Effect of The Birth Process On The Neonatal Line in Primary Tooth Enamel
Effect of The Birth Process On The Neonatal Line in Primary Tooth Enamel
Effect of The Birth Process On The Neonatal Line in Primary Tooth Enamel
Abstract
The neonatal line is a histologic landmark in primary tooth 1980). The ultrastructural basis for the NNL was
enamel corresponding to the event of birth. The average width believed to be a localized change in configuration of
of the neonatal line (NNL) in primary tooth enamel of 147 enamel prisms along with possible reduction in crystal
children was measured. In children with normal birth concentration (Weber and Eisenmann 1971).
histories the width of the NNL was found to be 12.9 ± 4.8 \Lm. The formation and accentuation of the NNL were
It was wider (18.6 ± 5.7 \un) in children born by difficult attributed to the abrupt change in the environment and
operative delivery and thinner (7.6 ±1.5 \an) in children born nutrition of the newborn (Schour and Kronfeld 1938;
by Caesarean section. Massler et al. 1941; Orban 1980). Noren (1984a)
The data suggest that concomitant with the change from described a wider NNL in children born to diabetic
intrauterine to extrauterine environment, the birth process mothers and hypothesized that the wider NNL is a
itself also contributes to the width of the NNL. structural response to neonatal hypocalcemic stress
(Noren 1984b). Except for the influence of maternal
The incremental nature of enamel and dentin devel- diabetes, no other factors (asphyxia, low birth weight, or
opment has been known and described for more than a intrauterine malnutrition) were identified as being
century. Retzius (1837) reported brown lines observed associated with a wider NNL (Magnusson et al. 1978;
in the enamel which were caused by periods of enamel Noren et al. 1978; Noren 1983).
formation and rest — the incremental lines (striae) of The diagnostic possibilities of microscopic
Retzius. The distance between the lines of Retzius was examination of enamel, using the NNL as a marker
measured and found to be about 16 ^m (Schour and together with the known mean rate of enamel
Hoffman 1939). deposition to determine
When the very sensitive ameloblasts are subjected to the timing of noxious
a noxious episode of either internal or external origin, a events, was shown by
temporary change in the rhythmic enamel matrix Levine et al. (1979). A
formation may occur, causing some striae of Retzius to significant association
appear more prominent than normal. One such between case histories of
accentuated Retzius line corresponds to the event of brain damaged children
birth and is known as the "neonatal line" (NNL; Fig. 1). and histologic enamel
Schour (1936) described the NNL and estimated its findings was reported
distance from the dentinoenamel junction for the byjudesetal. (1985) and
various teeth. He indicated the absence of the NNL in Jaffe et al. (1985a, b).
teeth of unborn fetuses. By injecting sodium fluoride These studies concen-
into rats, Schour and Poncher (1937) were able to trated on the identifi-
estimate the average rate of enamel formation as 4 (am/ cation of any prominent
24 hr. The NNL was described as a border between the Retzius striae as a sign of
prenatal enamel created during gestation and interference with the
characterized by its regularity and high degree of developing fetus' tis-
calcification, and the postnatal enamel created after sues, an interference Fig 1. Histologic representation
birth which is less regular and less homogeneously which could be the cause of NN , L (arrow > in a 100^m
, . . . . „, sagittal ground section of a
calcified (Schour 1936,1938; Massler et al. 1941; Orban of the brain damage. To primary tooth
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TABLE 3. MeanWidth of NNL(~,m) in Children Born be continuous, the lower percentage of the NNL
by NormalDelivery Comparedto Children Born by identified in other studies may be due to lack of
Operative Delivery
appearance of the NNLin some areas of the tooth
Normal Operative* crown.
Levelof N = 125 N = 17 Statistical The present findings suggest that the normal NNL
crown~Delivery "~ SD ~ SD Significancd
width in primary teeth is about 12 ~tm. This is in
Incisal 12.1 5.1 17.4 6.4 P < 0.05 agreement with Jackobsen (1975) as to the NNLwidth
(N = 40) (N = 6)
first permanent molars and those cited by Magnussonet
Middle 12.4 7.0 18.3 5.7 P < 0.05
(N = 46) (N = 8) al. (1978) and Nor6net al. (1978) for primary incisors.
Gingiva! 11.9 4.8 18.6 5.7 P < 0.05 Unlike Jackobsen (1975) who claimed that the NNL
(N = 39) (N = width is highly dependent upon the distance of the
Operativedelivery - breech, vacuum,forceps. section from the cusp tip, the present data demonstrate
According
to t-test. that the level at which the sample is obtained (incisal,
middle, or gingival) has little influence on the value
obtained. As the NNLapparently is created by the
trauma caused to the newborn during or immediately
OPERATIVE
D. following the birth process, this trauma simultaneously
affects all ameloblasts at the different tooth levels,
NORMAL O.
establishing a basically uniform line. The fact that the
NNLwidth increases significantly in children born by
ELECTIVEC.S
operative delivery and decreases in children who have
undergone no active birth process, suggests that the
change from the intrauterine to the extrauterine
environment is responsible for only part of the arrest of
the ameloblast function, and that the trauma of the birth
process itself also has a major impact on the newborn’s
cells.
If we refer to the NNLwidth in children born by
elective Caesarean section as indicating the effect on the
ameloblast of the transition from intra- to extrauterine
life (without active birth process), this transition
I=ig 2. Averagewidthof NNL(gingival level) in childrenwith responsible for only about 63% of the NNLwidth (7.6/
variousbirth histories: normaldelivery, difficult (operative)
delivery, andelective Caesareansection. TheNNLin children 11.9). The magnitude of such transitional effect on the
bornby operativedeliverywassignificantly widerthanthat in ameloblasts may vary under different environmental
children born by normaldelivery. A muchlower value was conditions. Schour and Kronfeld (1938) suggest that the
foundin the elective Caesareansection group. NNLshould be more prominent in teeth of prematurely
born children, due to the relatively greater nutritional
Discussion difficulties usually encountered by premature infants.
Transient metabolic or environmental disturbances Thus, the fact that the NNLwidth was assessed by
during the fetal or early newborn period are likely to Weber and Eisenmann (1971) to be about 20-30
affect the physiological functions of various body probably is due to the fact that most of their specimens
systems adversely. The ameloblasts (and odontoblasts) were acquired from a prematurely delivered child. The
are unique in that the cell layers continue their steady effect of premature delivery on the NNLwidth and
retreat from the dentinoenamel junction, and any prominence is under investigation.
abnormal tissue produced by the disturbance becomes Tooth enamel can serve as a sensitive diagnostic tool,
part of the tooth structure and is permanently recorded permanently recording various pre-, peri-, and
(Orban 1980). postnatal events. The accurate definition of 12 ~tm as a
In the present study, the NNLwas identified in all "normal" NNLwidth, which is partly caused by the
teeth examined, a result which is higher than that environmental shock to the newborn (about 63%) and
reported in primary dentition by Magnusson et al. partly by the birth process itself (about 37%), maybe
(1978) and Nor6n(1984a). This finding maybe due to value when investigating causes to various pathologic
detailed protocol of measurements performed in this conditions. Further research in this field will broaden
study (3 measurementsat 3 levels of each tooth crown). our understanding of the changes occurring in the
Since only 60-78% of the NNLexamined were found to fetus during the birth process.
Jackobsen K: Neonatal lines in human dental enamel. Acta Odontol Retzius A: Microscopic investigation of the structure of the teeth.
Scand 33:95-105, 1975. Arch Anat U Physiol 486-91, 1837.
Jaffe M, Attias D, Dar H, Eli I, Judes H: Prevalence of gestational and Schour I: The neonatal line in the enamel and dentin of the human
perinatal insults in brain damagedchildren. Isr J MedSci 21:940- deciduous teeth and first permanent molar. J AmDent Assoc
44, 1985a. 23:1946-55, 1936.
Jaffe M, Attias D, Dar H, Eli I, Judes H: The etiology of brain damage Schour I: Calcium metabolism and teeth. J AmMed Assoc 110:870-
in children, in The At-Risk Infant: Psycho/Socio/Medical 77, 1938.
Aspects, Harel S, Anastasiow NJ, eds. Baltimore, London; Paul H.
Brooks Pub Co Inc, 1985b pp 227-34. Schour I, Hoffman MM:Studies in tooth development. The 16
microns calcification rhythm in the enamel and dentin from fish
Judes H, Eli I, Jaffe M, Attias D, Jagerman K: The histological to man. J Dent Res 18:91-102, 1939.
examination of primary enamel as a possible diagnostic tool in
developmental disturbances. J Pedod 10:68-75, 1985. Schour I, Kronfeld R: Tooth ring analysis. IV. Neonatal dental
hypoplasia: Analysis of the teeth of an infant with injury to the
Levine RS, Turner EP, Dubbing J: Deciduous teeth contain histories brain at birth. Arch Path 26:471-90, 1938.
of developmental disturbances. Early HumDev 3:211-20, 1979.
$chour I, l?oncher HG: Rate of apposition of enamel and dentin,.
MagnussonBOet al: Neonatal asphyxia and mineralization defect of measured by the effect of acute fluorosis. AmJ Dis Child 54:757-
the primary teeth. SwedDent J 2:9-15, 1978. 76, 1937.
Massler M, Shour I, Poncher HG: Developmental pattern of the child Weber DF, Eisenmann DR: Microscopy of the neonatal line in
as reflected in the calcification pattern of the teeth. AmJ Dis Child developing human enamel. AmJ Anat 132:375-92, 1971.
62:33-67, 1941.
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