Katherine Daiy

ANTH 425-500
4/27/2016
Scoring Enamel Hypoplasias and the Chronology of Childhood Stressors

Introduction
Metabolically stressful life events, such as illness and nutritional deficiency, are often
marked by corresponding osteological degeneration. Enamel of the dentition, produced by
appositional layering known as amelogenesis in utero and in childhood, reflects the fluctuations
in metabolic function, or stressors, during early childhood development. An enamel hypoplasia is
a defect caused by a disruption in normal enamel development as a result of metabolic stressors
(Goodman and Rose 1990). The distance of an enamel hypoplasia from the cemento-enamel
junction can be utilized to determine the age at which the defect was formed, and thus to draw
conclusions about pathological and nutritional environments during childhood. The enamel
hypoplasias of a single individual were measured using a regression analysis method outlined by
Goodman and Rose (1990) to determine the chronology of childhood stressors
Background
Enamel is a hard, acellular covering on tooth crowns, and is composed primarily of
inorganic salt (Goodman and Rose, 1990). The substance is formed in amelogenesis, a two-stage
process that initiates enamel development of deciduous and permanent teeth in the sixth week in
utero, and continuing to the eighth year after birth (MacCord 2013). In the first stage, enamelforming cells known as ameloblasts secrete a protein matrix on the cusps of a developing tooth in
response to odontoblast activity in dentin formation. After the organic matrix is formed, the
secretory ameloblasts change functions to form transport ameloblasts that carry organic

material and water out of the matrix, forming the hard, primarily inorganic salt of enamel
(Goodman and Rose, 1990). This calcification results in keyhole-shaped enamel prisms, which
are laid in an appositional manner in 24 hour-cycles to form distinctive, microscopic cross
striations (MacCord 2013). The slowing of enamel secretion is marked by more distinctive lines,
called the striae of Retzius, that form in weekly cycles (MacCord 2013). Though technically
cumbersome, the number of cross-striations or Retzius striae may be used to record the time of
enamel formation (Goodman and Rose 1990){, #22@@hidden}.
The rate of amelogenesis is susceptible to metabolic stressors such as nutrient-deficiency or
illness. Stress-induced enamel deficiency may result in various permanent developmental
defects, such as grooves, lines or pits resulting from decreased enamel thickness, known as
hypoplasias (Wright, 1997). Although enamel hypoplasias may result from genetic inheritance or
localized trauma, they are often manifested as horizontal linear grooves, or linear enamel
hypoplasias (LEH) as a result from systemic metabolic stressors. Since chronologies of enamel
formation are determined by the position of cross-striations, the distance of enamel hypoplasias
from the cement-enamel junction (CEJ) can be used to sequence and illustrate stress-induced
childhood events, such as weaning (Wright 1997). In the cuspal-cervical direction of enamel
formation, earlier events are reflected in cuspal LEHs and later events in more cervically-located
defects (Wright 1997). Anterior teeth, particularly mandibular canines and maxillary incisors, are
more susceptible to hypoplasia formation, possibly as a result of greater genetic influence or
slower rates of enamel formation (Goodman, Armelagos, and Rose 1984).
Methods

To determine the chronology of stress-induced metabolic life events, the distance of

enamel hypoplasias to the cement-enamel junction (CEJ) was measured in millimeters using a
sliding calipher and used in regression equations outlined by Goodman and Rose (1990).
Because hypoplasias are often difficult to distinguish from normal enamel variations, a dental
pick and magnifying glass were used to affirm them. The equations, specific to different tooth
types, calculated the age in years of the individual at the time of the defects formation. The
number for defects per tooth were noted and ages of hypoplastic formation were averaged.
Results

Maxillary
I1
I2
C
P3
P4
M1
M2
Mandibular
I1
I2
C
P3
P4
M1
M2

Left
# of Defects

Table 1. Hypoplasia Data by Tooth Type

Right
Mean Distance from CEJ
Mean Age
# of Defects

Average Distance from CEJ

Mean Age

1
2
1
1
1
1
1

2.35
1.825
2.59
2.31
3
2.58
2.57

3.4
3.8
4.4
4.9
4.6
2.3
5.9

1
2
1
2
1
unobservable
unobservable

2.1
1.27
1.38
0.99
2.93
n/a
n/a

3.5
4.0
5.1
5.5
4.6
n/a
n/a

1
1
2
1
1
1
2

2.42
1.85
1.76
4.86
4.6
2.34
3.02

2.9
3.2
5.5
4.9
6.5
2.9
5.3

1
unobservable
2
1
1
unobservable
unobservable

2.63
n/a
3.47
1.85
2.11
n/a
n/a

2.8
n/a
4.5
4.8
5.6
n/a
n/a

Table 1 outlines the results of LEH defect measurement and calculations. It should be
noted that all defects were present as linear horizontal grooves, with very little variation in shape.
All observable teeth exhibited at least one LEH, with the mandibular canines and maxillary
incisors exhibiting the most (Table 1). The LEHs were typically less than 5 millimeters away
from the CEJ; however, there was no distinctive pattern of defect distance from the CEJ among
tooth types (Table 1). The number of LEH defects per tooth was matched in the left and right
sides of the dental arcade (Table 1). Age of defect formation generally increased anteriorly-

posteriorly, with earlier ages present in anterior teeth. Ages were typically in a 2-6 year range,
with few outliers (Table 1). Dental calculus was omnipresent in the dental arcade, particularly
around the CEJ in posterior teeth, rendering the enamel of a few teeth unobservable (Table 1).
Discussion
The examination of linear enamel hypoplasias yielded a rudimentary chronology of
childhood stressors for the specimen through the differences in formation age between anterior
and posterior teeth, as well as the ages calculated using the regression equations outlined by
Goodman and Rose (1990). It is thought that a greater genetic influence on the anterior teeth is
responsible for their sensitivity to metabolic stressors (Goodman and Rose, 1990), which is
reflected in the results (Table 1). Anterior teeth in both the maxillary and mandibular dental
arcade exhibited earlier ages of LEH formation, indicating the earliest childhood stressors at as
young as 2.8 years of age. Mandibular canines and maxillary incisors had two hypoplasias on
each side of the arcade, the highest number of defects per tooth (Table 1), also reflective of the
greater genetic influence imposed on anterior teeth. The earliest ages of stressors were exhibited
in the mandible around 2.8 to 2.9 years (Table 1), indicating the onset of a stable chronology of
childhood stress. The ages of LEH formation increased consistently anteriorly to posteriorly,
with only a few outliers exhibited in the maxillary and mandibular first molars that showed a
decrease in the opposite direction (Table 1). This fairly consistent pattern reflects a stable period
of childhood metabolic stress from 2 to 6 years of age.
Although the chronology of childhood stress is easily established, the determination of a
precise cause of LEH formation is severely limited. There are numerous possible causes of
hypoplastic incidence, including nutritional and non-nutritional stressors (Goodman and Rose,

1990). Weaning, or the end of breastfeeding, is a nutritional stressor that can be associated with
LEH formation in childhood. This period in childhood reflects a change in diet from the nutrientrich breastmilk to solids. Breastmilk provides immune defenses such as IgA immunoglobulins,
that when removed from the diet gradually or abruptly, may provide metabolic stress and disrupt
amelogenesis (Wright 1997). The gradually increasing ages of the enamel hypoplasias and stable
LEH chronology of the observed individual (Table 1) may reflect a period of weaning, as it
occurs between 2 to 6 years of age, the typical age range for weaning (Wright, 1997). However,
drawing such conclusions is often aided by other osteological evidence, individual life history or
historical evidence of population-wide stressors, such as famine. It is impossible to establish the
precise cause of the LEH formation as weaning with confidence without additional evidence
(Goodman and Rose 1990){Goodman, 1990 #22}{Goodman, 1990 #22@@author-year}
{Goodman, 1990 #22}{Goodman, 1990 #22}{Goodman, 1990 #22}. Pathologies exhibited in
cranial and postcranial data, as well as a context of death would provide more certainty to the
assumption that the LEH formation observed was a result of weaning and not of childhood
pathological conditions or another source of nutrient deficiency.
Conclusion
Enamel hypoplasias provide a wealth of evidence to construct a chronology of childhood
stressors. The examination of LEH defects in the maxillary and mandibular dentition indicated a
stable period of metabolic stress from 2 to 6 years of age, progressing in LEH formation from the
anterior to posterior aspects of the dental arcade. Ages of defect formation from 2 to 6 years may
reflect a period of weaning, where the gradual loss of breastmilk nutrients and substitution of
solid foods constitute a source of metabolic stress. However, the absence of additional evidence
from the crania and postcrania, this conclusion cannot be supported with much certainty.

References
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DISTRIBUTION OF ENAMEL HYPOPLASIAS FROM PREHISTORIC DICKSON
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PERTURBATIONS FROM DENTAL ENAMEL HYPOPLASIAS AND ASSOCIATED
HISTOLOGICAL STRUCTURES. Yearbook of Physical Anthropology 33:59-110.
MacCord, Kate. 2013. Biological Clocks and the Formation of Human Tooth Enamel. The
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Wright, L. E. 1997. Intertooth patterns of hypoplasia expression: Implications for childhood
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