Full text of DOI:10.1111/j.1834-7819.2000.tb00246.x

ADRF RESEARCH REPORT
Australian Dental Journal 2000;45:(2):83-90
Localised enamel hypoplasia of human deciduous
canines: genotype or environment?
Sue Taji,* Toby Hughes,* Jim Rogers,* Grant Townsend*
aetiological factors within any given environment in
Abstract
different ethnic groups may provide better insight
into the ambiguous aetiology of the hypoplastic
enamel defect.
A discrete area of defective enamel formation that
appears on the labial surface of the crowns of
deciduous canine teeth has been described in both
recent and prehistoric human populations, with
reported frequencies varying from 1 to 45 per cent.
Suggestions about the aetiology of this localized
hypoplasia range from genotypic factors to environ-
mental conditions and systemic effects. The major
aims of this study were to describe the frequency of
occurrence and pattern of expression of the lesion
in Australian Aboriginal and Caucasian ethnic
groups, and to clarify the role of genetic factors by
examining a sample of twins.
The study sample consisted of dental casts of 181
pairs of Australian Caucasian twins, 215 Aborigines
and 122 Caucasian singletons, together with 253
extracted deciduous canines. Examination of
dental casts and extracted teeth was undertaken
under 2ϫ magnification with emphasis being
placed upon location and expression of the lesion.
The defect was observed in 49 per cent of twins
and 44 per cent of Aborigines, but only 36 per cent
of singletons. The percentages of affected teeth in
each group were: 18 per cent in twins, 17 per cent
in Aborigines and 13 per cent in Caucasians. A
significant proportion of the defects occurred on the
mesial aspect of the labial surface, in the middle
area incisocervically, with the majority in the lower
jaw. Anumber of significant differences in frequency
were observed between groups, sexes, arches and
sides.
The results confirm some of the findings of previous
studies, but also suggest that none of environmental,
genetic or systemic factors can be ruled out as
being involved in aetiology of the defect. The higher
incidence of the lesion occurring on the mesial
aspect of the labial surface is suggestive of physical
trauma. Also, the vulnerability of the prominent
developing mandibular canine, with its thin or
missing labial covering of bone, would be expected
to lead to higher prevalence of the lesion in the
lower jaw. Although not definitive, the results of
concordance analyses in twins were suggestive of
a possible genetic predisposition in the formation of
the lesion. Further research with a greater clinical
orientation and emphasis on determining specific
Key words: Enamel defects, trauma, genetics, twins.
(Received for publication October 1998. Revised
December 1998. Accepted December 1998.)
Introduction
A discrete area of defective enamel formation on
the labial surface of the crowns of deciduous canine
teeth has been described in both recent and
prehistoric human populations.1 The lesion usually
manifests as a flat-bottomed crater covering an area
of about 1-2 mm, extending either partially or
completely through the enamel to the dentine (Fig.
1). A solitary lesion is most frequent, although
multiple defects have been observed also on
individual teeth.2
Many suggestions have been proposed to explain
the aetiology of the lesion. Jorgensen,2 the first to
report the defect, found no difference between
medieval and modern Danes with respect to the
frequency of the defect. He believed that this
consistency over time indicated at least a partial
genetic basis. However, no other studies appear to
have been carried out to verify whether genetic
factors play a role.
Skinner and Hung3 have used the location of the
lesion, most commonly at mid-crown level, to
support their view that the defect is initiated shortly
after birth. Skinner4 further suggested that minor
trauma to the developing canine crown of neonates
(for example, sharp objects placed in the mouth) is
an important environmental factor. At birth the
cortical bone forming the labial bulge of the crypt of
the primary canine is either thin or absent, and thus
the crown may not receive adequate protection from
4
early physical trauma (Fig. 2). Skinner has argued
that this differentiates the canine with respect to
other adjacent primary teeth, which are either less
labially positioned, or have largely completed crown
*Dental School,The University of Adelaide.
Australian Dental Journal 2000;45:2.
83

2
Fig. 1. – Extracted deciduous mandibular canine showing a distinct
hypoplastic defect on the labial surface of the crown.
Fig. 2. – Neonate skull showing distinct bulges in the regions of
developing deciduous canines, with deficiency of labial bone
on the left side.
1
5
4
formation at birth. Nation et al. have hypothesized
that the high prevalence of the defect in mandibular
canines at a level corresponding to the perinatal
period of tooth formation may be due to the
protruded position of these teeth during formation.
They have suggested also that, during the act of
birth, trauma of the canines is induced by
compression of the lower labial alveolar wall due to
Skinner has looked at the onset and duration of
the lesion in detail and notes that the time interval
during which a specific defect formed can be deter-
mined by relating the height of the defect to rates of
deciduous canine formation. An intermediate for-
mation rate for the deciduous canine is 0.33 mm per
month, corresponding to an average time of 5.2
4
months for the formation of the defect. To
5
pressure from the maxilla.
determine the time of onset and cessation of the
lesion, its vertical extent is drawn on an outline of a
representative deciduous canine, adjusting the data
to allow for differences in observed tooth heights.
Nutritional status of the expectant mother has
also been implicated as a possible contributing
6
factor to the defect. Skinner and Hung have
2
5
Both Jorgensen and Nation et al. commented on
attributed reduced cortical bone in the jaws of the
infant to nutritional factors, involving calcium
deficiency of the mother and/or developing infant.
Calcium deficiency may either be due to unavail-
ability of calcium-rich food or lactose intolerance. It
has been proposed that diets composed of high fibre
and phytate contribute directly to low calcium levels
by interfering with absorption of vitamin D required
the presence of apparent prenatal defects in
4
Caucasian subjects. However, Skinner suggested
that defects assumed to occur prenatally may result
from an individual being born at an early stage of
canine formation due to retarded crown formation
and/or premature birth. A link between size of the
hypoplastic defect and apparent prematurity has also
4
1
been demonstrated. Lesions commencing close to
for phosphorous and calcium deposition. Deficiency
the crown tip appear significantly larger than those
initiated near the cervical margin.
of such nutritional elements can affect epithelial cell
7
function and the mineralization process. Such a
situation may produce a developmental setting
conducive to formation of the hypoplastic defect.
The prevalence of labially located enamel
hypoplasia of the primary canine was first reported
by Jorgensen, with lesions observed in 21 per cent
1
2
Other studies have reported a strong association
between socio-economic status and prevalence of
the defect together with differences in frequencies
between developing and developed countries. This
suggests that differences in nutritional status, or
obstetric and paediatric care, may be important
of modern Danish and 28 per cent of medieval
Danish primary canine teeth. Other studies in
modern populations have found a varied prevalence
1,4
ranging from 45 per cent or more to less than 1 per
3
cent. Such variation depends on the population
1,6,8
aetiological factors.
studied, the sample size of teeth examined and the
84
Australian Dental Journal 2000;45:2.

criteria used for diagnosis.7 The lesion occurs twice
as commonly in the lower jaw.4 Jorgensen2 noted that
the hypoplastic areas appeared to occur within or on
the boundary of the mesiogingival quadrant of the
labial surface. Variation in the defect has been
observed between ethnic groups. Nation et al.5 have
suggested that variation in occurrence of the defect
between different ethnic groups may be due to
differences in susceptibility to trauma of the cells
taking part in amelogenesis or to a difference in the
tendency to develop general disorders or diseases
affecting indirectly amelogenesis. Population
differences in the prevalence of the lesion may reflect
innate and acquired variation in thickness of the
alveolar bone and soft tissues overlying the bulging
4
crypt of the deciduous canine.
Fig. 3. – Dental cast showing a distinct hypoplastic defect on the
labial surface of a mandibular deciduous canine.
In studies conducted previously, the lesion has
most commonly presented as a solitary defect in the
cervical half of the deciduous canine crown.
However, little is known about the shape of the
defect or the relevance of its location to its aetiology.
Previous studies also lack any examination of the
lesions over time (longitudinal assessment).
of the lesion and to confirm that the dental casts
provided a valid representation of the various forms,
ranging from pinpoint to larger defects. Dental casts
were examined for evidence of the defect on the
labial surface of deciduous canines from the four
dental quadrants. Presence or absence of the defect
and its position on the tooth crown were recorded
(Fig. 3). Crowns were subdivided into thirds in two
planes. These were denoted incisal, middle and
cervical in the incisocervical plane, and mesial,
middle and distal in the mesiodistal plane, following
The current study aimed to address many of these
issues. The main aims of the study were:
1. To determine the range of expression of the
lesion by examination of a sample of extracted teeth.
2. To compare the frequency of occurrence and
range of expression between large samples of
Australian Caucasians and Aborigines.
11
Wheeler.
3. To examine a sample of twins in order to
determine the relative contributions of genetic and
environmental influences to variation in expression
of the lesion.
Detection was based on the presence of a
depressed area on the labial surface of the deciduous
canines presenting as pinpoint, oval, circular or tri-
angular in shape. Observation was carried out
initially under 2ϫ magnification adjusting the light
angulation for clear demarcation of the border of the
lesion. Further observations were conducted using a
stereo-microscope to aid detection of pinpoint
defects. Apart from their characteristic position and
shape, localized hypoplastic defects in the extracted
teeth were differentiated from possible carious
lesions by confirming with a dental explorer that the
enamel or dentine at the base of the lesion was hard.
Given that it was impossible to use tactile methods
of discrimination on the dental models, hypoplastic
lesions were distinguished solely on the basis of their
appearance and location.
4. To examine serial dental casts of selected
Aboriginal subjects to determine whether any trends
in expression of the lesion were evident with time.
Materials and methods
The sample consisted of dental casts of 181 pairs
of Australian Caucasian twins, 122 Caucasian sin-
gletons and 215 Australian Aborigines. The twins
were part of an ongoing study of dentofacial
variability and ranged in age from around 4 to 9
years.The dental casts of Caucasian singletons, aged
from 3 to 6 years, were collected during an earlier
9
study of deciduous tooth size variability. The dental
casts of Aborigines belonging to the Wailbri tribe
were obtained during a longitudinal growth study
that was undertaken in the 1960s and 70s.10 Their
ages ranged from approximately 6 to 10 years. A
total of 253 extracted deciduous canines collected in
South Australia during the early 1900s were also
examined.
Frequency of occurrence was calculated on an
individual-by-individual basis and also on a tooth-
by-tooth basis. Due to the availability of serial dental
casts for the Aborigines, it was possible to determine
whether lesions were always present from the
youngest age or whether they became apparent at
later ages.
The extracted deciduous canines were examined
initially to assess the extent of variation in expression
Genetic analysis was conducted on the twin
samples by comparing percentage concordances in
Australian Dental Journal 2000;45:2.
85

monozygotic (MZ) twins with dizygotic (DZ) twins.
Under the assumption that MZ twins share the same
genes, the theoretical maximum expected
concordance is 100 per cent, whereas the DZ twins
share only half of their genes, leading to maximum
values of 50 per cent.
Table 1. Frequencies of occurrence of
hypoplastic lesions on human deciduous
canines within three distinct populations
Twins
n %
Aborigines
n %
Singletons
n%
Individuals with no
lesions
Individuals with one
tooth affected
Individuals with two
teeth affected
Individuals with three
teeth affected
184 (50.8)
115 (31.8)
43 (11.9)
16 (4.4)
121 (56.3)
62 (28.8)
23 (10.7)
6 (2.8)
78 (63.9)
30 (24.6)
12 (9.8)
2 (1.6)
The ethical guidelines issued by the National
Health and Medical Research Council (NHMRC)
of Australia were followed in the study and informed
consent was obtained from human subjects.
Chi-square tests were used to examine associa-
tions between presence or absence of the defect and
several variables, including ethnicity, sex, twin
zygosity, age, dental arch, side and location of the
lesion.
Individuals with four
teeth affected
4 (1.1)
3 (1.4)
0 (0.0)
Individuals with at
least one lesion
178 (49.2)
94 (43.7)
44 (36.1)
Frequency of occurrence (at least one lesion) differed significantly
between the three groups (␹2 = 6.89,p<0.05).
Double determination tests were carried out on
10 per cent of the sample to assess the reliability of
the scoring method. Concordances between repeated
measures were high (80 per cent) for all measured
traits.
occurred predominantly (58 per cent) in the mesial
region, followed by the middle (34 per cent) and
distal (8 per cent) regions. Fifty-six per cent of all
lesions were round, 37 per cent were oval, 4 per cent
were triangular and 3 per cent were irregularly
shaped.
Results
Extracted teeth
Nineteen per cent of the extracted teeth
demonstrated some form of hypoplastic lesion.
There was a significant difference (␹2=10.96,
p<0.001) in frequencies between arches. Only 11
per cent of maxillary canines were affected, compared
with 28 per cent of the mandibular canines.
Group differences
Table 1 presents frequencies of occurrence of the
lesion for the three groups. There was a significant
difference in frequencies between the groups
(␹2=6.89, p<0.05); Aborigines and twins showed
similar frequencies of individuals with at least one
lesion (44 per cent and 49 per cent respectively) but
singletons displayed lower frequencies (36 per cent).
Incisocervically, 10 per cent of lesions were in the
incisal third, 29 per cent were in the middle third
and 61 per cent were in the cervical third. Mesio-
distally, 65 per cent were in the mesial third, 2 per
cent were in the middle third and 33 per cent were
in the distal third. No significant arch or side
differences were observed in lesion distribution.
Fifty-eight per cent of lesions were round, 35 per
cent were ovoid and 6 per cent were triangular or
irregular in shape.
On a tooth-by-tooth basis, there was also a
significant difference between groups (␹2=8.81,
p<0.05). Twins had the highest frequency at 18 per
cent, closely followed by Aborigines (17 per cent),
with the Caucasian singletons having the lowest
frequency at 13 per cent.
Table 2 presents frequencies of occurrence of the
lesion for the three groups by arch and side.All three
groups exhibited a frequency in the mandible greater
than that in the maxilla. Furthermore, there were
group differences in frequency, averaged for right
Dental casts
Forty-seven per cent of all individuals were affected
by at least one detectable hypoplastic lesion. Of
these, 64 per cent had only a single affected tooth,
26 per cent had two, 8 per cent had three and only 2
per cent had lesions on all four canines. Overall, 17
per cent of all canines were affected.
Table 2. Frequencies of occurrence of
hypoplastic lesions by arch and by side
There was
a highly significant difference
Twins
n %
Aborigines
n %
Singletons
n %
(␹2=82.35, p<0.001) between maxillary and
mandibular frequencies (11 per cent and 24 per cent
respectively); however, there was no difference
between left and right sides.
Maxilla
Right
Left
Mandible
Right
48 (13.3)
46 (12.8)
8 (3.9)
25 (12.2)
12 (9.8)
6 (4.9)
99 (27.4)
72 (19.9)
54 (29.7)
48 (26.1)
21 (17.2)
22 (18.0)
Overall, lesions occurred predominantly (59 per
cent) in the middle region of the incisocervical
plane, followed by the cervical (32 per cent) and the
incisal (9 per cent) regions. Mesiodistally, lesions
Left
Frequency in mandible significantly greater than maxilla for all three
groups: twins (␹2=26.65, p<0.001), Aborigines (␹2=52.86,
p<0.001),singletons (␹2= 11.71, p<0.001).
86
Australian Dental Journal 2000;45:2.

Table 3. Frequency distribution of localized enamel hypoplasia incisocervically
Twins
Aborigines
Singletons
Mid %
Inc %
Mid %
Cer %
Inc %
Mid %
Cer %
Inc %
Cer %
Maxilla
Right
Left
20.8
15.0
47.9
70.0
31.3
30.0
0.0
8.0
37.8
48.0
62.5
44.0
0.0
16.7
66.7
16.7
33.3
66.6
Mandible
Right
Left
10.2
5.6
66.3
70.8
23.5
23.6
7.4
6.2
61.1
41.7
31.5
52.1
9.5
0.0
61.9
72.7
28.6
27.3
Inc=incisal third;Mid=middle third; Cer=cervical third.
No significant difference in distribution of lesions between the three groups.
and left sides, within both the maxilla (8 per cent, 7
per cent and 13 per cent for Aborigines, singletons
and twins respectively; ␹2=10.05, p<0.01) and the
mandible (28 per cent, 18 per cent and 24 per cent;
␹2=8.52, p<0.05). However, the relative differences
between arches were similar between groups (14 per
cent higher in the mandible).
demonstrate concordance for lesion presence.
Subsequent sample sizes were relatively low (33 for
dizygous twins, 19 for monozygous twins) and the
results should be considered accordingly. Mono-
zygous twins had slightly higher concordance for
incisocervical location but were similar to their
dizygous counterparts for mesiodistal location.
Tables 3 and 4 present frequencies of occurrence
of the lesion with regard to vertical and horizontal
position respectively. In all three groups the lesions
occurred predominantly in the middle region inciso-
cervically, followed by the cervical and incisal
regions.With respect to mesiodistal location, again a
similar pattern of expression was noted in all three
groups, with mesially positioned lesions tending to
be most common, particularly in the mandible,
followed by those located in the middle, then distal
thirds of the crown.
Discussion
Most of this study’s findings with regard to
location, occurrence and the influence of gender on
the hypoplastic defect were similar to those observed
by other investigators. However, some new insights
into the defect’s aetiology were gained.
Observation of 253 extracted Caucasian deciduous
canines indicated that around 19 per cent of the
teeth showed the defect. Results from examination
of dental casts were similar overall (17 per cent) and
for all groups studied (18, 17 and 13 per cent for
twins, Aborigines and singletons respectively),
supporting the use of casts as an appropriate
medium for detecting the defect. It should be
acknowledged, however, that there are limitations in
using dental casts for studies of hypoplastic lesions,
as mild forms of hypoplasia including opacities
cannot be distinguished and differential diagnosis of
hypoplastic lesions from carious lesions is generally
not possible.
There were no significant differences between
sexes in the frequency of occurrence of the lesion,
either on an individual-by-individual basis or on a
tooth-by-tooth basis.
Twin concordances
Twin concordances are presented in Table 5.
Dizygous twin pairs had a higher concordance for
presence of at least one lesion than their monozygous
counterparts, whereas concordances for number of
teeth affected were similar in both groups.
The results derived from dental casts were
comparable to those found by Lukacs1 but were
lower than other studies such as Jorgensen’s2 Danish
data (21 per cent and 28 per cent for modern and
medieval Danes respectively), and Skinner’s4
Calcutta data (29 per cent).
Concordances for vertical and horizontal location
were determined by accumulating the pair-wise
comparisons of each of the four canine types (upper
right, upper left, lower right and lower left).This was
after removal of any canine pairs that did not
Table 4. Frequency distribution of localized enamel hypoplasia mesiodistally
Twins
Aborigines
Singletons
Mid %
Mes %
Mid %
Dis %
Mes %
Mid %
Dis %
Mes %
Dis %
Maxilla
Right
Left
39.6
26.1
47.9
50.0
12.5
23.9
62.3
44.0
37.5
52.0
0.0
4.0
25.0
66.7
66.7
33.3
8.3
0.0
Mandible
Right
Left
57.1
70.8
33.6
27.8
9.2
1.4
75.9
81.3
18.5
14.6
5.5
4.2
61.9
68.2
33.3
31.8
4.8
0.0
Mes=mesial third; Mid=middle third;Dis=distal third.
No significant difference in distribution of lesions between the three groups.
Australian Dental Journal 2000;45:2.
87

It has been suggested that an acquired hypoplastic
defect may be a result of a systemic effect on the
ameloblasts.4 In the case of a systemic insult to the
ameloblasts, a bilateral expression of the defect and
its presence in both jaws is expected. However, as
ameloblasts do not become secretory simultaneously,
presence of a lesion in less than all four quadrants
need not rule out systemic influence.4 Of the
subjects studied, only 17 per cent of the twins, 15
per cent of the Aborigines and 11 per cent of the
singletons showed two or more affected teeth (Table
1). Furthermore, absence of the defect on other
tooth types whose crown formation overlaps that of
the canines, and the observation of a greater
frequency of occurrence of the defect in the lower
jaw, lessen the possibility of a systemic cause.
Table 5. Twin concordances for frequency,
position and size of hypoplastic lesions
Concordance %
Trait
Monozygous
Dizygous
Presence of at least one lesion
Number of teeth affected
Incisocervical position
Mesiodistal position
55
43
42
53
73
54
30
48
Frequency
In the current study, the defect has been shown to
occur more frequently in the lower jaw with no
detectable difference in prevalence between sexes.
1,3,4
This has also been reported in previous studies.
Skinner4 suggested that this may be a reflection of
the presence of a thicker layer of soft tissue,
especially fat cheeks, overlying and protecting the
upper canines from trauma, or alternatively, it may
result from a reduction or total absence of protective
alveolar bone in the lower jaw. An increased
frequency in the mandible may also reflect the
marked protrusion of the lower canines during early
growth and development.This is illustrated in Fig.2.
Such exposure may make mandibular canines more
susceptible to physical trauma. This is an example
where environmental influences may be interacting
with an underlying genetic predisposition to produce
a phenotypic effect.
The susceptibility of deciduous canines to display
the defect may indeed have some genetic basis. In
the current study involving the twin data set, seven
pairs of MZ twins and six pairs of DZ twins showed
mirror-imaging for size and location of lesions. This
indicates subjectively that there may be an under-
lying genetic predisposition to lesion development.
However, the concordance value for presence of at
least one lesion in MZ twin pairs was only 55 per
cent, indicating substantial environmental variation.
This is further evidence that lesion development
reflects a complex interplay between genetic and
environmental factors. Further analysis using more
advanced genetic modelling is warranted to quantify
the relative contributions of genotype and
environment.
Localized trauma as an aetiological factor in
formation of the hypoplastic defect has been
supported by the majority of previous studies.
However, none of these studies have employed the
three very distinct groups of subjects who were
included in this study.
1,3-5,7
The highest percentage of subjects with at least
one lesion was noted in twins. Twinning has long
been associated with both prenatal and perinatal
mortality and morbidity, with perinatal mortality
estimated to be 11 times that of normal singleton
Ethnic differences in frequency may reflect either
genetic or environmental differences, or more likely
a combination of the two. It is difficult to quantify
the relative contributions of these two components
based only upon interpopulation comparisons,
however some inferences may be drawn about the
impact of various socio-economic and cultural
differences.
12
births. Twins have a much higher incidence of pre-
mature birth, and gestation is on average three weeks
shorter than singletons. Parity is also important.The
second-born twin is at greater risk of oxygen
deficiency and birth trauma due to abnormal uterine
positioning.13 A higher frequency of low birth weight
resulting from nutritional deficiency has also been
observed.14 Perinatal and prenatal growth retardation
and prematurity observed in twins may be factors
associated with the aetiology of the hypoplastic lesion.
Seow15 has commented on the high prevalence of
enamel hypoplasia (both localized and generalized)
in low birth weight and premature children with a
range of 43-96 per cent. Such dental defects have
been variously associated with low bone mineral
stores, traumatic laryngoscopy and prolonged
endotracheal intubation.15 With respect to the
greater risk of nutritional and oxygen deficiency in
twins, the chance of an abrupt cessation of enamel
formation through sudden ameloblast death, and
If the aetiology were dictated by environmental
factors alone, in particular physical trauma, one may
have expected a greater frequency of affected teeth
within the Aboriginal population, who were exposed
to harsher environmental conditions and a greater
likelihood of developmental trauma. More
importantly, one would have expected a greater
frequency of individuals with multiple teeth affected,
but this was not the case. The results in this study
suggest that the large differences between the two
groups in lifestyle, diet and socio-economic status
are having only a small impact on the frequency of
occurrence of the lesion.
88
Australian Dental Journal 2000;45:2.

thus development of the hypoplastic lesion, may be
much greater.
study provides some further insights. Where serial
dental models were available for Aborigines, changes
in lesion appearance were noted over time. In five
cases, defects were only evident on casts representing
older age, suggesting the possibility of a subclinical
lesion early in development that deteriorates with
age due to factors within the local environment of
the tooth. Two or more pinpoint lesions in close
proximity were observed in 23 per cent of affected
extracted canines. It is possible that these may unite
in some teeth, through wear or enamel breakdown,
leading to the formation of typical crater-like
defects.
Location
The deciduous canine crown forms from the
cuspal tip to the cervix at linear rates.4 It is known
that ameloblasts do not become secretory at the
same time, cells in the presumptive cuspal regions
being more differentiated than those placed more
laterally and cervically. Correspondingly, the cuspal
region contains the advanced organic front in which
mineralization will subsequently follow. The pattern
of mineral deposition and growth appears to follow
the incremental lines of Retzius, laid down by the
matrix-secreting ameloblasts, thus transversing the
cuspal zones in an arc-like fashion; ending
bisymmetrically at the cervical regions of the dento-
enamel junction with a decreasing gradient of
mineralization.16 Kraus and Jordan17 observed that
both maxillary and mandibular deciduous canines
have one-third of their enamel formed at birth with
crown formation being completed by nine months
after birth.The vertical position of the lesions in our
study was mostly in the middle third of the tooth
incisocervically, followed by the cervical third and
then the incisal third, suggesting a perinatal
commencement of the defect, with some defects
commencing up to a few months after birth.The few
examples of the lesion being positioned in the incisal
third may in fact reflect a premature birth and/or a
retarded crown formation.
Conclusion
The results of this study have shown a specific
trend in the location of the hypoplastic defect. A
significant proportion of the lesions occur on the
mesial aspect of the labial surface of the crown, and
are centralized vertically.There is a higher frequency
of occurrence in the mandibular canines relative to
the maxillary canines, but there is no effect of
gender. Overall, there is some suggestion of an
underlying genetic predisposition to lesion formation
but the developmental environment seems to be the
main determinant of trait expression. A more
comprehensive analysis involving genetic modelling
of twin data is warranted to elucidate the relative
contributions of genotype and environment. Further
research with a clinical orientation may also provide
insight into the ambiguous aetiology of the
hypoplastic enamel defect.
Of note was evidence of two or more pinpoint
lesions presenting in close proximity on some teeth.
This was observed in approximately 5 per cent of the
dental casts that displayed lesions and 23 per cent of
affected extracted primary canine teeth. This
suggests that the crater-like appearance of at least
some lesions may result from contiguous pinpoint
lesions uniting through enamel wear or breakdown.
Acknowledgements
The support of the Australian Dental Research
Foundation, which awarded an Undergraduate
Scholarship to Sue Taji, is gratefully acknowledged.
The support of the National Health and Medical
Research Council (NHMRC) of Australia and the
Australian NHMRC Twin Registry is also
acknowledged.
The high prevalence of the lesion on the mesial
aspect of the labial surface may be indicative of the
action of physical trauma in the aetiology of the
defect.This is demonstrated in part by the data from
the different ethnic groups studied. The Aboriginal
tribe from whom dental casts were obtained lived in
harsher environmental conditions compared with
the twins or Caucasians who participated in the
study. Such conditions may have had an impact in
terms of early postnatal access to damaging agents in
a non-urban environment.Finding a higher incidence
of the mesially located lesions in the Aboriginal data
than in twins or singletons supports this hypothesis.
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