Archs oral Biol. Vol. 30, No. 6, pp. 503-507,
Printed in Great Britain. All rights reserved
1985
Copyright
THE CHRONOLOGICAL
DISTRIBUTION
HYPOPLASIA
IN HUMAN PERMANENT
CANINE TEETH
0
0003-9969/85 $3.00 + 0.00
1985 Pergamon Press Ltd
OF ENAMEL
INCISOR AND
A. H. GOODMAN’ and G. J. ARMELAGOS~
‘Department of Orthodontics, University of Connecticut Health Center, Farmington, CT 06032 and
*Department of Anthropology, University of Massachusetts, Amherst, MA 01003, U.S.A.
Summary-The Frequencies and chronology, based on a standard tooth development chart, of enamel
hypoplasia derived from permanent upper central incisors and mandibular canines were compared for 42
prehistoric Amerindians. Between 0.5 and 4.5 years, when the crowns of both these teeth are developing,
hypoplasias were 1.36 times more common on the incisors (54 hypoplasias/incisor; 40 hypoplasias/canine).
Hypoplasias on incisors occurred earlier (mean = 2.50; median at 2.G2.5 years) compared to the canine
(mean = 3.51; median at 3.54.0 years). Differences in published frequencies and chronologies of
hypoplasias may be explained, in part, by an indefinable variation in the teeth studied. The highest density
of hypoplasias on both tooth crowns was just cervical to the midpoint, suggesting that developmental rates
and crown geommetrymay influence the ability of the crown to record stressful events,
INTA ODUCTION
Chronologic
or systemic enamel hypoplasia
is a
decrease in enamel thickness resulting from a tempo-
rary disruption in enamel matrix formation (Pindborg, 1970, 1982; Sarnat and Schour, 1941; Yaeger,
1980). As a wide variety of nutritional deficiencies
and diseases may cause enamel hypoplasias; they can
be put in the general category of non-specific
physiological disruption (stress; Kreshover, 1960;
Pindborg, 1982).
As enamel once developed remains more or less
unchanged and in man its time of development can
be ascertained, enamel hypoplasia has great potential
as an indicator of stress during the prenatal to
childhood periods (Sarnat and &hour, 1941). The
frequency of enamel hypoplasia has been used to
assess the genera1 health status of living (Infante and
Gillespie, 1974; Sweeney et al., 1969) and prehistoric
populations (Cook and Buikstra, 1979; Goodman,
Armelagos and Rose, 1980; Swlrdstedt, 1966). The
chronological distribution of enamel hypoplasia in
populations has been used as evidence for peak
periods of stress (Goodman Armelagos and Rose,
1984; Sarnat and Schour, 1941; Schulz and McHenry,
1975; Swardstedt, 1966).
Sarnat and Schour (1941) presented the chronological distribution of hypoplasias in 60 individuals
from the Chicago area. Two-thirds of the episodes of
hypoplasias occurred within the first year of life,
approximately one-thl rd occurred during the next 22
months and less than 2 per cent occurred between 34
and 80 months. Sarnat and Schour (1941) concluded
that this distribution
of hypoplasias is more a
reflection of a biologically-universal
pattern of host
resistance, than of the chronological pattern of environmental stressors (Massler, Schour and Poncher,
1941).
If Sarnat and Schour’s conclusion is correct,
enamel hypoplasia chronologies from other populations should accord with their findings. Their
findings have not been repeated for other contemporary or industrial populations but hypoplasia
chronologies have been constructed for at least four
prehistoric populations. The chronological distribution of hypoplasias in a medieval Swedish population
had a peak at two to four years, with low frequencies
before two years (Swardstedt, 1966). Similarly,
chronological distribution of hypoplasias in two
time-successive ancient American Indian populations
from Dickson Mounds had few hypoplasias before
two years of age and after four years, with a peak
frequency between two and four years (Goodman
et al., 1984). Finally, a prehistoric California population showed few hypoplasias in the first two years
and increases in frequency to a peak between four
and six years (Schulz and McHenry, 1975).
The differences in enamel hypoplasia chronologies
do not support Sarnat and Schour’s (1941) contention referred to above. Rather, these data support
the view that hypoplasia chronologies are a reflection
of different chronological patterns of environmental
stressors affecting these populations.
Still unevaluated, however, is the potential role of methodological factors as causes of the differences and
observed
among
these hypoplasia
similarities
chronologies.
Our purpose was to determine whether uppercentral incisors and lower canines, the two teeth
which are most often studied (Rose, Condon and
Goodman, 1985) and most frequently hypoplastic
(Goodman et al., 1980), differ in susceptibility to
hypoplasia and yield different chronologies.
503
MATERIALS
AND METHODS
The sample is derived from the Dickson Mounds,
a multicomponent habitation and burial site (A.D.
950-1300) located near Lewiston, Illinois (Harn,
1980). In a study of 111 individuals with permanent
dentitions, Goodman et al. (1980) found that 73 (65.8
A. H.
504
GOODMAN
and G. J.
AKMELAWS
probability
of this difference being due to random
variations is near zero (p i 0.001). as estimated by
the sign test (2 = 3.47).
The occurrence
of hypoplasias
in both teeth
showed a normal distribution (Text Fig. 2). However,
the distributions
differed in the place of their means
and modal ages. The incisor-chronology
mode was at
2.0-2.5 years with a mean of 2.50 years; the canine
mode was at 3.54.0 years, with a mean of 3.5 1 years.
The incisor and canine hypoplasia
distributions
differed
significantly
even within
the common
0.5-4.5-year period. By 3.0 years, 39 of 54 (72.2 per
cent) incisor lesions had occurred compared to 12 of
40 (30.0 per cent) canine lesions. The significance of
the 42.2 per cent difference between these cumulative
frequencies
was tested by applying KolmogorovSmirnov test for differences in distributions
(Siegel,
19.56). The 42.2 per cent difference is far greater than
the critical value of 29 per cent for rejection of the
null hypothesis
(distributions
are not significantly
different) at the p > 0.01
level
of confidence (twotailed).
For all 12 occurrences of a hypoplasia on a canine
before 3.0 years, a corresponding
hypoplasia
was
found on the incisor in the same skull. However,
before 3.0 years there were 27 hypoplasias found on
the incisor without a corresponding
hypoplasia
on
the canine. Between 0.5 and 3.0 years of age, the
incisor yielded over three times the frequency
of
defects as did the canine.
After 3 years of age, the distribution
of defects on
these teeth changed. Between 3.0 and 3.5 years there
was an equal frequency of lesions on each tooth class.
However, between 3.5 and 4.5 years 20 canines had
lesions, whereas only 7 incisors had lesions. For this
time period, the canine yielded nearly three times the
frequency of defects found on the incisor.
per cent) had one or more systemic enamel hypoplasias. Forty-two individuals with at least one intact
and unworn upper-central
incisor and mandibular
canine were included in our study.
Hypoplasias
were defined as circumferential
lines,
bands or row of pits of decreased enamel thickness
(Plate Fig. 1). Using a binocular
microscope
and
dental probe, these crown-surface
lesions were easily
distinguished
from other surface irregularities.
In order to determine
the age of the individual
when the lesions developed, their distance from the
cementum-enamel
junction
was measured.
These
measurements
were converted to a half-year period
by reference to the chronology
of enamel-crown
development
of Massler
et al.
(1941), slightly
modified by Swlrdstedt
(1966). This method involves
the division of the incisor crown into 9 (birth to 4.5
years) and the canine crown into 12 (birth to 6.0
years) half-year developmental
periods.
RESULTS
There were more hypoplasias
on the incisor than
on the canine. Of the 378 half-year periods (9 periods
times 42 teeth) in respect of incisors, 54 were hypoplastic (1.29/incisor; O.l4/half-year
interval). Of the
504 half-year canine periods (12 periods times 33
hypoplastic
(1.1 O/canine;
were
teeth),
46
O.O9/half-year period). The significance of the greater
frequency of defects on the incisor was tested by
applying
the Wilcoxon
matched-pairs
sign test
(Siegel, 1956) and yielded a two tailed p = 0.026
(Z = 2.21). Furthermore,
all the incisor hypoplasias
and 40 (87 per cent) of the canine hypoplasias
occurred
between 0.5 and 4.5 years. During this
4-year period, the incisor can be said to be 1.36 times
more susceptible
than the canine. The two-tailed
O-
05-
LO-
1.5-
20-
25-
30-
35-
40-
4.5-
50-
55-
6 O-
05
to
15
20
25
30
3.5
40
45
5.0
55
60
65
1
0
0
Developmental
0
( years)
age
1
0
2
4
5
8
11
9
2
3
8
16
10
8
5
2
5
Fig. 2. Percentage
of hypoplasias
by half-year intervals for maxillary central incisors and mandibular
canines (n = 33). Numbers below the graph are frequencies of hypoplasias for each half-year period during
which these tooth crowns were developing.
505
Enamel hypoplasia chronology
DI!XUSSION
The greater frequency of hypoplasias on the incisor
does not appear to be due to local factors, random
variation, or methodological errors. When a hypoplasia was present on only one of these two teeth,
other teeth were exammed to determine whether the
defect might be due to a local factor. It was decided
that one defect was due to local trauma and it was not
included in the analys!.s. Attrition is the only factor,
we are aware of, which could limit our ability to
record defects. However, we excluded all teeth from
study in which attrition had begun to wear into the
incisal edge (beyond stage 2 attrition; Brothwell,
1981).
Differences in the frequency of defects by tooth
have been noted (Cutress and Suckling, 1982; ElNajjar, DeSanti and Ozebek, 1978; Pindborg, 1970).
In general, the anterior teeth in series are mostly
hypoplastic. Because they are the earlier developing
teeth, these differences are usually attributed to the
difference in time of mineralization (Pindborg, 1970;
Yaeger, 1980). In our study, however, variation was
found while both tooth crowns are mineralizing.
Thus, we propose thz.t variations in frequency may
also be due to differential susceptibility of tooth
crowns to hypoplasias.
The reason why teeth might be differentially susceptible to hypoplasias can only be speculated on.
One possible explanation is that teeth which are most
stable in developmental timing, the teeth at the polar
centres of dental fields (Bailit, 1975; Butler, 1939;
Dahlberg, 1945), are most susceptible to disruption.
Teeth, in which the genetic control over development
is strongest, may be more likely to be hypoplastic
because they are less able to alter developmental
timing. In a sense, different teeth may favour different
developmental reacti#Dns to stress, depending upon
the degree of genetic control over their development.
If this hypothesis is c#Brrect,recognition of variations
in susceptibility of enamel to developmental disturbance should aid in understanding patterns of
genetic control over and evolution of the human
dentition.
Between-tooth differences in the chronology of
defect could be partly related to systemic error in the
mineralization standard and its application to prehistoric Amerindian teeth. However, the majority of the
difference in chronology is not reasonably attributed
to the method. The choice of the Massler et al. (1941)
standard is justified for a variety of reasons. First, it
has been used in previous studies, therefore, its use
allows for direct comparisons. Secondly, this standard is in general agreement with other mineralization standards; thus large errors are not to be
expected (Gustafson and Koch, 1974). Thirdly, it
contains data on the development of the anteriorpermanent teeth before 3 years of age. Information
on the early stages of development of these teeth was
critical to our study, but is infrequently found in
studies based on serial radiographs. Finally, the
modification of SwLrdstedt (1966) accounts for variation in the rate of mineralization of tooth crowns
(Moorrees, Fanning and Hunt, 1963a) by allowing
for differences in the amount of enamel which is
equivalent to a half-life interval.
Although teeth differ in their chronology of enamel
hypoplasias, the distribution of defects is remarkably
similar in regard to the position of the defects on
tooth crown. For both the incisor and canine, there
is a low frequency of defects in the incisal third and
gingival sixth of the crown, and a high frequency in
the remaining half of the crown. The peak frequency
is near the midpoint of the crown. The enamel prisms
at this point on the tooth crown are most nearly
perpendicular to the surface. This orientation may
render it easier to discern variations in rod lengths.
Gleiser and Hunt (1955) and Moorrees et al. (1963a,
1963b) noted that there is an increase in velocity of
crown development at this time. The greater rate of
development may render the’tooth more vulnerable
to disruption.
These data may help to explain variations in results
of studies which use different teeth. For example,
among the prehistoric
hypoplasia
chronologies,
the
late-peak frequency in the California population may
be due to Schulz and McHenry’s (1975) exclusive use
of mandibular canines. The California chronology is
more similar to the Dickson Mound chronology for
the same tooth (Fig. 1).
Our findings warn against comparing results of
enamel-hypoplasia studies which do not use the same
teeth. In order to begin to understand the importance
of host resistance and environmental factors in the
aetiology of hypoplasias, differences in susceptibility
of various teeth to hypoplastic disruption should be
ascertained. Once these sources of variation are
known, teeth may prove to be better recorders of
previous physiologic stresses than has hitherto been
realized.
Acknowledgements-We
gratefully acknowledge the assistance of Alan Harn and the staff of the Dickson Mounds
Museum, Lewiston, Illinois for allowing access to the
skeletal materials upon which this study is based. Kenneth
Sassaman provided the Figures. Ideas presented in this
paper were improved by numerous discussion with, among
others, Michael Blakey, Howard University; Della Cook,
University of Indiana; Keith Condon, University of Illinois;
Simon Hillson, University of Lancaster; Ed Hunt, Pennsylvannia State University; Ann Magennis, University of Massachusetts; Debra Martin, Hampshire College; Conraad
Moorrees, Harvard University; Jerome Rose, University of
Arkansas; and James Yaeger, University of Connecticut.
This project is supported by a N.I.D.R. Postdoctoral
Fellowship (T-32-DE07047).
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1
on the maxillary incisors and canine in a prehistoric Amerindian.
on the teeth suggests a common time of formation around 3 years
of age.
Enamel
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Plate
chronology
1.
507