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Relationship of enamel hypoplasia to abnormal events of gestation and birth
Relationship of enamel hypoplasia to abnormal events of gestation and birth
William F. Via, J r.* D.D.S., and John A. Churchill, f M .D., Detroit
Enamel hypoplasia was seen in 119 (54 per cent) of 219 children with some form of cerebral disorder, whereas only 8 (9 per cent) of 93 normal children had enamel hypoplasia. The highest incidence of enamel hypoplasia was seen in those children with choreo-athetosis (100 per cent) and simple spastic diplegia (84 per cent) , and the lowest incidence in chil dren with focal cerebral seizure and hemi plegia (38 per cent). Among the 312 chil dren studied, enamel hypoplasia and one or more of 11 other abnormal factors studied occurred in 93. A definite cor relation was found between the time the abnormal factors occurred and the time the enamel hypoplasia was estimated to have occurred.
Enamel hypoplasia occurs as a direct re sult of disturbances in the metabolism of the ameloblastic layer of the enamel or gan. The specific etiologic agents or events responsible for deleterious changes in the metabolism of ameloblasts fall into three general categories: localized me chanical trauma, hereditary factors and systemic disease. The present study is concerned with hypoplasia in regard to those abnormal events of gestation and birth which are known to be associated with high rates of infant mortality and morbidity.
Kronfeld and Schour1 in 1947 defined enamel hypoplasia as a deficient or ar rested state of enamel formation mani fested by irregularities and indentations on the enamel surface, the result of inter ference with the metabolism o f amelo blasts. The causes o f enamel hypoplasia have been studied by several investigators. Hereditary enamel hypoplasia has re cently been studied by Witkop.2 He de scribed five types of amelogenesis imper fecta characterized by disturbances in either enamel matrix formation or mat uration, or both and showed that all of these types are the result of hereditary factors. Sarnat and Schour3 found a pos sible correlation between enamel defects and rickets; but they found no relation ship between childhood diseases and enamel hypoplasia. Stein4 in 1947 found that 8 of 16 premature children had enamel hypoplasia. The position of the defect on the teeth corresponded in time with the time of their births. Forrester and Miller5,6 found enamel hypoplasia in 13 patients with kernicterus. They also noted that the sites of hypoplasia on the teeth corresponded to the age at which metabolism was disturbed. Kreshover,7,8 in studies of human teeth, found that it is possible to correlate in many instances the occurrence of enamel hypoplasia with abnormalities of gestation or parturition. Kreshover9'13 has
V IA — C H U R C H IL L . . . V O LU M E 59, OCTO BER 1959 • 703
shown that enamel hypoplasia could be produced in rodents given artificially in duced fever, alloxan diabetes, injections o f tubercle bacilli and the viruses of vac cinia, and lymphocytic choriomeningitis. The enamel hypoplasia produced was vis ibly and microscopically similar to that seen in humans. A recent study14 of the relationship of cerebral disorders to faults in dental enamel showed that there was a much higher incidence of enamel de fects in children with cerebral disorders than there was in a corresponding group of normal children. Certain abnormal factors of gestation and birth were found to coincide in time with the hypoplasia, suggesting a possible correlation in time between the factor and the enamel hy poplasia. M ETHOD
In this study, detailed information con cerning gestation, birth and subsequent development was obtained by one investi gator from the parents or medical rec ords o f 312 children. On the basis of neurologic examination, the patients were segregated into a group with definite signs of cerebral dysfunction and a group hav ing no indications of cerebral dysfunction. The patients admitted into the study were those upon whom a dental examina tion had been performed, and whose teeth were in such condition as to allow a definite determination of whether hy poplasia was present or absent. Most of the patients were between two and six years o f age. Children under two have too few teeth for adequate evaluation of enamel hypoplasia; those over six have lost their deciduous incisors, and caries and abrasions o f their deciduous molars may have caused the obliteration of the enamel formed during the neonatal period. The teeth of two and three year old children are in the most suitable con dition for evaluation of enamel hypo plasia occurring during the prenatal and neonatal periods.
A child was considered to have hypo plasia if a defect in the enamel was ob served which was characterized by a grooved ring of visible and palpable depth about the crown of the tooth. The defect could be either smooth or pitted, discolored or not discolored. Hypoplasia was considered to be distinct from hypomaturation. The estimation of the time hypoplasia occurred, by its position on the tooth (Fig1. 1), was based on Logan and Kronfeld’s16 chart of the development of the dentition. Faults in the enamel which were on the incisal one fourth of the deciduous central incisors and incisal one fifth of the lateral incisors were estimated to have occurred during the fourth and fifth months of gestation (Fig. 2 ). Hypo plasia of the middle one third of the de ciduous central incisors, and at the junc tion of the middle one third and incisal one third of the lateral incisors occurred during the sixth or seventh month of ges tation (Fig. 3 and 4 ). Faults located at the tips of the deciduous cuspids, and junction of the occlusal and middle one third of the first deciduous molars were designated as occurring in the eighth or ninth month of gestation (Fig. 5 ). The term factor is used to denote those abnormal events of gestation and parturi tion which are known to be associated with high rates of infant mortality and morbidity. The abnormal event in itself, however, may not be the direct cause of death or injury, but may have occurred as a result of the operation of other po tentially injurious agencies. The following abnormalities compli cating gestation or parturition, or both, were studied : ( 1) R h incompatibility proved by a positive Coombs test and kernicterus in the infant; (2) maternal diabetes; (3 ) toxemia of pregnancy, acute infections, urinary tract and kid ney infections and congenital heart dis ease; (4) prematurity, birth weight being less than 5J/2 lbs.; (5) breech presenta tion; (6) twinning; (7) cesarean section;
704 • TH E J O U R N A L O F TH E A M E R IC A N D ENTAL A S S O C IA T IO N
(8) labor in excess of 20 hours; (9) in trapartum hemorrhage and placenta previa; (10) poor respiratory response at birth in which the children did not breathe spontaneously and required re suscitation. RESULTS
The cerebral damage group was divided into the types of disorders shown in Table 1. The first column in Table 1 refers to the number of patients who had hypo plasia which occurred during the prenatal period but was not associated with pre mature birth. The second column refers to those patients whose hypoplasia was associated with premature birth. The third column refers to those patients born at term whose hypoplasia occurred dur ing the neonatal period. The rate of enamel hypoplasia in the group of 219 children with cerebral dam age was 54 per cent. In contrast, only 9 per cent o f the 93 normal children had
Cent.
Lat.
Cuspid
enamel hypoplasia. A chi square test of these data results in a X 2 value of 56.5, indicating a P value far less than 1 X 10'4. T he incidence of hypoplasia in the nor mal and abnormal groups in this study compares favorably with the incidence of hypoplasia reported previously in a com parable study.14 One or more abnormal factors of ges tation and parturition were recorded in the medical history of 93 patients who also had hypoplasia. The hypoplasia ob served in all of these patients was esti mated to have occurred during the pre natal and neonatal periods. The times of the occurrence of a factor or factors and the times of the occurrence of enamel hypoplasia in the 93 patients in whom hypoplasia was found and who had sus tained abnormal events of gestation and parturition were plotted on a graph (Table 2 ). The X axis indicates the time the abnormal event occurred. The Y axis indicates the estimated time the hypo plasia occurred. T o test for a correlation
I st. M 2nd.M
1st.
Mand.
H ill 4 - 5 months 8 - 9 months
6 -7 months 10-12 months
Fig. ! • The tim e hypoplasia occurred ind ica te d by position on te e th . Time indicates months fro m onset o f,g e s ta tio n
V IA — C H U R C H IL L
. V O LU M E 59, OCTOBER 1959 • 705
Fig. 2 • Enamel hypoplasia which occurred dur- Fig. 3 • Enamel hypoplasia which occurred during ing fo u rth and fifth months o f gestation sixth and seventh months o f gestation
Fig. 4 • Side view o f p a tie n t shown in Figure 3
between the times of occurrence of ab normal events of gestation and parturi tion and hypoplasia, the correlation coeffi cient, r, was calculated using the formula: r= V " The correlation coefficient, r, was .933. Perfect cor relation is i.ooo; therefore, there is strong evidence to support the contention that the time when the abnormal factors oc curred correlated with the time when the enamel hypoplasia occurred. The prob ability that chance rather than a rela tionship between factors and hypoplasia was responsible for the distribution of cases was exceedingly remote as shown by an analysis of variance using the formula
Fig. 5
•
Enamel hypoplasia o ccu rring a t term
F-
(1 .
(n
2 ),
Vi — 1 and Vo = 91. F was found to be 21,203.00. P from the table of F in Biometrika Tables for Stat isticians10 was far less than 1X10~20. D IS C U S S IO N
The visible enamel hypoplasia observed in the patients of this study is regarded as an abnormal extreme of the micro scopic neonatal line found in most de ciduous teeth of normal persons. A visible hypoplastic defect is consid ered abnormal, for this lesion is observed
706 • TH E J O U R N A L O F THE A M E R IC A N DENTAL A S S O C IA T IO N
Table 1 • D istribution o f hypoplasia P rior to term N o t born prem aturely Id io p a th ic epilepsy Focal ce re b ra l seizures and hem iplegia M e nta l d e ficie n cy C om plex d ip le gia Simple spastic d ip le g ia C h o re o -a th e to sis O th e r N o rm a l
Term
H ypo p lasia in Born prem aturely n eo n a ta l p e rio d
T otal patients
% H ypoplasia
48
0
3
13
16
33
3 3 2 0 0 0 0
4 5 4 26 0 4 4
11 11 6 0 7 9 4
18 19 12 26 7 13 8
48 49 20 31 7 31 93
in a large proportion of children with cerebral diseases but in only a small pro portion of normal children. Furthermore, enamel hypoplasia can be produced ex perimentally in animals by disturbing the animals’ physiology. A strong correlation between enamel hypoplasia and central nervous system diseases suggests that the cerebral disease is a result of generalized physiologic dis orders which also affect the teeth. Enamel hypoplasia was observed most frequently in those children who had choreo-athetosis and Little’ s disease, con ditions in which the central nervous sys tem is involved bilaterally; the occurrence of enamel hypoplasia was lowest in those children with focal cerebral seizures or
Table 2 • C o rre la tio n o f abnorm al gesta tion a l and p a rtu ritio n a l events and enamel hypoplasia
X = Time o f íaciors. Y = Time of hypoplasia.
T o ta l hypoplasia
38 39 60 84 100 . 42 9
hemiplegia, conditions which can be ac counted for by the operation of injurious processes acting locally within the central nervous system. The relationship of enamel hypoplasia and cerebral disease was further sup ported by finding that the time when the cerebral abnormality was estimated to have occurred coincided closely with the times when the hypoplasia was estab lished. This temporal coincidence of hy poplasia and cerebral disease was most striking in patients with simple spastic diplegia, all of whom were born prema turely and in patients with choreo-athetosis who had kernicterus in the neonatal period. N o conclusions can be reached identi fying the particular mechanisms which are responsible for either hypoplasia or cerebral abnormalities. In many instances several factors such as prematurity, in trapartum hemorrhage, toxemia, abnor mal presentation at birth and poor res piratory response coincided in the same individual. Thus, two or more mecha nisms such as circulatory or respiratory failure, asphyxia, nutritional deficiency or toxicity may have been operative in a single person. It is pertinent at this time to question whether or not anoxia pro duces enamel hypoplasia since anoxia is cited as the outstanding factor in the pathogenesis of cerebral palsy and allied diseases. The present study yields no de cisive information regarding the effect of
V IA — C H U R C H IL L . . . V O LU M E 59, OCTO BER 1959 • 707
anoxia but this aspect o f the problem is being investigated currently.
between the time the factors occurred and the time the enamel hypoplasia was estimated to have occurred.
SUM M ARY
Dental examinations and medical his tories including prenatal, birth, and sub sequent development information have been obtained for 312 children. A neuro logical examination revealed that 219 of these children had some form of cerebral disorder, whereas 93 had no evidence of cerebral disorder. Enamel hypoplasia was seen in 119 (54 per cent) of the children with cerebral disorders, whereas only 8 (9 per cent) of the normal children had enamel hypoplasia. The highest incidence o f hypoplasia was seen in those children with choreoathetosis (100 per cent) and simple spastic diplegia (84 per cent). The children in the focal cerebral seizure and hemiplegia group had the least hypoplasia (38 per cen t). The abnormal factors of gestation and birth studied were: Rh incompatibility, maternal diabetes, toxemia of pregnancy, prematurity, breech presentation, twin ning, cesarean section, labor in excess of 20 hours, intrapartum hemorrhage and placenta previa, and poor respiratory re sponse at birth. Among the 312 children studied, enamel hypoplasia and one or more o f the abnormal factors occurred in 93. A definite correlation was found
*Associate in dentistry, Henry Ford Hospital. fAssociate in neurology, Henry Ford H ospital. 1. Kronfeld, R., and Schour, I. Neonatal dental hypo plasia. J.A .D .A . 26:18 Jan. 1939. 2. W itkop, C. J. H ereditary defects in enamel and dentin. Acta Genet, et Stat. M ed. 7:236, 1957. 3. Sarnat, B. G., and Schour, I. Enamel hypoplasia (chronologic enamel aplasia) in relation to systemic disease. J.A .D .A . 28:1989 Dec. 1941; 29:67 Jan. 1942. 4. Stein, George. Enamel damage o f systemic origin In premature birth and diseases o f early infancy. Am . J. O rthodont. & O ral Surg. 33:831 Dec. 1947. 5. Forrester, R. M., and M ille r, J. Dental changes associated with kernicterus. Arch. Dis. C hildhood 30:224 June 1955. 6. M ille r, J. Pigmentation o f teeth due to Rhesus fa cto r. Brit. D. J. 91:121 Sept. 1951. 7. Kreshover, S. J. H istopathologic studies o f a b normal enamel form ation in human teeth. A m . J. O rtho dont. & O ral Surg. 26:1083 Nov. 1940. 8. Kreshover, S. J .; Clough, O . W ., and Bear, D. M. Study of prenatal influences on tooth developm ent in humans. J.A .D .A . 56:230 Feb. 1958. 9. Kreshover, S. J. Pathogenesis o f enamel hypo plasia: an experimental study. J. D. Res. 23:231 Aug. 1944. 10. Kreshover, S. J .; Clough, O. W ., and Bear, D. M. Prenatal influences on tooth developm ent: I. Alloxan diabetes in rats. J . D. Res. 32:246 A p ril 1953. 11. Kreshover, S. J .t and Clough, O . W . Prenatal influences on tooth developm ent: II. A rtific ia lly induced fever in rats. J. D. Res. 32:565 Aug. 1953. 12. Kreshover, S. J.; Clough, O . W ., and Hancock, J. A . Vaccinia infection in pregnant rabbits and its effect on maternal and fetal dental tissues. J.A .D .A . 49:549 Nov. 1954. 13. Kreshover, S. J., and Hancock, J. A. Effect of lymphocytic^ choriom eningitis on pregnancy and dental tissues in mice. J. D. Res. 35:467 June 1956. 14. Via, W . F., Jr., and Churchill, J. A . Relation ships of cerebral disorder to faults in dental enamel. A .M .A . Am . J. Dis. C h ild . 94:137 A ug. 1957. 15. O rban, Balint. O ral histology and embryology, ed 2. St. Louis, C. V. Mosby Co., 1949, p. 305. 16. Pearson, E. S., and H artley, H . O. Bio.metrika tables fo r statisticians, vol. I. C am bridge, University Press, 1956, p. 157-163.
Luck and Intelligence • One of the apparent injustices of the human condition is that the lucky man does not need intelligence, but the intelligent man does need luck. Sydney ] . Harris, Strictly Personal.
William F. Via, J r.* D.D.S., and John A. Churchill, f M .D., Detroit
Enamel hypoplasia was seen in 119 (54 per cent) of 219 children with some form of cerebral disorder, whereas only 8 (9 per cent) of 93 normal children had enamel hypoplasia. The highest incidence of enamel hypoplasia was seen in those children with choreo-athetosis (100 per cent) and simple spastic diplegia (84 per cent) , and the lowest incidence in chil dren with focal cerebral seizure and hemi plegia (38 per cent). Among the 312 chil dren studied, enamel hypoplasia and one or more of 11 other abnormal factors studied occurred in 93. A definite cor relation was found between the time the abnormal factors occurred and the time the enamel hypoplasia was estimated to have occurred.
Enamel hypoplasia occurs as a direct re sult of disturbances in the metabolism of the ameloblastic layer of the enamel or gan. The specific etiologic agents or events responsible for deleterious changes in the metabolism of ameloblasts fall into three general categories: localized me chanical trauma, hereditary factors and systemic disease. The present study is concerned with hypoplasia in regard to those abnormal events of gestation and birth which are known to be associated with high rates of infant mortality and morbidity.
Kronfeld and Schour1 in 1947 defined enamel hypoplasia as a deficient or ar rested state of enamel formation mani fested by irregularities and indentations on the enamel surface, the result of inter ference with the metabolism o f amelo blasts. The causes o f enamel hypoplasia have been studied by several investigators. Hereditary enamel hypoplasia has re cently been studied by Witkop.2 He de scribed five types of amelogenesis imper fecta characterized by disturbances in either enamel matrix formation or mat uration, or both and showed that all of these types are the result of hereditary factors. Sarnat and Schour3 found a pos sible correlation between enamel defects and rickets; but they found no relation ship between childhood diseases and enamel hypoplasia. Stein4 in 1947 found that 8 of 16 premature children had enamel hypoplasia. The position of the defect on the teeth corresponded in time with the time of their births. Forrester and Miller5,6 found enamel hypoplasia in 13 patients with kernicterus. They also noted that the sites of hypoplasia on the teeth corresponded to the age at which metabolism was disturbed. Kreshover,7,8 in studies of human teeth, found that it is possible to correlate in many instances the occurrence of enamel hypoplasia with abnormalities of gestation or parturition. Kreshover9'13 has
V IA — C H U R C H IL L . . . V O LU M E 59, OCTO BER 1959 • 703
shown that enamel hypoplasia could be produced in rodents given artificially in duced fever, alloxan diabetes, injections o f tubercle bacilli and the viruses of vac cinia, and lymphocytic choriomeningitis. The enamel hypoplasia produced was vis ibly and microscopically similar to that seen in humans. A recent study14 of the relationship of cerebral disorders to faults in dental enamel showed that there was a much higher incidence of enamel de fects in children with cerebral disorders than there was in a corresponding group of normal children. Certain abnormal factors of gestation and birth were found to coincide in time with the hypoplasia, suggesting a possible correlation in time between the factor and the enamel hy poplasia. M ETHOD
In this study, detailed information con cerning gestation, birth and subsequent development was obtained by one investi gator from the parents or medical rec ords o f 312 children. On the basis of neurologic examination, the patients were segregated into a group with definite signs of cerebral dysfunction and a group hav ing no indications of cerebral dysfunction. The patients admitted into the study were those upon whom a dental examina tion had been performed, and whose teeth were in such condition as to allow a definite determination of whether hy poplasia was present or absent. Most of the patients were between two and six years o f age. Children under two have too few teeth for adequate evaluation of enamel hypoplasia; those over six have lost their deciduous incisors, and caries and abrasions o f their deciduous molars may have caused the obliteration of the enamel formed during the neonatal period. The teeth of two and three year old children are in the most suitable con dition for evaluation of enamel hypo plasia occurring during the prenatal and neonatal periods.
A child was considered to have hypo plasia if a defect in the enamel was ob served which was characterized by a grooved ring of visible and palpable depth about the crown of the tooth. The defect could be either smooth or pitted, discolored or not discolored. Hypoplasia was considered to be distinct from hypomaturation. The estimation of the time hypoplasia occurred, by its position on the tooth (Fig1. 1), was based on Logan and Kronfeld’s16 chart of the development of the dentition. Faults in the enamel which were on the incisal one fourth of the deciduous central incisors and incisal one fifth of the lateral incisors were estimated to have occurred during the fourth and fifth months of gestation (Fig. 2 ). Hypo plasia of the middle one third of the de ciduous central incisors, and at the junc tion of the middle one third and incisal one third of the lateral incisors occurred during the sixth or seventh month of ges tation (Fig. 3 and 4 ). Faults located at the tips of the deciduous cuspids, and junction of the occlusal and middle one third of the first deciduous molars were designated as occurring in the eighth or ninth month of gestation (Fig. 5 ). The term factor is used to denote those abnormal events of gestation and parturi tion which are known to be associated with high rates of infant mortality and morbidity. The abnormal event in itself, however, may not be the direct cause of death or injury, but may have occurred as a result of the operation of other po tentially injurious agencies. The following abnormalities compli cating gestation or parturition, or both, were studied : ( 1) R h incompatibility proved by a positive Coombs test and kernicterus in the infant; (2) maternal diabetes; (3 ) toxemia of pregnancy, acute infections, urinary tract and kid ney infections and congenital heart dis ease; (4) prematurity, birth weight being less than 5J/2 lbs.; (5) breech presenta tion; (6) twinning; (7) cesarean section;
704 • TH E J O U R N A L O F TH E A M E R IC A N D ENTAL A S S O C IA T IO N
(8) labor in excess of 20 hours; (9) in trapartum hemorrhage and placenta previa; (10) poor respiratory response at birth in which the children did not breathe spontaneously and required re suscitation. RESULTS
The cerebral damage group was divided into the types of disorders shown in Table 1. The first column in Table 1 refers to the number of patients who had hypo plasia which occurred during the prenatal period but was not associated with pre mature birth. The second column refers to those patients whose hypoplasia was associated with premature birth. The third column refers to those patients born at term whose hypoplasia occurred dur ing the neonatal period. The rate of enamel hypoplasia in the group of 219 children with cerebral dam age was 54 per cent. In contrast, only 9 per cent o f the 93 normal children had
Cent.
Lat.
Cuspid
enamel hypoplasia. A chi square test of these data results in a X 2 value of 56.5, indicating a P value far less than 1 X 10'4. T he incidence of hypoplasia in the nor mal and abnormal groups in this study compares favorably with the incidence of hypoplasia reported previously in a com parable study.14 One or more abnormal factors of ges tation and parturition were recorded in the medical history of 93 patients who also had hypoplasia. The hypoplasia ob served in all of these patients was esti mated to have occurred during the pre natal and neonatal periods. The times of the occurrence of a factor or factors and the times of the occurrence of enamel hypoplasia in the 93 patients in whom hypoplasia was found and who had sus tained abnormal events of gestation and parturition were plotted on a graph (Table 2 ). The X axis indicates the time the abnormal event occurred. The Y axis indicates the estimated time the hypo plasia occurred. T o test for a correlation
I st. M 2nd.M
1st.
Mand.
H ill 4 - 5 months 8 - 9 months
6 -7 months 10-12 months
Fig. ! • The tim e hypoplasia occurred ind ica te d by position on te e th . Time indicates months fro m onset o f,g e s ta tio n
V IA — C H U R C H IL L
. V O LU M E 59, OCTOBER 1959 • 705
Fig. 2 • Enamel hypoplasia which occurred dur- Fig. 3 • Enamel hypoplasia which occurred during ing fo u rth and fifth months o f gestation sixth and seventh months o f gestation
Fig. 4 • Side view o f p a tie n t shown in Figure 3
between the times of occurrence of ab normal events of gestation and parturi tion and hypoplasia, the correlation coeffi cient, r, was calculated using the formula: r= V " The correlation coefficient, r, was .933. Perfect cor relation is i.ooo; therefore, there is strong evidence to support the contention that the time when the abnormal factors oc curred correlated with the time when the enamel hypoplasia occurred. The prob ability that chance rather than a rela tionship between factors and hypoplasia was responsible for the distribution of cases was exceedingly remote as shown by an analysis of variance using the formula
Fig. 5
•
Enamel hypoplasia o ccu rring a t term
F-
(1 .
(n
2 ),
Vi — 1 and Vo = 91. F was found to be 21,203.00. P from the table of F in Biometrika Tables for Stat isticians10 was far less than 1X10~20. D IS C U S S IO N
The visible enamel hypoplasia observed in the patients of this study is regarded as an abnormal extreme of the micro scopic neonatal line found in most de ciduous teeth of normal persons. A visible hypoplastic defect is consid ered abnormal, for this lesion is observed
706 • TH E J O U R N A L O F THE A M E R IC A N DENTAL A S S O C IA T IO N
Table 1 • D istribution o f hypoplasia P rior to term N o t born prem aturely Id io p a th ic epilepsy Focal ce re b ra l seizures and hem iplegia M e nta l d e ficie n cy C om plex d ip le gia Simple spastic d ip le g ia C h o re o -a th e to sis O th e r N o rm a l
Term
H ypo p lasia in Born prem aturely n eo n a ta l p e rio d
T otal patients
% H ypoplasia
48
0
3
13
16
33
3 3 2 0 0 0 0
4 5 4 26 0 4 4
11 11 6 0 7 9 4
18 19 12 26 7 13 8
48 49 20 31 7 31 93
in a large proportion of children with cerebral diseases but in only a small pro portion of normal children. Furthermore, enamel hypoplasia can be produced ex perimentally in animals by disturbing the animals’ physiology. A strong correlation between enamel hypoplasia and central nervous system diseases suggests that the cerebral disease is a result of generalized physiologic dis orders which also affect the teeth. Enamel hypoplasia was observed most frequently in those children who had choreo-athetosis and Little’ s disease, con ditions in which the central nervous sys tem is involved bilaterally; the occurrence of enamel hypoplasia was lowest in those children with focal cerebral seizures or
Table 2 • C o rre la tio n o f abnorm al gesta tion a l and p a rtu ritio n a l events and enamel hypoplasia
X = Time o f íaciors. Y = Time of hypoplasia.
T o ta l hypoplasia
38 39 60 84 100 . 42 9
hemiplegia, conditions which can be ac counted for by the operation of injurious processes acting locally within the central nervous system. The relationship of enamel hypoplasia and cerebral disease was further sup ported by finding that the time when the cerebral abnormality was estimated to have occurred coincided closely with the times when the hypoplasia was estab lished. This temporal coincidence of hy poplasia and cerebral disease was most striking in patients with simple spastic diplegia, all of whom were born prema turely and in patients with choreo-athetosis who had kernicterus in the neonatal period. N o conclusions can be reached identi fying the particular mechanisms which are responsible for either hypoplasia or cerebral abnormalities. In many instances several factors such as prematurity, in trapartum hemorrhage, toxemia, abnor mal presentation at birth and poor res piratory response coincided in the same individual. Thus, two or more mecha nisms such as circulatory or respiratory failure, asphyxia, nutritional deficiency or toxicity may have been operative in a single person. It is pertinent at this time to question whether or not anoxia pro duces enamel hypoplasia since anoxia is cited as the outstanding factor in the pathogenesis of cerebral palsy and allied diseases. The present study yields no de cisive information regarding the effect of
V IA — C H U R C H IL L . . . V O LU M E 59, OCTO BER 1959 • 707
anoxia but this aspect o f the problem is being investigated currently.
between the time the factors occurred and the time the enamel hypoplasia was estimated to have occurred.
SUM M ARY
Dental examinations and medical his tories including prenatal, birth, and sub sequent development information have been obtained for 312 children. A neuro logical examination revealed that 219 of these children had some form of cerebral disorder, whereas 93 had no evidence of cerebral disorder. Enamel hypoplasia was seen in 119 (54 per cent) of the children with cerebral disorders, whereas only 8 (9 per cent) of the normal children had enamel hypoplasia. The highest incidence o f hypoplasia was seen in those children with choreoathetosis (100 per cent) and simple spastic diplegia (84 per cent). The children in the focal cerebral seizure and hemiplegia group had the least hypoplasia (38 per cen t). The abnormal factors of gestation and birth studied were: Rh incompatibility, maternal diabetes, toxemia of pregnancy, prematurity, breech presentation, twin ning, cesarean section, labor in excess of 20 hours, intrapartum hemorrhage and placenta previa, and poor respiratory re sponse at birth. Among the 312 children studied, enamel hypoplasia and one or more o f the abnormal factors occurred in 93. A definite correlation was found
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Luck and Intelligence • One of the apparent injustices of the human condition is that the lucky man does not need intelligence, but the intelligent man does need luck. Sydney ] . Harris, Strictly Personal.