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Correspondence between enamel hypoplasia and odontometric bilateral asymmetry in Australian twins.

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Correspondence Between Enamel Hypoplasia and
Odontometric Bilateral Asymmetry in Australian Twins
Robert S. Corruccini,1* Grant C. Townsend,2 and Wendy Schwerdt2
Department of Anthropology, Southern Illinois University, Carbondale, Illinois 62901-4502
Dental School, University of Adelaide, Adelaide 5005, South Australia
enamel hypoplasia; odontometrics; directional asymmetry; fluctuating
asymmetry; Australians; twins
Four aspects of enamel hypoplasia of the
maxillary central incisor and mandibular canine (hypoplasia presence, width, cumulative width, and crown position) were correlated with directional and fluctuating
measures of bilateral odontometric asymmetry in a large
panel (n ⫽ 950) of South Australian twins. Hypoplasia and
asymmetry are thought to reflect general developmental
disruption, but they show few correlations beyond the
expected statistical type I error. This may relate to differences in their specific etiology, the composite nature of
overall crown dimensions, a general lack of stress, and the
extended period of formation of dental crowns. In contrast,
asymmetry is marginally more detectable in a subsample
separated according to hypoplastic teeth, suggesting that
correspondence may be clearer in comparisons at the population rather than individual level. The most notable
difference is the greater variability of asymmetry measures in hypoplastic individuals. Am J Phys Anthropol
126:177–182, 2005. © 2004 Wiley-Liss, Inc.
Enamel hypoplasia (EH), a developmental defect
visible on the external surface of teeth, and bilateral
asymmetry (BA), an odontometric difference between antimeres, continue to attract substantial research attention. A review by Hoover (2001) cited 72
hypoplasia articles and 42 concerning asymmetry
that pointed to disturbed growth due to developmental insult as the cause of these anomalies. For instance, Townsend (1983) found sharply increased
dental fluctuating asymmetry in Down’s syndrome
individuals. Contemporary reviews established that
generalized stress between ages 0 –5 years underlies
most permanent tooth hypoplasias (Goodman and
Rose, 1990, 1991; Hillson, 1996; Larsen, 1997), and
this span need not be raised much to encompass the
likely range of formation of detectable crown asymmetries.
Perzigian (1977) noted increased asymmetry in
the Indian Knoll sample as compared with later
prehistoric and historic collections, and noted another study suggesting that Indian Knoll also had
the most frequent hypoplasia; he did not report individual BA-EH correspondence. Surprisingly, only
the analysis by Hoover (2001) seemed to approach
this issue. However, some preceding analyses suggested that disrupted calcification and disturbed
odontometric growth relate generally to each other
(Rose and Pasley, 1980; McKee and Lunz, 1989;
Manzi et al., 1997; Van Gerven et al., 1990), so direct
analyses of hypoplasia and asymmetry correspondence seem overdue.
On the other hand, there are various theoretical
reasons to doubt such a BA-EH correspondence. Po-
lar teeth in genetic “fields” (e.g., first molars) may
show increased effects of growth canalization but
halted calcification in response to stress (Townsend
and Brown, 1980; Goodman and Armelagos, 1985),
while nonpole teeth may react differently. Specific
stresses and their duration may affect BA and EH
differently. Growth of pulp and dentin contributes to
overall crown dimensions, not just enamel. Furthermore, the occluso-gingival position on tooth crowns
differs for recording maximum mesiodistal and buccolingual crown diameters, and for the location of
EH; perhaps only prolonged or repeated growth disruptions should significantly coeffect EH and BA.
Twins tend to undergo more morbidity and mortality than singleton human births (Taji et al., 2000;
Bryan, 1983; Townsend and Richards, 1990). They
are also systematically lower in birth weight than
singletons, and low-birth-weight and premature infants show increased enamel hypoplasia of both localized and generalized kinds (Seow, 1997). Therefore, twins offer a valid approach to exploring
BA-EH associations. The University of Adelaide has
a large collection of high-quality dental casts of
*Correspondence to: R.S. Corruccini, Anthropology Department,
Southern Illinois University, Carbondale, IL 62901-4502.
Received 28 January 2003; accepted 25 July 2003.
DOI 10.1002/ajpa.20113
Published online 6 July 2004 in Wiley InterScience (www.
twins that formed the basis of the study by Taji et al.
(2000) of localized hypoplasia of deciduous teeth. In
the same materials, Townsend and Farmer (1998),
Townsend et al. (1999), and Dempsey et al. (1995)
found rather extensive directional dental asymmetry but no more fluctuating asymmetry than in singletons.
Our purpose in this study is to analyze the hypoplasia correspondence to odontometric bilateral
asymmetry according to the various quantifications
of both entities, both among individuals and among
The dental stone casts, collected as part of an
ongoing study of dental and facial development in
twins being carried out at the Dental School, University of Adelaide, were obtained during two time
periods: an earlier group between 1983–1993, and a
second group commencing in 1995 and continuing
today. In the first project, 308 twin pairs of adolescent-to-adult Australians of European descent living
in Adelaide were examined, and records were obtained to determine the relative contributions of genetic and environmental influences to observed variations in dento-facial morphology. With an
approximate median age of 20 in 1985, this sample
has a median year of birth of roughly 1965. Adequate casts presenting the appropriate teeth allowed incisor hypoplasia data to be collected for 590
individuals (275 males and 315 females) among
these 616 cotwins. The second twin panel comprised
4 –5-year-olds, born in Australia and of European
descent, living in Adelaide and Melbourne, whose
parents had agreed could participate in a longitudinal study of dental and facial development. Follow-up castings of these children were obtained at
around 8 –10 years in 1998 –2000; thus the sample
had a modal year of birth of 1990 and fully erupted
incisors, but usually did not yet present the erupted
permanent canine. This sample comprised 296 pairs
in 2001, of whom 360 individuals (176 boys and 184
girls) out of 184 twin pairs allowed adequate assessment of the incisor/M1 group, but only 53 of the
canine/premolar group. Thus the total pooled sample size at maximum was 950, but the largest single
BA to EH bivariate sample size (owing to missing
data) was 818.
Data collection methods were approved by the
Committee on Ethics of Human Experimentation,
University of Adelaide (approval no. H/07/84A), and
all participants were informed volunteers. There
were 147 monozygotic (MZ) and 148 dizygotic (DZ)
pairs in the earlier cohort, and 83 MZ and 101 DZ in
the later cohort. Zygosity was determined to more
than 99% probability using 17 serum and protein
polymorphisms in the earlier cohort, and 6 hypervariable DNA loci in the later cohort. The sex and
zygosity variation would be expected more than 33%
of the time with random sampling.
The procedure one of us (R.S.C.) followed, to diagnose enamel hypoplasia prevalence was based on
current recommendations (Goodman and Rose,
1990, p. 92, 1991, p. 281; Goodman et al., 1992, p.
121; Hillson, 1996, p. 172, 2000, p. 253; Larsen,
1997, p. 44 –50). Only two focal teeth most susceptible to hypoplastic calcification, the permanent maxillary central incisor and mandibular canine, were
examined. If either antimere presented a macroscopic linear defect, hypoplasia was scored, provided
one of the following confirmatory signs was also
present: 1) the defect was a palpable (by fingernail)
depression on both antimeres at the same level of
the crown; 2) a defect was also observed on a different tooth class of roughly equivalent calcification
timing (i.e., I2 or I1/2 or less likely M1 in concert with
I1, or mesial or distal premolars, here referred to as
P1/2, or C1 supplementing an observation on C1 at
roughly the same crown height); or 3) a lingual as
well as labial manifestation of the line circumscribed the tooth. Illuminated magnifier observation
was only used to confirm and measure, not to initially diagnose, the hypoplasias (Goodman and Rose,
1990; Hillson, 2000). These criteria are in keeping
with the current practice of delimiting “definite”
cases. However, if a linear or limited (pitting) phenomenon seemed to be observed (or was only microscopically detectable) but none of the confirmatory
signs was found, this was considered a “possible”
EH, in keeping with less stringent requirements
that seem to have led to very high (90%⫹) hypoplasia prevalences reported for some modern (El Najjar
et al., 1978) and many prehistoric (Goodman and
Rose, 1990, 1991; Hoover, 2001) samples. Thus five
ranks of scoring were employed (not, possibly, and
definitely present, with two occasional intermediate
stages noted between these three).
In keeping with Blakey and Armelagos (1985),
Hutchinson and Larsen (1988), Larsen and Hutchinson (1992), and especially Ensor and Irish (1995),
hypoplasia width was ranked as a separate variable
in stages of absent, present but less than 1 mm,
between 1–1.5 mm, between 1.5–2 mm, and just one
case of ⬎2 mm as judged by a handheld magnifier
with a reticle. Vertical hypoplasia width may relate
to duration of metabolic insult, although hypoplastic
area might be a more revealing measure (Hoover,
2001). If there was more than one discrete hypoplasia, their width ranks were added together to create
a third variable, total hypoplasia width. Finally, in
cases of hypoplasia presence, it was noted whether
the event occurred relatively early in calcification
(occlusal 1/3 of crown location), intermediate (middle third), or late (apical 1/3), with borderline cases
decided with the reticle.
The maximum mesiodistal and buccolingual diameters of the crowns of all emerged permanent
teeth were measured following the definitions of
Seipel (1946) and Moorrees et al. (1957). Any teeth
in which wear or restorations had affected dimensions were excluded, together with those in which
the stage of emergence precluded measurement of
maximum dimensions. Third molars were excluded.
The measuring equipment comprised sharpened Mitutoyo digital vernier calipers connected via a multiplexer unit to a computer that provided readings to
the nearest 0.1 mm.
To estimate the reliability of the measurement
procedure, all 56 tooth-size variables were remeasured in 50 individuals selected at random. Mean
differences between repeated measurements were
small, with none exceeding 0.1 mm. Only 2 of 56
values were significantly different from zero, a finding that can be attributed to type 1 errors at the 5%
probability level, and which indicate no systematic
differences between first and second measurements.
The technical error of measurement, or Dahlberg
statistic (Dahlberg, 1940), averaged 0.06 mm, with a
range of 0.04 – 0.07 mm. The reliability of the measurement technique was also estimated as the ratio
of true to observed variance, where the true variance
was calculated as the observed minus the error variance. For our test-retest data, the estimated reliability of measuring the dental casts was 0.98, on average.
Odontometric directional asymmetry was calculated as (L ⫺ R)/((L ⫹ R)/2) for each mesiodistal and
buccolingual dimension. When using the absolute
value of (L ⫺ R), the formula gives fluctuating asymmetry which is irrespective of the larger side. A
common alternative formula, log(L) ⫺ log(R), produces directional asymmetries more than 99% correlated with the first formula over narrowly varying
dimensions such as these.
While fluctuating asymmetry has been the norm
for most stress assessments in both humans and
nonhuman experiments, Corruccini and Potter
(1981), Corruccini et al. (1982), Boklage (1987),
Hoover (2001), and Townsend et al. (1999) provided
cautionary evidence that the directional variant
may be just as or even more indicative of environmental responses (especially in nonpolar teeth).
For the time being, we relinquish consideration of
root mean square and other methods for assessing
dentition-wide asymmetry levels, as well as possible
multivariate correspondence between assessments
of hypoplasia and asymmetry in multiple groups of
teeth. These shall remain topics for possible future
Correspondence was assessed by using productmoment and rank-order correlations over the entire
sample. The former might be the better indicator of
strength of relationship. The latter might be more
reliable for assessing probabilities for the null hypothesis in the presence of non-normal distributions. The distribution of the fluctuating type of
asymmetry and of all hypoplasia measures except
crown position (i.e., early vs. late) was decidedly
non-normal. In two-sample comparisons, t-tests
were used, which with these large sample sizes
should be fairly robust despite the non-normalities.
As we are testing numerous null hypotheses with
the same sample, an adjusted Bonferroni probability
of 0.05/N should be the proper critical probability,
where N is the number of different variables tested.
The use of twins could raise an objection of redundancy of sampling. Genetically, this would be true,
but hypoplasias and asymmetries are putatively environmental markers. Nevertheless, one might expect environmental covariance to be channeled by
similar genotypes, so a correlated response to environmental exposure could be possible. However,
most “definite” hypoplasias (77%) are discordant between cotwins (Corruccini and Townsend, 2003),
and the genetic variance of asymmetries is very low
(Corruccini et al., 1988; Corruccini and Sharma,
In this and previous studies, there are no obvious
consistent differences between males and females or
between MZ and DZ individuals for either hypoplasia or asymmetry, justifying pooling into one sample.
Correlations between hypoplasia and asymmetry
variables total 448 (four hypoplasia variables for
each of the two teeth, and both directional and fluctuating types of asymmetry over the 28 mesiodistal
and buccolingual dimensions; thus, 8 ⫻ 56). Rankorder correlations and their probability levels differ
by minuscule amounts from parametric Pearsonian
correlation coefficients, usually only in the third decimal place, as is the conventional wisdom when sample sizes are very large. Therefore, only the productmoment correlations are presented here, despite
non-normality. The various hypoplasia measures intercorrelate at about r ⫽ ⫹0.19 between canines and
The width and total width measures very consistently give correlations very close to those for the
variable of simple presence (usually differing in only
the third decimal place), but also consistently
slightly lower. This suggests that no extra information resides in thickness variables as regards their
correspondence to asymmetries, so further consideration of the former is omitted here. It is somewhat
surprising that usually slightly lower but otherwise
thoroughly redundant correlations are found for
those thicknesses.
Of the 112 correlations between the two hypoplasia positions and 56 asymmetry variables, just four
attain the critical probability of P ⬍ 0.05, which is
less than expected at random for type I error (0.05 ⫻
112 ⫽ 5.6), and all are well below the r ⫽ 0.20 level.
Therefore, hypoplasia location (whether near or far
from the occlusal apex) is considered unrelated to
asymmetries of any tooth class.
Table 1 shows the remaining information, i.e.,
nine asymmetry variables which correlate significantly with hypoplasia presence. Eight of these involve incisor hypoplasia, and only one involves hypoplastic canines. These are all very low correlations,
TABLE 1. Correlations that achieved statistical significance
between hypoplasia presence and asymmetry at ordinary p ⬍
0.05 level and at Bonferroni level of 0.05/112 ⫽ p ⬍ 0.00051
I1 hypoplasia
C1 hypoplasia
MD, mesiodistal; BL, buccolingual; DA, directional asymmetry;
FA, fluctuating asymmetry.
* p ⬍ 0.05.
** p ⬍ 0.0005.
so while there may be a significant correspondence,
there certainly is not a very useful or predictive one.
The strongest correlation, r ⫽ ⫺0.159 between incisor hypoplasia and C1 mesiodistal directional asymmetry, does not inspire us with its strength, and
furthermore seems rather illogical, as canines and
incisors have fairly different calcification and eruption schedules. However, this correlation alone
among the 112 between hypoplasia presence and
asymmetry variables falls below a critical Bonferroni probability of 0.0005 (0.05/112). This adjusted
alpha probability is divided by the number of repeat
tests performed on the same sample of subjects,
raising confidence that this might reflect a real biological relationship.
Another problem in Table 1 is that 2 of 4 correlations involving fluctuating asymmetry are negative,
illogically suggesting that hypoplastic individuals
tend to show less asymmetry. However, the nine
total significant findings exceed an expected type I
error rate of 5% (0.05 ⫻ 112 ⫽ 5.6), and there are 33
positive as opposed to 23 negative correlations for
the fluctuating asymmetries overall, where 28 each
would be the perfectly random expectation. Perhaps
therefore there is a real (but very faint) overall hypoplasia-asymmetry correspondence at the level of
the individual.
There is clearly a difference (Corruccini and
Townsend, 2003) in the sharply lowered hypoplasia
frequencies in the later (born ca. 1990) twin cohort.
This may bear a strong relation to the introduction
of fluoridated city water in the study population.
Frequencies are about four times as high in the
earlier cohort for the “possible” I1 hypoplasias, and
all other incisor and canine contrasts are even stronger. In view of the time lag involved in measuring
the two cohorts and the paucity of hypoplasias in the
later one, pairwise sample comparison of asymmetries according to whether the case did or did not
evince a hypoplasia was limited to the earlier cohort.
Table 2 shows only those asymmetry variables
that differ between the incisor hypoplastic and con-
trol subsamples of twins. Of 56 t-tests, only 6 attain
a significant difference at P ⬍ 0.05, with none at a
Bonferroni level of P ⬍ 0.001. Much like the correlation analysis, this gives a weak signal. One result,
for buccolingual fluctuating asymmetry of M1, is
illogical in that the nonhypoplastic individuals averaged higher values.
Logically expectable results attaining convincing
levels of statistical improbability for the null hypothesis are attained only when comparing the variability of the asymmetries. One quarter of the 56 F
tests for variance are significant at P ⬍ 0.05; 6 of
these 14 are significant even at P ⬍ 0.001. There is
consistency also in that most of the BA effects according to EH involve teeth in the same, earlier
erupting calcification group, i.e., permanent incisors
and first molars. The hypoplastic individuals are
quite consistently more variable in asymmetry. This
signal is much clearer than it is for any central
tendency of asymmetry.
The only exception is the buccolingual M1 dimension in both fluctuating and directional asymmetry,
where the hypoplastic subsample is significantly
less variable. In examining the raw data, no outlier
values are obvious for this dimension, but in contrast to all the other asymmetries, the largest values
for M1 buccolingual asymmetry are consistently associated with individuals showing smaller or reversed asymmetries in other dimensions, and are
also associated with contrasting values in the individual cotwin. Perhaps some sort of mirror imagery
is involved.
The few asymmetry-hypoplasia correlations attaining nominal statistical significance do not attain
statistical usefulness, such as an r of greater than
⫹0.50. Overall there is just a hint of meaningful
correspondence at the level of the individual, comparable to the results of Hoover (2001). Perhaps the
scoring of hypoplasias only in the more susceptible
polar teeth of incisor and canine genetic fields affected results, because such teeth are likely more
canalized in their growth response to the same stressors. However, if that were the case there should
have been detectable asymmetric responses in the
lateral incisors (compared to the maxillary central),
and in the premolars and M2 compared to the canine
Nevertheless, it could be that comparisons across
stressed and unstressed samples (rather than individuals) could reveal shared differences in asymmetry and hypoplastic calcification. This approach will
be more profitable in prehistoric archeological samples with more variable infection and nutrition profiles than the present affluent Westernized subjects.
Perhaps in these Australians there simply is insufficient stress of any kind to bring about sufficient
growth disruption to cause any measurable correlated response. However, Hoover (2001) found quite
similar results among nonelite Imperial Romans.
TABLE 2. Descriptive statistics of asymmetry in earlier (ca. 1965) born subsample divided by maxillary central incisor hypoplasia1
Directional asymmetry
Fluctuating asymmetry
mean (S.D.)
mean (S.D.)
⫺0.0014 (0.0384)
⫺0.0121 (0.0296)
⫺0.0146 (0.0480)
0.0036 (0.0477)
⫺0.0003 (0.0271)
0.0029 (0.0263)
⫺0.0006 (0.0240)
0.0013 (0.0337)
⫺0.0010 (0.0162)
⫺0.0045 (0.0368)
⫺0.0188 (0.0579)
0.0096 (0.0259)
0.0185 (0.0317)
⫺0.0054 (0.0212)
⫺0.0028 (0.0283)
⫺0.0006 (0.0541)
0.0119 (0.0213)
0.0066 (0.0309)
0.0243 (0.0296)
0.0183 (0.0206)
0.0243 (0.0437)
0.0280 (0.0267)
0.0343 (0.0329)
0.0212 (0.0169)
0.0177 (0.0156)
0.0182 (0.0156)
0.0259 (0.0206)
0.0258 (0.0217)
0.0307 (0.0183)
0.0122 (0.0106)
0.0307 (0.0201)
0.0185 (0.0203)
0.0283 (0.0285)
0.0233 (0.0174)
0.0158 (0.0152)
0.0217 (0.0183)
0.0192 (0.0151)
0.0264 (0.0224)
F is a variance ratio and tests difference in variability, t-tests are of mean difference.
* Ordinary two-tailed significance at p ⬍ 0.05.
** signifies Bonferroni corrected significance at p ⬍ 0.001 (0.05/56).
The major noteworthy finding concerns the increased variability of asymmetry in individuals constituting the hypoplastic sample. Hypoplastic individuals calcify tooth crowns that are both more and
less asymmetrical than controls, increasing variance. Perhaps two different processes are at work,
one disrupting development and mutually increasing the risk of hypocalcification and asymmetry,
while another sort or intensity of stress incurs canalization of development and therefore decreases
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