. All family members were enjoying good health, with no report of serious illness in any of the members. The proband and the father have had wavy hair since birth. The father’s hair is thin and fine in texture. The father, grandfather, and brothers are of average height and reportedly have no bone abnormality. Radiographs, other than panoramic and periapical films, were not available for review. Neither the proband nor his father have fingernail abnormalities. DISCUSSION Both amelogenesis imperfecta and taurodontism, as separate conditions, have been recognized for many years and in various populations.‘, 4* 6* 73 g, lo3 l4 Recently, patients with a combination of amelogenesis imperfecta and taurodontism have been reported. “2 i6 Other authors have recognized that the combination of amelogenesis imperfecta and taurodontism may occur
542
Congleton
and Burkes
Fig. 2.
Oral Surg. December,1979
Male Proband. family No. 1. Pitted dysplastic enamel on erupted permanentteeth. Pedigree
#2
7
Fig. 4. Proband, family No. 3. Deciduous teeth with thin enamel and dentin, and large pulp chambers.
Fig. 3.
Family No. 2
with abnormalities of the hair and the bones.“. ‘. I3 Othc:r combinations of abnormalities of enamel and Pulp have been the subject of reports by Jorgenson and War son5 and Stewart and associates.” Many of the rep0 rts, such as those of Crawford,’ Parker and associates, I1 and Widerman and Serene” did not specifically
mention hair and bone with the dental abnormalities. Because of the variability of expression evidently seen in this group of conditions, there is reason to question whether amelogenesis imperfecta and taurodontism can occur together without other abnormalities or whether this combination must include hair, bone, and other abnormalities. The families examined in this report would seem to settle that question. None of the patients had kinky hair, observable or demonstrable skull changes, known skeletal abnormalities, or fingernail changes. All were in good health and had progressed through growth milestones uneventfully. Members of these families not examined by us could have some of the extraoral abnormalities observed by other writers,
Amelogenesis
Volume 48 Number 6
imperfecta
with
taurodontism
543
Pedigree #3
Fig. 6. Father of the proband, family No. 3. The enamel is dysplastic. The teeth have large pulp chambers and taurodontism.
Fig.
5. Family No. 3.
but reliable historians in the families reported no observable stigmata. The condition was seen in successive generations and there was male-to-male transmission. Similar abnormalities were seen in males and females. These findings would be consistent with autosomal dominant inheritance. The exact type of the amelogenesis imperfecta seen with taurodontism is difficult to determine from the literature. In all the families reported here, the teeth were smaller than normal and had thin, hard, rough enamel. The teeth varied from white to yellow in color. Radiographically, there was little contrast between the enamel and the dentin; however, this is due in large part to its thinness. Histologic and biochemical evaluation in a number of these patients would be helpful in further understanding of the enamel and dentin abnormalities. In all of the examined affected members of each family, the primary teeth and erupted permanent teeth were altered, showing both the amelogenesis imperfecta and taurodontism. None of the examined patients were found to have either amelogenesis imperfecta or taurodontism as separate entities. Radiographic examination of the early primary dentition showed teeth with a small amount of dentin and enamel and very large pulp chambers. With time, these pulp chambers appear to deposit secondary dentin and become smaller, but they still retain the taurodont morphology. Long-term follow-up is not available on any family member in this series. As the members have become old enough to be bothered by the appearance of the teeth, or as multiple
Fig. 7. Father of the proband, family No. 3. The enamel is dysplastic. The teeth have large pulp chambers and taurodontism.
abscesses have developed, the treatment has been to remove all of the teeth and construct dentures. We wish to thank Drs. Burton Horowitz, and Victor radiographs
Rodman for their cooperation for family No. 3.
William Trolley, in providing the
REFERENCES I. Coon, S. C.: The Origin of the Races, ed. 1, New York, 1961, Alfred A. Knopf, Inc. 2. Crawford, J. L.: Concomitant Taurodontism and Amelogenesis lmperfecta in the American Caucasian, J. Dent. Child 37: 171175, 1970.
544
Congleton
and Burkes
Oral Surg. December, 1979
3. Gulmen, S., Pullon, P. A., and O’Brien, L. W.: Tricho-Dento-Osseous Syndrome, J. Endodont. 2: 117- 120, 1976. 4. Hamner, J. E., III, Witkop, C. J., Jr., and Metro, P. S.: Taurodontism: Report of a Case, ORAL SURG. 18: 409-418, 1964. 5. Jorgenson, R. J., and Watson, R. W.: Dental Abnormalities in the Tricho-Dento-Osseous Syndrome. ORAL SURG. 36: 693. 700, 1973. 6. Keith, A.: Problems Relating to the Teeth of the Earlier Forms of Prehistoric Man. Proc. Royal Sot. Med. (Odont. Sect.) 6: 103. 124, 1913. 7. Mangion, J. J.: Two Cases of Taurodontism in Modern Human Jaws, Br. Dent. J. 113: 309-312, 1962. 8. Melnick, M., Shields, E. D., and El-Kafrawy. A. H.: TrichoDento-Osseous Syndrome: A Scanning Electron Microscopic Analysis, Clin. Gen. 12: 17-27, 1977. 9. Metro, P. S.: Taurodontism: A Dental Rarity in Modern Man, ORAL SURG. 20: 236-237. 1965. IO. Mjor, I. A.: The Structure of Taurodont Teeth, J. Dent, Child 39: 459-463. 1972. 11. Parker. J. L., Regattieri. L. R., and Thomas, J. P.: Hypoplastic-Hypo-maturation Amelogenesis Imperfecta with Taurodontism: Report of a Case, J. Dent. Child. 42: 379-383, 197.5.
INFORMATION
12. Stewart, R. E.. Lourien, E. W.. and Wyandt, H. E.: Unusual Dental Findings in a Patient with a Rare Bone Dysplasia (dyschondrosteosis) and a Chromosomal Anomaly, ORAL SURF. 32: 596-604, 1971. 13. Robinson, G. C., Miller. J. R., and Worth, H. M.: Hereditary Enamel Hypoplasia: Its Association with Characteristic Hair Structure, Pediatrics 37: 498-501. 1966. 14. Weinman, J. P.. Svoboda, J. F., and Woods. R. W.: Hereditary Disturbances of Enamel Formation and Calcifications, J. Am. Dent. Assoc. 32: 397, 1945. 15. Widerman, F. H., and Serene, T. P.: Endodontic Therapy Involving a Taurodont Tooth, ORAL SURG. 32: 6 18-620. 197 1. 16. Winter. G. B., Lee, K. W., and Johnson, N. W.: Hereditary Amelogenesis Imperfecta: A Rare Autosomal Dominant Type, Br. Dent. J. 127: lS7- 164. 1969. Reprinr wyuc.~ t.\ to: Dr. E. Jeff Burkes Department of Oral Diagnosis School of Dentistry University of North Carolina Chapel Hill, N. C. 27514
FOR AUTHORS
Most of the provisions of the Copyright Act of 1976 became effective on January 1, 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author: “The undersigned author transfers all copyright ownership of the manuscript entitled (title of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warrants that the article is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility for releasing this material on behalf of any and all co-authors.” Authors will be consulted, when possible, regarding republication of their material.
D.D.S., OF ORAL
MS., DIAGNOSIS,
and E. Jeff Burkes, Jr., D.D.S., SCHOOL
OF DENTISTRY,
MS.,
UNIVERSITY
Chapel Hill, OF NORTH
N. C.
CAROLINA
Reports of families having a combination of amelogenesis imperfecta and taurodontism are limited. This study of members of three families shows that the combination is inherited as an autosomal dominant trait. In each of the patients examined, neither condition was seen without the other. The enamel was rough and dysplastic and varied in color from white to yellow. Radiographically, taurodontism was present in the deciduous and permanent dentitions. The pulp chambers of the incisor teeth were larger than is usually seen at all ages. All patients had normal-appearing hair, fingernails, and bones. The distinction between amelogenesis imperfecta with taurodontism and the tricho-dento-osseous syndrome is discussed.
A
melogenesis imperfecta with taurodontism is an unusual combination of defects that has been reported in a limited number of families. In many cases the description of the affected members has been incomplete, creating confusion as to whether this combination can occur alone or whether it must be accompanied by hair and bone abnormalities. In this report, three families with amelogenesis imperfecta and taurodontism will be described.
dysplastic enamel was present on the erupted permanent teeth. Three relatives were examined; each one exhibited amelogenesis imperfecta with taurodontism. Teeth of other family members could not be examined because they had been removed and no preextraction records were available. In none of the family members has tightly curled or kinky hair been seen or reported at birth or anytime during life. They vary from average to above average in height and show no frontal bossing or square jaw forms.
CASE REPORTS Family No. 1
Family
A 3-year-old white boy was referred to the University of North Carolina School of Dentistry. The parents were concerned that the child might have the same dental characteristics as his father. After further questioning, it was reported that several generations of the family had exhibited similar dental findings (Fig. 1). Initial examination of the child revealed that the oral soft tissues were within normal limits. A full complement of primary teeth was present, but the enamel was thin and had areas of discoloration (Fig. 2). There was interproximal spacing between the anterior teeth. Radiographic examination revealed a normal complement of developing permanent tooth buds. The enamel of all teeth showed a radiodensity similar to or slightly greater than that of dentin. All teeth had pulp chambers which were larger than normal. The first and second primary molars exhibited very large pulp chambers with the bifurcation of the roots in the apical third of the root structure. The patient had slightly wavy hair and no fingernail abnormalities. A regular trabecular and bone growth pattern was present on radiographs taken for cephalometric studies. The patient was followed for restorative and routine care at the dental school. At age 9 the first permanent molars exhibited taurodont pulp chambers radiographically. All the primary molars showed a decrease in the size of the pulp chambers, but they were still noted to be largerthan normal. Pitted, 540
No. 2
Two children were referred to the University of North Carolina School of Dentistry because of significant tooth abnormalities. The mother reported that her teeth had poor enamel and that the same dental trait could be traced to her great-grandmother (Fig. 3). The oldest child, a 9-year-old white boy, was first seen in 1971 in the late mixed-dentition stage. Interproximal spacing was noted between all teeth. The enamel on all teeth was rough and yellow. Radiographic examination revealed that the permanent maxillary lateral incisors and the mandibular second premolars were congenitally missing. The enamel on every tooth was thin and had the same radiodensity as the dentin. The second primary molars exhibited large pulp chambers, and the first permanent molars exhibited moderately enlarged pulp chambers, with the bifurcation starting in approximately the middlethird of the root. At age 12, radiographs showed that the roots of the second permanent molars had an extremely conical shape with a very short bifurcation. The second child, a L/-year-old girl, was seen with her mother. She was in the early mixed-dentition stage. The enamel on all teeth was rough and yellow. There was interproximal spacing between all teeth. Radiographic examination revealed that the enamel on all teeth had the approximate radiodensity of dentin. All first and second primary molars and first permanent molars had large pulp chambers and short roots, consistent with taumdontism. A full complement of 00304220/79/120540+05$00.5010
0
1979 The C. V. Mosby Co.
Amelogenesis imperfecta with taurodontism
Volume 48 Number 6
541
Pediirw #l
Fig. 1. Family No. 1. developing permanent teeth was present radiographically. At age 12, each of the second permanent molars exhibited one large conical root with no evidence of bifurcation formation. The permanent teeth were small; there was interproximal spacing between all teeth. The enamel on all permanent teeth was thin, very rough, and discolored. A younger brother was seen at the School of Dentistry at age 4. Intraoral examination revealed a full complement of primary teeth. The enamel was similar to that of the older brother and sister. Radiograpic examination revealed that the primary molars had very large pulp chambers with only a suggestion of bifurcation of the root. The permanent maxillary lateral incisors and the mandibular second premolars were not evident on the radiographs. All of these patients have had straight to slightly wavy hair since birth. Their growth has been within the average for their ages, and bone density on skull radiographs has been within normal limits. The family members examined showed no evidence of growth disturbance, bossing or unusual facial form, or fingernail abnormality. Family No. 3 A 2%-year-old white boy was referred to the University of North Carolina School of Dentistry for diagnosis of unusual tooth formation and pulp chamber configuration. The father was concerned that his first child might have the same conditon he remembered being affected with when he was a child and for which his teeth had been removed. Examination of the boy revealed rough yellow enamel on the teeth. There was no
interproximal contact between the teeth throughout the mouth. Radiographs showed large pulp chambers in all the primary incisors and taurodontism of the primary molars (Fig. 4). The child’s two paternal uncles, his grandfather, and his great-grandfather had had their teeth removed at an early age because of a similar condition. It was further determined from history and dental records that a female cousin had the same condition (Fig. 5). Taurodontism with amelogenesis imperfecta was demonstrated radiographically from preextraction records in the father of the proband (Figs. 6 and 7). There was no other known hereditary condition in the family. All family members were enjoying good health, with no report of serious illness in any of the members. The proband and the father have had wavy hair since birth. The father’s hair is thin and fine in texture. The father, grandfather, and brothers are of average height and reportedly have no bone abnormality. Radiographs, other than panoramic and periapical films, were not available for review. Neither the proband nor his father have fingernail abnormalities. DISCUSSION Both amelogenesis imperfecta and taurodontism, as separate conditions, have been recognized for many years and in various populations.‘, 4* 6* 73 g, lo3 l4 Recently, patients with a combination of amelogenesis imperfecta and taurodontism have been reported. “2 i6 Other authors have recognized that the combination of amelogenesis imperfecta and taurodontism may occur
542
Congleton
and Burkes
Fig. 2.
Oral Surg. December,1979
Male Proband. family No. 1. Pitted dysplastic enamel on erupted permanentteeth. Pedigree
#2
7
Fig. 4. Proband, family No. 3. Deciduous teeth with thin enamel and dentin, and large pulp chambers.
Fig. 3.
Family No. 2
with abnormalities of the hair and the bones.“. ‘. I3 Othc:r combinations of abnormalities of enamel and Pulp have been the subject of reports by Jorgenson and War son5 and Stewart and associates.” Many of the rep0 rts, such as those of Crawford,’ Parker and associates, I1 and Widerman and Serene” did not specifically
mention hair and bone with the dental abnormalities. Because of the variability of expression evidently seen in this group of conditions, there is reason to question whether amelogenesis imperfecta and taurodontism can occur together without other abnormalities or whether this combination must include hair, bone, and other abnormalities. The families examined in this report would seem to settle that question. None of the patients had kinky hair, observable or demonstrable skull changes, known skeletal abnormalities, or fingernail changes. All were in good health and had progressed through growth milestones uneventfully. Members of these families not examined by us could have some of the extraoral abnormalities observed by other writers,
Amelogenesis
Volume 48 Number 6
imperfecta
with
taurodontism
543
Pedigree #3
Fig. 6. Father of the proband, family No. 3. The enamel is dysplastic. The teeth have large pulp chambers and taurodontism.
Fig.
5. Family No. 3.
but reliable historians in the families reported no observable stigmata. The condition was seen in successive generations and there was male-to-male transmission. Similar abnormalities were seen in males and females. These findings would be consistent with autosomal dominant inheritance. The exact type of the amelogenesis imperfecta seen with taurodontism is difficult to determine from the literature. In all the families reported here, the teeth were smaller than normal and had thin, hard, rough enamel. The teeth varied from white to yellow in color. Radiographically, there was little contrast between the enamel and the dentin; however, this is due in large part to its thinness. Histologic and biochemical evaluation in a number of these patients would be helpful in further understanding of the enamel and dentin abnormalities. In all of the examined affected members of each family, the primary teeth and erupted permanent teeth were altered, showing both the amelogenesis imperfecta and taurodontism. None of the examined patients were found to have either amelogenesis imperfecta or taurodontism as separate entities. Radiographic examination of the early primary dentition showed teeth with a small amount of dentin and enamel and very large pulp chambers. With time, these pulp chambers appear to deposit secondary dentin and become smaller, but they still retain the taurodont morphology. Long-term follow-up is not available on any family member in this series. As the members have become old enough to be bothered by the appearance of the teeth, or as multiple
Fig. 7. Father of the proband, family No. 3. The enamel is dysplastic. The teeth have large pulp chambers and taurodontism.
abscesses have developed, the treatment has been to remove all of the teeth and construct dentures. We wish to thank Drs. Burton Horowitz, and Victor radiographs
Rodman for their cooperation for family No. 3.
William Trolley, in providing the
REFERENCES I. Coon, S. C.: The Origin of the Races, ed. 1, New York, 1961, Alfred A. Knopf, Inc. 2. Crawford, J. L.: Concomitant Taurodontism and Amelogenesis lmperfecta in the American Caucasian, J. Dent. Child 37: 171175, 1970.
544
Congleton
and Burkes
Oral Surg. December, 1979
3. Gulmen, S., Pullon, P. A., and O’Brien, L. W.: Tricho-Dento-Osseous Syndrome, J. Endodont. 2: 117- 120, 1976. 4. Hamner, J. E., III, Witkop, C. J., Jr., and Metro, P. S.: Taurodontism: Report of a Case, ORAL SURG. 18: 409-418, 1964. 5. Jorgenson, R. J., and Watson, R. W.: Dental Abnormalities in the Tricho-Dento-Osseous Syndrome. ORAL SURG. 36: 693. 700, 1973. 6. Keith, A.: Problems Relating to the Teeth of the Earlier Forms of Prehistoric Man. Proc. Royal Sot. Med. (Odont. Sect.) 6: 103. 124, 1913. 7. Mangion, J. J.: Two Cases of Taurodontism in Modern Human Jaws, Br. Dent. J. 113: 309-312, 1962. 8. Melnick, M., Shields, E. D., and El-Kafrawy. A. H.: TrichoDento-Osseous Syndrome: A Scanning Electron Microscopic Analysis, Clin. Gen. 12: 17-27, 1977. 9. Metro, P. S.: Taurodontism: A Dental Rarity in Modern Man, ORAL SURG. 20: 236-237. 1965. IO. Mjor, I. A.: The Structure of Taurodont Teeth, J. Dent, Child 39: 459-463. 1972. 11. Parker. J. L., Regattieri. L. R., and Thomas, J. P.: Hypoplastic-Hypo-maturation Amelogenesis Imperfecta with Taurodontism: Report of a Case, J. Dent. Child. 42: 379-383, 197.5.
INFORMATION
12. Stewart, R. E.. Lourien, E. W.. and Wyandt, H. E.: Unusual Dental Findings in a Patient with a Rare Bone Dysplasia (dyschondrosteosis) and a Chromosomal Anomaly, ORAL SURF. 32: 596-604, 1971. 13. Robinson, G. C., Miller. J. R., and Worth, H. M.: Hereditary Enamel Hypoplasia: Its Association with Characteristic Hair Structure, Pediatrics 37: 498-501. 1966. 14. Weinman, J. P.. Svoboda, J. F., and Woods. R. W.: Hereditary Disturbances of Enamel Formation and Calcifications, J. Am. Dent. Assoc. 32: 397, 1945. 15. Widerman, F. H., and Serene, T. P.: Endodontic Therapy Involving a Taurodont Tooth, ORAL SURG. 32: 6 18-620. 197 1. 16. Winter. G. B., Lee, K. W., and Johnson, N. W.: Hereditary Amelogenesis Imperfecta: A Rare Autosomal Dominant Type, Br. Dent. J. 127: lS7- 164. 1969. Reprinr wyuc.~ t.\ to: Dr. E. Jeff Burkes Department of Oral Diagnosis School of Dentistry University of North Carolina Chapel Hill, N. C. 27514
FOR AUTHORS
Most of the provisions of the Copyright Act of 1976 became effective on January 1, 1978. Therefore, all manuscripts must be accompanied by the following written statement, signed by one author: “The undersigned author transfers all copyright ownership of the manuscript entitled (title of article) to The C. V. Mosby Company in the event the work is published. The undersigned author warrants that the article is original, is not under consideration by another journal, and has not been previously published. I sign for and accept responsibility for releasing this material on behalf of any and all co-authors.” Authors will be consulted, when possible, regarding republication of their material.
