AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 000:000–000 (2005)
Linear Enamel Hypoplasias as Indicators
of Systemic Physiological Stress: Evidence
From Two Known Age-at-Death and Sex Populations
From Postmedieval London
T. King,1* L.T. Humphrey,1 and S. Hillson2
1
2
Human Origins Group, Department of Palaeontology, Natural History Museum, London SW7 5BD, UK
Institute of Archaeology, University College London, London WC1H 0PY, UK
KEY WORDS
linear enamel hypoplasias; dental defects; dentition; perikymata; developmental
stress; early environment; growth; morbidity; mortality
ABSTRACT
Enamel hypoplasias are useful indicators of systemic growth disturbances during childhood,
and are routinely used to investigate patterns of morbidity and mortality in past populations. This study examined the pattern of linear enamel hypoplasias in two different burial populations from 18th and 19th Century
church crypts in London. Linear enamel hypoplasias on
the permanent dentitions of individuals from the crypt
of Christ Church, Spitalfields, were compared to enamel
defects on the teeth of individuals from St. Bride’s. The
method used involves the identification of enamel defects
at a microscopic level, and systemic perturbations are
detected by matching hypoplasias among different tooth
classes within each individual. The pattern of linear
enamel hypoplasias was contrasted between individuals
from the burial sites of Spitalfields and St. Bride’s,
between males and females, and between those aged less
than 20 years of age and those aged over 20 years at
death. Six different parameters were examined: frequency of linear enamel hypoplasias, interval between
defects, duration of hypoplasias, age at first occurrence
of hypoplasia, age at last occurrence of hypoplasia, and
the percentage of enamel formation time taken up by
growth disturbances. All individuals in the study displayed linear enamel hypoplasias, with up to 33% of
total visible enamel formation time affected by growth
disruptions. Multiple regression analysis indicated a
number of significant differences in the pattern of
enamel hypoplasias. Individuals from Spitalfields had
shorter intervals between defects and greater percentages of enamel formation time affected by growth disturbances than did individuals from St. Bride’s. Females
had greater numbers of linear enamel hypoplasias,
shorter intervals between defects, and greater percentages of enamel formation time affected by growth disturbances than males. There were also differences in the
pattern of enamel hypoplasias and age at death in this
study. Individuals who died younger in life had an earlier age at first occurrence of enamel hypoplasia than
those who survived to an older age. The pattern of
enamel hypoplasias detected in this study was influenced by tooth crown geometry and tooth wear such that
most defects were found in the midcrown and cervical
regions of the teeth, and greater numbers of defects were
identified on the anterior teeth. Differences in sensitivity
of the parameters used for the detection of enamel
hypoplasias were found in this study. The percentage
of visible enamel formation time affected by growth
disturbances was the parameter that identified the
greatest number of significant differences among the
subgroups examined. Am J Phys Anthropol 000:000–000,
2005. ' 2005 Wiley-Liss, Inc.
Enamel hypoplasias are deficiencies in enamel
thickness or quantity of enamel that are initiated
during enamel matrix secretion (Goodman and
Rose, 1990; Skinner and Goodman, 1992). They
occur when a wider-than-normal band of ameloblasts (enamel-secreting cells) ceases matrix production early, resulting in the formation of pits,
furrows, or even entire areas of missing enamel
(Hillson and Bond, 1997). Linear enamel hypoplasias (furrow form defects) are produced when a
broader-than-normal band of ameloblasts ceases
matrix secretion at each perikymata groove. They
are recognized as a disruption in the contour of the
tooth crown surface resulting from an increased
spacing between perikymata (King et al., 2002).
Systemic growth disruptions can be identified by
matching linear enamel hypoplasias across different tooth classes with overlapping developmental
schedules (Hillson, 1992, 1996; King et al., 2002;
Malville, 1997). Such markers are considered to be
nonspecific indicators of systemic stress suffered
#
2005 WILEY-LISS, INC.
Grant sponsor: Wellcome Trust; Grant sponsor: English Heritage;
Grant sponsor: Nuffield Trust.
*Correspondence to: T. King, Human Origins Group, Department
of Palaeontology, Natural History Museum, Cromwell Road, London
SW7 5BD, UK. E-mail: [email protected]
Received 13 August 2003; accepted 5 March 2004.
DOI 10.1002/ajpa.20232
Published online in Wiley InterScience (www.interscience.wiley.com).
2
T. KING ET AL.
during the period of tooth crown formation (Duray,
1996; Goodman and Rose, 1990). Enamel defects
that cannot be matched across teeth may be
caused by localized traumas or infections rather
than by systemic growth disruption (Hillson, 1992;
Malville, 1997).
The examination of enamel hypoplasias has
advantages over other indicators of developmental
disruption. First, since enamel does not remodel, it
provides a more permanent record of developmental disruption during infancy and childhood than
osteological indicators (Goodman and Rose, 1990).
Second, it is possible to quantify the frequency, age
of occurrence, duration, and periodicity of enamel
defects (King et al., 2002) and make comparisons
between populations or other social and demographic groups.
In recent years, numerous studies have focused
on enamel hypoplasias as indicators of developmental disruption in past populations. Several different
issues have been addressed, including the relationship between enamel defects and age at death
(Cucina, 2000; Duray, 1996; Goodman et al., 1980;
Malville, 1997; Palubeckaite et al., 2002; Saunders
and Keenleyside, 1999; Šlaus, 2000; Stodder, 1997),
comparisons between males and females (Duray,
1996; Lanphear, 1990; Lovell and Whyte, 1999;
Malville, 1997; Palubeckaite et al., 2002; Saunders
and Keenleyside, 1999; Šlaus, 2000; Van Gerven
et al., 1990), comparisons between individuals of
differing social status (Palubeckaite et al., 2002),
comparison between population groups (Hutchinson
and Larsen 1988; Keenleyside, 1998; Wood, 1996),
diachronic change (Cucina, 1999; Goodman et al.,
1980; Hutchinson and Larsen, 1988; Lovell and
Whyte, 1999; Malville, 1997; Manzi et al., 1999;
Šlaus, 2000; Wright, 1997), and comparison
between individuals with and without evidence of
skeletal infection (Stodder, 1997).
Early studies have also focused on the frequency
of enamel defects (e.g., Blakey and Armelagos,
1985; Goodman and Armelagos, 1988; Rose et al.,
1978). Although these can be obtained independently of tooth formation schedules, there is a risk
of including defects that are caused by local rather
than systemic factors. Other studies have attempted to establish the chronology of growth-disruption
events by relating the position of a hypoplastic
event on the enamel surface to tooth formation
chronologies (e.g., Blakey and Armelagos, 1985;
Ensor and Irish, 1995; Goodman et al., 1980, 1984,
1987; Lanphear, 1990; Rose et al., 1985; Saunders
and Keenleyside, 1999). The traditional method
involves using population averages for the age of
onset and completion of tooth crown calcification to
determine the age range during which a tooth
crown forms. The tooth crown was then divided
into a number of equal-sized increments considered
to reflect a standard time interval (usually 6 months).
Enamel defects are assigned to one of these time
intervals by measuring the distance between the
midpoint of the defect and the cemento-enamel junction (e.g., Goodman et al., 1980).
The age of occurrence and periodicity of stress
episodes can be more reliably determined by reference to tooth formation schedules, such as those
presented by Malville (1997) or Reid and Dean
(2000), which take hidden (appositional) enamel
into account. Nevertheless, these techniques still
rely on average tooth crown formation schedules
that will typically have been generated in a different population from that being studied. In addition, with worn teeth it is still necessary to use
population averages for tooth crown height to infer
the age of occurrence (e.g., Malville, 1997; Saunders and Keenleyside, 1999). A more exact chronology can be obtained relating the position of each
defect to incremental structures at the enamel surface (Hillson and Bond, 1997; King et al., 2002).
Studies have examined the internal surface of
enamel only visible in tooth crown sections, such
as Wilson lines or accentuated striae of Retzius,
and found a relationship between these histological
structures and defects visible at the crown surface
(e.g., Goodman and Rose, 1990). A recent study
determined an exact chronology for enamel growth
disruptions in a deciduous tooth from the church
crypt of Christ Church, Spitalfields, also found a
clear relationship between disruptions that can be
seen through inspection of the internal histology of
the tooth and defects visible on the external surface of the tooth crown (Hillson et al., 1999).
In this paper, we present a detailed evaluation of
the chronological distribution of linear enamel hypoplasias (LEH) in the permanent dentitions of individuals buried in the crypts of Christ Church, Spitalfields, and St. Bride’s Church, London, UK. Interments in both crypts date from the 18th and 19th
centuries and reflect a population that lived through
a period of unprecedented social and economic
change. This study develops individual chronologies
for the formation of LEH by relating the position of
defects to perikymata, and uses dental formation
schedules to match defects across teeth. The use of
these individual chronologies makes it possible to
quantify and compare a wider range of parameters
than those of previous studies. The purpose of the
present study is to investigate variation in the
expression of LEH within and between samples of
individuals from these two sites.
MATERIALS AND METHODS
The sample was drawn from the 18th and 19th
century London crypts of Christ Church, Spitalfields, and St. Bride’s Church. The permanent dentitions of 24 individuals from Spitalfields and 10
individuals from St. Bride’s were examined. The
individuals included in the sample, as well as their
actual or estimated age at death and sex, are listed
in Table 1. The age at death of these individuals
ranges from 9–39 years. Males and females are
Estimated age at death.
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
Spitalfields
St. Bride’s
St. Bride’s
St. Bride’s
St. Bride’s
St. Bride’s
St. Bride’s
St. Bride’s
St. Bride’s
St. Bride’s
St. Bride’s
2070
2139
2142
2156
2175
2296
2301
2308
2465
2601
2605
2655
2667
2677
2708
2721
2747
2752
2755
2777
2854
2890
2895
2903
10/182
12/183
1/53
18/89
43/1
46/96
48/89A
5/113
67/48
72/114
1
Place of
burial
Specimen
number
35
10
27
161
15
39
35
19
26
241
19
321
30
12
37
14
26
17
16
241
321
321
321
19
18
29
14
17
25
17
9
14
21
23
Age at
death
Female
Male
Female
Male
Female
Female
Female
Female
Female
Male
Female
Male
Female
Female
Female
Female
Female
Female
Male
Male
Male
Male
Male
Male
Female
Female
Female
Male
Female
Male
Male
Male
Male
Female
Sex
12
11
4
7
13
9
13
13
12
8
10
8
12
11
13
8
6
14
11
10
2
3
9
9
11
9
19
8
4
7
13
10
5
9
No. of
defects
38
38
22
36
48
28
43
36
38
24
37
23
30
31
53
28
34
55
36
39
7
11
37
30
39
30
65
25
15
22
22
38
18
32
No. of
perikymata
disrupted
3.2
3.3
5.4
4.7
3.7
3.1
3.3
2.8
3.5
3.6
3.7
3.8
2.5
2.8
4.1
3.5
5.7
3.9
3.3
3.3
3.8
3.2
3.5
3.3
3.6
3.4
3.4
3.8
3.6
3.1
3.4
3.8
3.5
3.5
Mean duration
(perikymata)
29
30
49
42
33
28
30
25
32
32
33
34
23
25
37
32
51
35
30
30
34
29
32
30
32
30
31
34
33
28
31
34
32
32
Mean
duration
(days)
11.7
9.7
12.8
20.3
10.5
17.2
7.5
6.9
7.6
17.8
10.6
12.5
12.9
10.8
10.1
10.1
12.8
8.2
13.1
13.0
13.7
16.6
12.6
12.5
13.2
17.6
9.8
27.3
12.5
18.6
9.2
9.9
17.8
10.8
Mean
interval
(perikymata)
TABLE 1. Enamel defect parameters observed for each individual included in study
105
87
115
183
95
155
68
62
68
160
95
113
116
97
91
91
115
74
118
117
123
149
113
113
119
158
89
246
113
168
83
89
160
97
Mean
interval
(days)
2.0
1.7
2.8
1.7
1.2
2.2
1.6
1.4
1.9
1.7
1.8
1.9
1.8
1.2
2.6
1.5
2.3
2.2
2.3
1.6
2.6
2.0
2.0
1.8
1.5
2.5
1.6
1.4
3.3
1.5
1.2
1.8
2.4
2.0
Age
at first
defect
5.2
4.2
3.8
4.6
3.8
5.6
3.6
3.4
3.9
3.3
4.2
2.5
5.4
4.2
5.6
3.2
3.5
4.8
5.7
5.9
2.8
2.9
4.8
4.2
4.5
6.1
6.3
4.7
4.4
4.2
3.8
3.9
4.1
4.1
Age
at last
defect
20
15
19
19
25
19
31
26
23
14
20
11
17
19
33
20
26
29
19
23
5
9
19
14
25
13
21
8
9
8
11
18
8
16
%
growth
4
T. KING ET AL.
equally distributed between the two populations.
Sex and age at death are known for all 10 individuals from St. Bride’s (Scheuer and Black, 1995).
The Spitalfields sample included 17 individuals
from the coffin plate sample. These individuals
could be securely identified from an associated coffin plate, which typically records name, date of
death, and age at death. This information enabled
many individuals in the coffin plate sample to be
traced in other historical sources, which allowed
details to be verified and provided additional bibliographic information (Molleson and Cox, 1993).
Sample size was restricted by the number of
young adults with relatively complete unworn dentitions available for study. The Spitalfields coffin
plate sample included comparatively few suitable
dentitions from young adult males. Sample size
was increased by including seven individuals from
the unidentified part of the collection. All seven
individuals were classified as young adult males,
using standard morphological criteria (Molleson
and Cox, 1993). A more precise estimation of age
at death was established for these seven unnamed
individuals by including them in a series of males
of known age from Spitalfields and St. Bride’s that
was seriated according to development of the postcranial skeleton. The youngest unnamed individual
was assigned an age at death of 16 years, with an
estimated error of 62 years, based on the state of
fusion of the long bones, calcaneus, scapula, pelvis,
and sacrum. Two individuals exhibited partial
fusion of the medial epiphysis of the clavicle. This
stage was observed in identified males aged
between 21–26 years, and these individuals were
assigned an age at death of 24 years with an estimated error of 63 years. The medial epiphysis of
the clavicle was fully fused in four individuals, a
state that was not observed in any male younger
than 28 years in the sample studied. These four
individuals were compared to a sample of males
aged between 28–37 years, and although a number
of developmental parameters were examined, it
was not possible to consistently subdivide this
group on the basis of skeletal maturation. These
four individuals were assigned an age at death of
32 years, with an estimated error of 65 years.
Replicas of teeth were made using Coltène President’s Jet Light Body Plus and Araldite (MY 753
epoxy resin and XD 716 hardener). A 20-nm coating of gold palladium was applied to the casts
using a Cressington 208HR sputter coater. The
coated replicas were used for light microscopy in
addition to electron microscopy, since a reflective
coating renders the incremental structures more
visible than does enamel (Hillson, 1992, 1996). A
sequence of photomicrographs of the labial surfaces
of the replicas from the crown cervix to the apex
were taken for each tooth, using a Philips XL30 FEG
in secondary electron mode at 50 magnification.
The methods for identification and verification of
LEH used in this study are detailed in King et al.
(2002). LEH are defined as a variation in the spacing and prominence of the perikymata, and thus
LEH are a band of the crown surface in which
there is a greater spacing between perikymata
than would be expected for that region of the
crown. In this study, LEH were identified using
perikymata spacing profiles generated using an
engineer’s microscope, as well as visual inspection
of both the tooth crown replicas using a binocular
microscope and the scanning electron microscope
(SEM) micrographs. A Union measuring microscope fitted with gauges that provided digital computer input was used to record spacing profiles.
Two coordinates for each perikymata groove along
a profile of the crown were recorded. The X coordinate measured the distance from the cusp tip. The
Z coordinate was taken at right angles to the
X coordinate and represented the topography of
the crown. The two coordinates were entered for
each perikymata groove into an Excel worksheet,
and these were used to calculate a perikymata spacing profile. This method was supported by visual
examination of the tooth replicas under a lowpower stereomicroscope and photomicrographs
taken using the SEM. Six tooth types that overlap
in their developmental schedules were included in
the study: first and second incisors, canine, premolar, and first and second molars.
To qualify as LEH, defects were matched between at least two different tooth classes in the
same individual (Fig. 1). This ensured that the
observed disruption was caused by systemic disturbances rather than localized trauma. Since different tooth types develop at varying times, enamel
defects will be located at different sites on the
crown surface (Hillson, 1992, 1996). Recently published tooth crown developmental schedules estimating the age at which different areas of the
tooth crown are formed were used for preliminary
LEH matches between teeth (Reid and Dean,
2000). The first perikymata visible at the crown
surface in the human dentition appear on the
lower central and lateral incisors at about 1 year
of age, with increments on the upper central incisor appearing shortly after this at approximately
1.1 years of age. The latest forming incremental
structures are visible at about 6 years of age on
the surface of the lower canine (excluding third
molars).
Several parameters were examined once the
matches had been made. Frequency of growth disruptions was calculated for each individual. The
duration of each LEH episode was recorded, and
this was expressed as the number of perikymata
affected by a growth disruption. The interval
between successive defects, from the beginning of
one LEH to the start of the next, was recorded.
Lastly, the total amount of dental formation time
taken up by growth disruptions was also determined. This was expressed as total number of
perikymata affected as a percentage of total
LEH IN POSTMEDIEVAL LONDON
5
Fig. 1. SEM images of (a) lower central and (b) lateral incisors, (c) lower canine, (d) lower third premolar, and (e) lower first
molar in individual 2721 from Spitalfields. Arrow indicates one enamel defect that was matched in each of these five tooth types.
Position of defect (arrow) varies on each tooth due to fact that these teeth vary in developmental schedules. Appearance of defects
is influenced by tooth crown geometry, perikymata spacing, and illumination under microscope.
number of perikymata in the spacing sequence for
each individual.
The timing of LEH events was calculated using
estimations for the timing of perikymata forma-
tion. A 9-day perikymata periodicity interval was
used in this study, which represents an average for
the variation generally seen in human populations
(Fitzgerald and Rose, 2000; Hillson, 1996). Individual
6
T. KING ET AL.
growth disruption chronologies were developed for
each dentition to describe the sequence and timing
of LEH events experienced by that person. The
determination of the age at which defects occurred
involves the use of crown formation schedules of
the anterior teeth (Reid and Dean, 2000) and
assumes a perikymata periodicity of 9 days. Reid
and Dean (2000) presented averages for the
amount of appositional enamel that is present
beneath the cusp tips in each anterior tooth, based
on samples of between 13–39 teeth for each tooth
type. These data were used to establish a baseline
for the LEH sequences recorded in this study.
Where possible, the upper central incisor was used,
since enamel visible at the crown surface appears
earliest in this tooth. However, the use of this
tooth depended on its being present and the state
of enamel preservation; if necessary, another anterior tooth was used.
The age at onset of earliest occurring LEH in
each individual was calculated by counting the
number of perikymata present between the cusp
tip and the first recorded defect, converting this
into days, and adding this to the average age in
days at which enamel becomes visible at the crown
surface on that tooth. The age of occurrence of the
second and subsequent defects was calculated by
adding the number of days between defects (duration plus interval) to the age of occurrence of the
previous defect. Although all calculations were
made in days, ages were converted into years by
dividing by 365.
RESULTS
All individuals in the Spitalfields and St. Bride’s
samples displayed LEH (Table 1). The frequency of
LEH ranged from 2–19 defects per individual.
Mean interval between episodes of LEH varied
from 6.9–27.3 perikymata, which represent intervals of between 62–246 days. The mean duration
of growth disruptions ranged from 2.5–5.7 perikymata, representing durations of between 23–51
days. The total number of perikymata that were
affected by growth disturbances varied from 7–55
perikymata for each person. Defects represent
growth disruption for between 5–33% of the visible
enamel formation time in the individuals studied.
The age of individuals when enamel defects first
occurred varied from 1.2–3.3 years of age, while
age at last defect ranged from 2.5–6.3 years of age.
The average age profile of enamel defects across
individuals examined in the study is shown in
Figure 2 and Table 2. The highest frequencies of
enamel growth disruptions occur between ages
2–4 years, with an average of more than three
events per year occurring in this age range. This
pattern is observed in males and females and in
individuals dying before and after age 20 years.
Males and females exhibit extremely similar age
profiles, but the frequency of LEH in males is
Fig. 2. Frequency distribution of LEH matched across six
permanent teeth. a: Comparison of females (circles) and males
(triangles). b: Comparison of Spitalfields (circles) and St. Bride’s
(triangles). c: Comparison of individuals under 20 years old (circles) and over 20 years old (triangles). Average number of
enamel defects shown for 1-year age categories between ages
1–7 years.
lower in every age group, and this is particularly
evident between ages 2–6 years. The average profile
between ages 1–5 years for individuals who were
older than 20 years at death is similar to that of individuals who were younger than 20 years at death,
but the frequency of LEH is consistently lower in
older age group between ages 1–5 years. Individuals aged over 20 years at death have a slightly
7
LEH IN POSTMEDIEVAL LONDON
1
TABLE 2. Age profile of enamel defects in total samples and subsets based on place of burial, sex, and age at death
Age range in years
Average number of defects
Total sample
Spitalfields
St. Bride’s
Females
Males
Under 20 years
Over 20 years
Sample size
1–1.99
2–2.99
3–3.99
4–4.99
5–5.99
6–6.99
34
24
10
19
15
16
18
0.97
0.92
1.10
1.00
0.93
1.63
0.39
3.24
3.50
2.60
3.53
2.87
3.63
2.89
3.06
2.92
3.40
3.42
2.60
3.63
2.56
1.47
1.38
1.70
1.74
1.13
1.75
1.22
0.50
0.50
0.50
0.79
0.13
0.31
0.67
0.06
0.00
0.20
0.11
0.00
0.06
0.06
1
Average number of enamel defects are shown for 1-year age categories between 1–7 years of age. Relatively few defects appear in
6–7-year age range, as no perikymata sequences extended into this age range.
TABLE 3. Multiple regression analysis of enamel growth disturbances1
Predictor variables (significance of t)
Parameter
Significance of F
Sex
Place of burial
Age at death
Frequency of defects
Average duration
Average interval
Age at first defect
Age at last defect
% growth affected
0.0342
0.9613
0.0077
0.0095
0.4124
0.0001
0.0079
0.8718
0.0043
0.7856
0.2504
0.0001
0.7032
0.7466
0.0467
0.2322
0.2268
0.0063
0.0778
0.8167
0.0909
0.0012
0.6437
0.2832
1
Significant differences are indicated in bold. Variables examined were number of events, average duration of events, average interval between events, age at first event, age at last event, and proportion of total enamel formation time affected by LEH. Three predictor variables were sex, age-at-death in years, and place of burial (Spitalfields or St. Bride’s).
higher prevalence of LEH when they were aged
between 5–6 years than the younger age group. The
samples from Spitalfields and St. Bride’s both exhibit a peak frequency of LEH between 2–4 years, but
the overall profile is shifted toward the right in the
St. Bride’s sample, such that frequency of LEH is
highest at 3–4 years as compared to 2–3 years in the
Spitalfields sample.
Multiple regression analysis was carried out to
investigate whether sex, age at death, or place of
burial predicted variation in the occurrence LEH
within the 34 individuals examined. The variables
examined were number of events, average duration
of events, average interval between events, age at
first event, age at last event, and proportion of
total enamel formation time affected by LEH. Significant linear relationships with the predictor
variables were observed for four of these parameters (Table 3). Place of burial predicted variation in two of six parameters examined. Individuals from Spitalfields displayed shorter intervals
between LEH and had a greater amount of their
dental formation times disturbed by enamel
growth disruptions than individuals from St.
Bride’s. Differences between males and females
were indicated for the three parameters. Females
displayed higher frequencies of LEH and a greater
proportion of disrupted enamel growth than males.
In addition, there were shorter intervals between
growth disruptions in females than males. Age at
death predicted variation in only one of six parameters examined. The age at first occurrence of
LEH was earlier in those who died at a younger
age. The analysis was repeated using 5-year age
categories due to the possible error associated with
the estimated age at death of seven individuals in
the sample. In all but one analysis, the same significant outcomes were obtained. The difference
between the two sites in intervals between LEH
was no longer significant when age categories were
used.
DISCUSSION
Tooth crown geometry
Previous studies report a higher prevalence of
enamel defects on the anterior teeth than on the
posterior teeth (El-Najjar et al., 1978; Goodman
and Armelagos, 1985; Goodman and Rose, 1990).
Goodman and Armelagos observed a higher prevalence of defects on the mandibular canine and
maxillary central incisor than on other teeth.
Within the anterior dentition, Saunders and Keenleyside (1999) found that the mandibular canines
displayed the highest frequencies of defects, followed by the maxillary canines and maxillary central incisors. Goodman and Armelagos (1985) suggested that the variation in occurrence of enamel
defects in different tooth types cannot be fully
accounted for by variation in the timing and duration of tooth crown formation in different teeth.
They noted that areas of enamel forming at the
same time on different teeth do not record hyploplasias to the same degree. These authors suggested that polar teeth in developmental fields are
more susceptible to hypoplasias than nonpolar
teeth, and suggested that teeth that are more
8
T. KING ET AL.
developmentally stable are more susceptible to
ameloblastic disruption.
Traditional methods for inferring the chronology
of enamel defects divide each tooth crown into
equal-sized zones that are considered to represent
half-year time intervals. These techniques are
based on the assumption that an increase in tooth
length occurs at a constant rate, in contrast to
other studies indicating that the rate of tooth
crown extension slows throughout the period of
enamel growth (Liversidge et al., 1993). Additionally, a variable number of enamel layers are hidden in the appositional zone of a tooth crown, and
this period of enamel growth is not accounted for
using traditional recording techniques (Hillson and
Bond, 1997). Hillson and Bond (1997) found that
when enamel defects are matched across teeth, the
size and prominence of defects resulting from a
single growth disruption vary between different
teeth forming at the same time. This reflects the
gradient of perikymata spacing on different parts
of the tooth crown and on different tooth types.
Defects are more difficult to identify on molar
teeth due to the steep gradient in perikymata spacing on molar crown surfaces. Furthermore, molar
teeth have more appositional enamel, so a smaller
proportion of enamel growth is represented at the
crown surface (Hillson and Bond, 1997). The theory that teeth differ in their susceptibility to systemic growth disruptions (Goodman and Armelagos,
1985) needs to be tested within a more accurate
chronological framework. Differences in frequencies
of enamel defects recorded on different teeth may
result from a combination of factors such as variation in the timing and duration of tooth crown formation, variation in the proportion of enamel layers
hidden in the appositional zone, and tooth crown
geometry.
The present study found that enamel defects
were more evident in the anterior teeth than the
posterior dentition, and it was easier to match
defects among anterior teeth. It was also difficult
to match defects identified on posterior teeth with
those on anterior teeth; second molars presented
the most difficulties. Table 4 displays the total
frequencies of defects identified in all teeth, and
these data are compared with matches made
between at least two anterior teeth, between two
or more posterior teeth, and between at least one
anterior and one posterior tooth. The highest frequencies of defects matched in at least two teeth
were achieved for the anterior teeth. However, it
should be borne in mind that although the different tooth types included in this study overlap in
their developmental schedules, it was often the
case that defects identified toward the end of formation of visible enamel on a particular tooth type
(e.g., a canine) were not visible on posterior teeth
(e.g., premolars and first molars), simply because
enamel formation in these teeth had already
ended. Another problem was that calculus was
often present on teeth and presented a particular
problem on the posterior teeth; thus defects were
often obscured and could not be matched with
those visible on the anterior teeth.
Defects were concentrated at midcrown and
toward the crown cervix in all teeth examined.
Goodman and Rose (1990) also noted that macroscopically visible hypoplasias are more common in the
middle and cervical thirds of teeth. This is related to
the decreased spacing between perikymata toward
the crown cervix, making hypoplastic events more
evident in these regions of the crown than near the
occlusal edge. It also reflects differential exposure
to wear of different parts of the tooth crown. Loss
of tooth enamel through wear leads to a reduction
in tooth crown height and the complete loss of evidence of enamel defects on that part of the tooth.
In addition, perikymata are worn away from all
areas of the crown surface during an individual’s
life, making it difficult, and sometimes impossible,
to see the incremental structures. While it is possible to find some older individuals who preserve
very clear incremental structures, it is in general
not possible to establish secure LEH chronologies
for individuals over age 40 years. Perikymata that
are situated toward the occlusal surface are more
likely to be obliterated by wear, such that defects
become less prominent or completely disguised. In
some cases, defects that were obliterated on one
tooth may still be detected on earlier-forming
teeth, where they are located more cervically.
Differential sensitivity of parameters
The variables examined in this study have varying utility for determining significant differences
between population groups. Frequency of enamel
defects simply records the number of enamel
defects displayed by an individual. However, an
individual who experienced a large number of
growth disruptions of short duration may in fact
have the same proportion of disrupted enamel
growth as an individual displaying fewer defects
that were longer-lasting. In the same way, duration of the interval between successive defects may
not be truly meaningful, since individuals who
experienced fewer enamel growth disturbances of a
long duration may have a similar mean interval
between defects as an individual with more defects
that were of shorter durations. The proportion of
enamel growth affected by a growth disturbance is
a cumulative record of both the number and duration of individual growth disruptions. In this study,
the percentage of enamel growth affected by a
growth disturbance was the most sensitive parameter for detecting differences within and between
populations and subgroups, since this variable
identified the greatest number of significant differences between groups. Other authors found that
different parameters vary in their ability to iden-
9
LEH IN POSTMEDIEVAL LONDON
TABLE 4. Comparison of frequencies of defects that were identified for individual teeth, compared with numbers
of defects matched between two or more anterior teeth, and two or more posterior teeth,
and in at least two teeth of different types
Specimen
number
Total no. of
defects identified
in all tooth types
in one or more teeth
No. of
defects matched
in two or more
anterior teeth
No. of defects
matched in
two or more
posterior teeth
No. of defects
matched between
anterior and
posterior teeth
No. of
defects matched
in two or more
tooth types
2070
2139
2142
2156
2175
2296
2301
2308
2465
2601
2605
2655
2667
2677
2708
2721
2747
2752
2755
2777
2854
2890
2895
2903
10/182
12/183
1/53
18/89
43/1
46/96
48/89A
5/113
67/48
72/114
17
17
10
10
17
9
15
14
21
6
15
6
16
14
17
16
9
21
19
12
6
8
11
16
13
14
20
17
10
7
15
12
15
15
12
11
3
7
13
9
13
9
12
5
10
6
12
11
10
8
6
14
10
8
2
3
8
9
11
7
19
8
4
8
12
10
5
8
4
0
0
6
3
0
0
0
2
N/A1
0
0
0
0
2
2
0
0
0
5
N/A1
0
0
0
1
3
0
1
0
0
2
1
0
0
8
0
3
6
11
2
0
6
5
3
0
0
0
6
7
4
0
7
1
10
N/A1
3
5
6
11
6
0
5
0
0
13
5
0
6
12
11
4
7
13
9
13
13
12
6
10
6
12
11
13
8
6
14
11
10
2
3
8
9
11
9
19
8
4
7
13
10
5
9
1
Fewer than two posterior teeth were available for study.
tify significant differences between groups in the
amount of LEH. Hutchinson and Larsen (1988)
found more significant differences using the average duration of stress episodes than for frequency
of LEH, and suggested that this represents a more
precise measure of metabolic insult.
The nature of the relationship between number of
perikymata affected by a growth disturbance and the
duration of metabolic insult is not clear. The duration
of growth disturbances may not be a simple reflection
of the number of perikymata involved in a hypoplastic defect. The current study estimates that disruptions to enamel formation could last for as long as 99
days. Although it is theoretically possible for a period
of inadequate nutrition to affect enamel growth for
this length of time, it is not clear how the duration of
an illness might relate to enamel growth disruptions
that last this length of time. One explanation for this
may be that the number of perikymata, and hence
duration of LEH, may reflect the time taken for full
recovery from an event, in addition to the duration
of the growth disruption, and thus may provide a
measure of severity.
Some studies have attempted to match enamel
defects to episodes of short-term illness. Pindborg
(1982, and references therein) reported that in a
group of children with nonspecific gastrointestinal
disease, 23% were found to have enamel hypoplasias. Furthermore, it was possible to match enamel
growth disturbances with bouts of gastrointestinal
disease in 31% of children who presented with these
enamel defects; thus, timing of enamel hyoplasias
was found to correspond to the course of the disease.
Infection with viruses such as rubella was also
linked with the formation of enamel defects,
although evidence is contradictory and study samples are small (see references in Pindborg, 1982).
Variation in distribution of LEH
The assumption that an adult exhibiting LEH
experienced impoverished or less favorable circumstances (including poor nutrition, high levels of
morbidity, and poor individual resistance to illness)
during childhood than an adult with unaffected
teeth is still widely accepted. A study of deciduous
10
T. KING ET AL.
and permanent dentitions of Mexican children
from poorer socioeconomic backgrounds found that
almost 50% of these children displayed one or more
enamel defects (Goodman et al., 1987). Moreover,
prevalence of hypoplasia in this population was 10
times greater than that of other less disadvantaged
groups, thus indicating an association between
impoverished conditions and disrupted enamel formation. Nutrition may play a particularly significant role in enamel defect formation. Goodman
et al. (1991) found a lower rate of linear enamel
hypoplasias in Mexican children who had received
nutritional supplements than in those who had
not. This result was supported by May et al.
(1993), who found a lower prevalence of enamel
hypoplasias in Guatemalan children who had been
given a high level of nutritional supplementation
compared with less supplemented children. Infante
and Gillespie (1974), in contrast, did not find a
reduced prevalence of enamel hypoplasias in Guatemalan children who had received protein supplements. However, it is possible that overall calorific
requirements for normal growth and development
were not achieved in these children through this
type of supplementation, and hence, growth arrests
did not decrease. A seasonal pattern to the prevalence of defects was found and may be related to
variation in diet or other environmental factors.
The authors suggested that acute diarrheal disease
or factors linked to diarrhea may account for the
seasonal distribution of defects. In addition,
Infante and Gillespie (1974) found that prevalence
of hypoplasia was higher among younger siblings
of affected individuals than in the population in
general, underlining the possible role of diarrheal
disease as a cause of enamel hypoplasias in this
population. The relationship between poor nutrition and increased prevalence of enamel growth
disturbances was further supported by a study of
individuals who experienced the Chinese famine of
1959–1961 (Zhou and Corruccini, 1998). A higher
prevalence of LEH was detected in individuals
whose teeth were developing during the famine
years than in those whose teeth were not forming
during this time. In addition, the study found that
defect frequency was higher in individuals who
were living in rural areas compared with urban
dwellers, and this pattern is associated with poorer
nutrition and standards in rural populations.
There is an increasing realization that drawing
conclusions about the general health of different
individuals and populations based on the quantification of LEH in osteological assemblages is not
straightforward (Wood et al., 1992). The presence
of LEH is evidence that an individual experienced
and survived a growth disturbance and resumed
normal enamel formation. This suggests that an
individual displaying LEH was able to survive
childhood environmental insults, and this in turn
suggests that the affected individual represents
a more advantaged section of society than those
individuals who did not survive such events.
Extrapolating from this, a population exhibiting a
high prevalence of LEH may have experienced a
better overall health status than a population exhibiting lower levels, as a low prevalence may be associated with high childhood mortality. Furthermore,
if the better health of an advantaged group results
in higher fertility as well as higher survivorship, the
mean age at death of skeletons from an advantaged
group would be lower than that of a disadvantaged
group with higher mortality and lower fertility
(Wood et al., 1992). This in turn would produce a
pattern of age-related variation in the prevalence of
LEH in a population comprised of relatively advantaged and disadvantaged groups of individuals
with differing levels of mortality and fertility. This
perspective suggests that comparison of LEH frequencies between populations or between particular demographic groups within a population should
not be undertaken independently of other indicators of morbidity and mortality.
Several studies have compared the prevalence of
enamel defects in individuals in different age categories as a way of investigating the relationship
between developmental stress and longevity (Goodman, 1996; Rudney, 1983; Simpson et al., 1990;
Šlaus, 2000; Stodder, 1997). Stodder (1997) carried
out a detailed analysis of the relationship between
the occurrence of dental enamel defects and age at
death for individuals from Latte Period sites on
Guam. At that site, juveniles (under 16 years) had
a lower frequency of enamel hypoplasias than
adults, and adults over 21 years had fewer hypoplasias than young adults. Other studies have
recorded a difference in prevalence of hypoplasia
between those who died during childhood and
those who survived into adulthood. Subadults from
two skeletal samples from Lower Nubia had significantly higher levels of enamel growth disturbances (accentuated striae of Retzius) than adults,
indicating that individuals displaying evidence of
exposure to stress during the period of tooth crown
formation suffered higher juvenile mortality than
the population as a whole (Rudney, 1983). Subadults from a Late Medieval sample from central
Croatia had significantly higher frequencies of
LEH in the central maxillary incisor than adults,
despite relatively low dental attrition (Šlaus,
2000). Juveniles from Santa Catalina de Guale had
a higher frequency of enamel defects than adults,
but the difference between juveniles and adults
was not significant (Simpson et al., 1990). Cucina
(2002) examined LEH in the mandibular canines
from 11 Italian sites, but observed significantly
higher frequencies of LEH in subadults (under 20
years) than adults in only two of the samples
examined. Malville (1997) found no significant differences between adults and subadults in the timing of hypoplasias or in the percentages of teeth
and individuals affected in ancestral Puebloan
populations from southwestern Colorado.
LEH IN POSTMEDIEVAL LONDON
An alternative strategy for investigating the
relationship between developmental stress and
longevity is to compare mean age at death of
adults with and without enamel defects (Duray,
1996; Goodman, 1996; Goodman and Armelagos,
1988; Palubeckaite et al., 2002; Rose et al., 1978;
Saunders and Keenleyside, 1999). Several such studies have found significantly lower mean ages at
death among adults exhibiting enamel defects than
in unaffected adults (Duray, 1996; Goodman, 1996;
Goodman and Armelagos, 1988; Rose et al., 1978).
For example, among adults from a Late Medieval
urban population from Lithuania, those with more
numerous and more marked LEH had a lower age
at death than those with fewer or less severe
enamel defects (Palubeckaite et al., 2002). Other
studies have found no significant difference in age
at death between individuals with and without
enamel defects (Saunders and Keenleyside, 1999).
Several different hypotheses were proposed to
account for the association between LEH and early
age at death observed in some past populations
(Duray, 1996; Goodman and Armelagos, 1988;
Humphrey and King, 2000; Wood et al., 1992).
Firstly, individuals within a population may differ
in their susceptibility to the effects of certain types
of stress factors, with some individuals suffering a
lifelong pattern of poor health that results in the
presence of LEH and early mortality. Secondly, disadvantaged individuals within a population are
exposed to a lifelong pattern of deprivation due to
the persistence of poor environmental circumstances throughout their lifetime, and these individuals exhibit more LEH and suffer premature mortality. Thirdly, individuals who are exposed to prenatal or early childhood stress, as evidenced by the
presence of LEH, may be ‘‘biologically weakened’’
so as to increase their susceptibility to factors
resulting in early mortality. This hypothesis complements an growing body of research indicating
that events in early life can have long-term consequences for health and mortality (Cameron and
Demerath, 2002; Barker and Osmond, 1986, 1987;
Henry and Ulijaszek, 1996). Each of these three
hypotheses assumes that those exhibiting LEH
represent individuals within a population who
were either culturally or biologically disadvantaged. It is also possible that individuals with LEH
have a lower age at death on average than individuals without defects because they are drawn from
a relatively advantaged group in the population
who enjoyed low mortality and high fertility (Wood
et al., 1992).
A particular concern for researchers investigating age-related variation in the occurrence of LEH
is the possibility that wear may obliterate enamel
defects (King et al., 2002; Šlaus, 2000). Since the
earliest-forming defects, which are expressed on or
close to the occlusal surface of the crown, are those
most susceptible to wear, there may be a particular
bias toward underscoring of earlier-forming LEH
11
in older individuals. A significant age-related trend
was found in only one of six parameters examined
here. The age of occurrence of earliest recorded
enamel defect increases with age at death. Individuals who died before age 20 years also have a
higher frequency of LEH, a slightly shorter interval between events, and a higher percentage of
enamel formation time affected. However, these
differences are not significant and may be confounded by differences in the age distribution of
males and females and of individuals buried at the
two different sites. The particular pattern of agerelated trends exhibited here could be explained by
the gradual and successive obliteration of earlyforming LEH following tooth emergence as a result
of tooth wear and abrasion.
Several studies of archaeological samples have
reported a higher prevalence of LEH in boys than
in girls (Palubeckaite et al., 2002; Saunders and
Keenleyside, 1999; Van Gerven et al., 1990). Other
studies have found a higher prevalence of LEH in
girls (Šlaus, 2000) or no significant difference
between sexes (Duray, 1996; Goodman et al., 1980;
Lanphear, 1990; Lovell and Whyte, 1999; Malville,
1997). Interpretation of differences in prevalence of
LEH between males and females in past populations is particularly complex, due to the interaction
of several different parameters. Males and females
may differ in vulnerability to environmental stress
or their teeth may record insults differently, and
they may be exposed to different levels of stress as
a result of cultural preferences for male or female
children. A higher prevalence of LEH in males is
often interpreted within the framework of their
greater sensitivity to environmental stressors.
Females show greater resistance to infectious disease, parasites, and famine than do males, but
overall the evidence for increased female buffering
against environmental stressors in postnatal life is
equivocal (Guatelli-Steinberg and Lukacs, 1999;
Stinson, 1985). A recent review of sex differences
in enamel hypoplasias suggested that female buffering does not strongly influence the expression of
defects (Guatelli-Steinberg and Lukacs, 1999). A
higher female prevalence of LEH is interpreted by
some as evidence of greater parental investment in
male children, including provision of better access
to nutritional and medical resources. The idea that
differential treatment of males and females can
influence the expression of LEH is supported by
studies of living children (May et al., 1993).
Another parameter that needs to be considered is
mortality bias, since studies of enamel hypoplasias
include only those individuals who survived
beyond the period of tooth crown formation (Wood
et al., 1992). Palubeckaite et al. (2002) observed a
significantly higher proportion of males with LEH
than females in a 15th–18th century aristocratic
sample from Lithuania. They interpreted this as
evidence of preferential treatment of boys, arguing
that boys had a greater chance of surviving a
12
T. KING ET AL.
particular metabolic insult and developing stress
markers than girls, who were more likely to die during the period of permanent tooth crown formation.
The variation seen in the distribution of enamel
defects in the individuals examined in the London
church crypt samples indicates that surviving
females had suffered more physiological stress
than surviving males. Females had higher frequencies of LEH, indicating more frequent growth disruptions, which is reflected in a shorter duration
between events and a higher percentage of enamel
growth affected. This finding may indicate less
favorable treatment of girls in 18th and 19th century London. Numerous direct and indirect factors
could be involved, including different nursing practices, inequality in access to suitable food and medical resources, and different behavioral expectations, perhaps resulting in reduced exposure to
sunlight in girls. Alternatively, males and females
may have been exposed to similar levels of environmental stressors, with a higher proportion of
males failing to survive for long enough to develop
enamel defects.
The coffin plate sample from Christ Church, Spitalfields, provides a rare opportunity to examine
sex differences in the number of burials at each
stage of life, since the sex of most of these individuals could be inferred from the name or title on
the associated coffin plate. There is an overrepresentation of males compared to females in the coffin plate sample as a whole, but the difference is
accounted for entirely by variation in the number
of male and female children buried in the crypt.
By age 15 years, 24% of males in the sample had
died, compared to only 16.8% of females (Rousham
and Humphrey, 2002). This difference may point
toward a large variation in male and female childhood mortality. However, the mortality profiles for
males and females in the coffin plate sample may
misrepresent the actual number of male and
female deaths at each age. Burial in the crypt of a
church was more expensive than burial in the surrounding churchyard, and was only available to
those whose families were willing and able to
afford the additional expense or to individuals who
had made provision for this prior to death. The coffin plate sample is therefore drawn from families
of higher socioeconomic status than was typical of
the Spitalfields area at that time, and members of
these relatively affluent families were not necessary treated equally in death.
Mortality rates under age 15 years are lower in
the coffin plate sample from Christ Church, Spitalfields, than was typical for London during the 18th
and 19th centuries. Bills of mortality for this period indicate that in the London population as a
whole, 45–57% of recorded deaths were of juveniles
(Molleson and Cox, 1993), whereas only 20.5% of
the coffin plate sample died between birth and
15 years (Rousham and Humphrey, 2002). Part of
this discrepancy may reflect higher socioeconomic
status in the Spitalfields community as a whole,
and in the coffin plate sample in particular, than
was typical of the London population at that time.
It seems likely, however, that children are genuinely underrepresented in the coffin plate sample
because they had not acquired the status that
would warrant a crypt burial. Similarly, the apparent large difference in male and female subadult
mortality in the Spitalfields sample could have
arisen because male children were more likely to
be buried in the crypt than female children (who
may have been buried in the churchyard). It is also
possible that male children buried in the crypt were
more likely to be afforded a coffin plate, thereby
enabling identification. At this stage, we cannot
exclude the possibility that the larger representation of male children in the coffin plate sample from
Spitalfields is an indication of higher male status
rather than higher male mortality. The documented
sample from St. Bride’s has a similar but more
extreme demographic bias than the Spitalfields
sample. Subadults are severely underrepresented
(individuals under age 19 years represent only 6.6%
of the total sample), and whereas the numbers of
adult males and females in the sample are almost
equal, the subadult sample is heavily biased in
favor of males (Scheuer, 1998).
Taken together, the higher frequency of hypoplasias in females and the higher number of male children in samples from Spitalfields and St. Bride’s are
compatible with two alternative explanations.
Firstly, female children may on average have been
exposed to greater environmental stress than male
children as a result of differential treatment, resulting in a higher incidence of enamel growth disruptions. The higher representation of nonsurviving
male children in the high-status coffin plate sample
could also reflect preferential burial treatment of
male children, and it does not necessarily reflect
the actual number of male and female deaths in
childhood. Alternatively, males and females may
have been exposed to similar levels of stress during
childhood, resulting in higher mortality in the
more vulnerable males and a higher frequency of
LEH among female survivors.
The samples from Spitalfields and St. Bride’s
exhibit slightly different patterns of enamel growth
disruptions. Individuals from Spitalfields have a
significantly higher average amount of dental formation time taken up by enamel growth disruptions than individuals from St. Bride’s, and shorter
intervals between LEH. The frequency of LEH
is highest at 3–4 years in the St. Bride’s sample
compared to 2–3 years in the Spitalfields sample,
and this reflects a general shift in LEH distribution toward a higher age range in the St. Bride’s
sample.
It is thought that the relatively high economic
status of families buried in the Spitalfields crypt
would have cushioned them from the effects of
severe weather, food shortages, and price fluctua-
13
LEH IN POSTMEDIEVAL LONDON
tions (Cox, 1996; Molleson and Cox, 1993), and the
same is probably true for those buried in the crypt
of St. Bride’s church. In addition, the children from
these middle-class families were less likely to be
wage earners, and more likely to live at addresses
that afforded less crowded living space and slightly
less unsanitary conditions. Other health risks,
including air pollution and the recurrent problem
of contaminated and adulterated foodstuffs, would
have affected all classes living in London during
this period. Perversely, the infants and children of
the wealthy did not necessarily receive better care
than those from less advantaged families, and
were more likely to be subjected to fashions affecting their treatment and diet. For example, affluent
families were more likely to have employed wet
nurses, or to have introduced the practice of artificial hand feeding that became increasingly popular
in the 18th century, or to follow the fashion of
keeping small children indoors (Cox, 1996). Hand
feeding would have increased the risk of nutritional deficiencies and introduced the risk of infection from contaminated foods and feeding implements at a very early age.
The differences in expression of LEH between
the samples from St. Bride’s and Spitalfields suggest that the risks resulting from these diverse
parameters differed between the two sites. Children from Spitalfields were either at greater risk
of physiological stress or were more able to survive
such events than those from St. Bride’s. These differences may reflect differences in socioeconomic
status, population density, and quality of housing
and amenities between these two areas of London,
or differences in the way in which children were
raised within the two different communities.
Detailed interpretation of these differences would
necessitate a comprehensive investigation of historical records to evaluate the socioeconomic context of each community and to consider additional
demographic and osteological evidence.
Dates of birth for the documented sample from
St. Bride’s ranged from 1676–1850 (Scheuer, 1998),
but those analyzed here were drawn from the more
recent period, with dates of birth between 1780–
1825, and a mean of 1805. Dates of birth for the
Spitalfields coffin plate sample range from 1646–
1844 (Molleson and Cox, 1993), and those analyzed
in this study were born between 1747–1825, with a
mean of 1779. Since the St. Bride’s sample represents, on average, a slightly more recent period
than the Spitalfields sample, differences in the pattern of enamel growth disruptions may also reflect
a change in living conditions during the time period represented by the two samples. However,
when year of birth was added to the regression
model, it did not prove to be a significant predictor
for any of the variables, whereas place of burial
remained a significant predictor of the amount of
enamel affected by growth disruptions and the
interval between LEHs.
CONCLUSIONS
The aim of this study was an investigation of linear enamel hypoplasias (LEH) in individuals buried in two London church crypts during the 18th
and 19th centuries. Differences in a number of
parameters were investigated: between males and
females, age at death, and place of burial. The following conclusions are suggested.
This study found that the parameter that had the
most utility for detecting variation within and
between populations and subgroups was percentage
of enamel growth affected by a growth disturbance.
Tooth crown geometry and wear influenced the
preservation and appearance of LEH. Defects were
concentrated at midcrown and toward the crown
cervix in all teeth examined, while erosion of perikymata from the occlusal regions of the crown
resulted in few defects being identified in this area
in older individuals. Matching of enamel defects in
the postcanine teeth was difficult and in some
cases impossible.
All individuals examined in this study displayed
LEH. These defects represented growth disruptions for up to 33% of the total visible enamel formation time. The earliest age at which enamel
defects first occurred was 1.2 years of age, and the
latest age at which hypoplasias were detected was
6.3 years of age. This reflects almost the entire age
range represented by visible enamel formation in
the six permanent teeth examined.
Age at death predicted variation in one of the
parameters examined in this study. Age at first
occurrence of LEH was earlier in the younger-aged
individuals in the sample. This finding may reflect
real differences in susceptibility to enamel growth
disruptions between younger and older individuals,
or may be an artifact resulting from tooth-wear
processes that result in the obliteration of earlierforming perikymata, and hence earlier defects, in
the older-aged individuals examined.
Significant differences between the two different
burial populations were found. Individuals from
Spitalfields had smaller intervals between enamel
defects and a greater proportion of the visible
enamel formation time affected by growth disturbances than individuals from St. Bride’s. These
variations may reflect differences in socioeconomic
status, standard of living, population density, or
child-rearing practices within these two different
communities. In addition, the differences in the
pattern of LEH displayed between individuals from
these two areas of London may indicate a change
in living conditions, since the St. Bride’s sample is
drawn from a slightly more recent period than the
Spitalfields sample. However, when included in a
multivariate analysis, year of birth did not prove
to be a significant predictor of variation in any of
the parameters examined.
Differences in LEH were also found between
sexes. Surviving females displayed higher frequen-
14
T. KING ET AL.
cies of enamel defects, shorter intervals between
growth disruptions, and greater percentages of
enamel formation time affected by growth disruptions than surviving males. This could indicate
either that female children experienced greater
physiological stress than male children as a result
of differential treatment, or it may reflect similar
levels of exposure resulting in higher mortality in
males and a higher frequency of LEH among
female survivors.
ACKNOWLEDGMENTS
We are grateful to the Canon of St. Bride’s
Church for permission to study the St. Bride’s
osteological collection. We thank Theya Molleson
for her help in interpreting the Spitalfields Project
Archive, and Chris Jones and Alex Ball for advice
and assistance with electron microscopy and preparation of images. We are also grateful to two
anonymous reviewers for their comments on an
earlier version of this paper. The Wellcome Trust
supported this study through a Bioarchaeology Fellowship to T.K. The Spitalfields Archaeological Project was funded by English Heritage and the Nuffield Trust.
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