orthodontic insight
“Maxillary lateral incisor partial
anodontia sequence”:
a clinical entity with epigenetic origin
Alberto Consolaro1,2, Maurício Almeida Cardoso3, Renata Bianco Consolaro4
DOI: https://doi.org/10.1590/2177-6709.22.6.028-034.oin
The relationship between maxillary lateral incisor anodontia and the palatal displacement of unerupted maxillary canines
cannot be considered as a multiple tooth abnormality with defined genetic etiology in order to be regarded as a “syndrome”.
Neither were the involved genes identified and located in the human genome, nor was it presumed on which chromosome
the responsible gene would be located. The palatal maxillary canine displacement in cases of partial anodontia of the maxillary lateral incisor is potentially associated with environmental changes caused by its absence in its place of formation and
eruption, which would characterize an epigenetic etiology. The lack of the maxillary lateral incisor in the canine region
means removing one of the reference guides for the eruptive trajectory of the maxillary canine, which would therefore, not
erupt and /or impact on the palate. Consequently, and in sequence, it would lead to malocclusion, maxillary atresia, transposition, prolonged retention of the deciduous canine and resorption in the neighboring teeth. Thus, we can say that we
are dealing with a set of anomalies and multiple sequential changes known as sequential development anomalies or, simply,
sequence. Once the epigenetics and sequential condition is accepted for this clinical picture, it could be called “Maxillary
Lateral Incisor Partial Anodontia Sequence.”
Keywords: Partial anodontia. Conical teeth. Impacted canines. Unerupted teeth.
A relação entre a anodontia parcial do incisivo lateral e o deslocamento palatino do canino superior não irrompido não pode
ser considerada uma anomalia dentária múltipla com etiopatogenia genética definida, a ponto de ser considerada como uma
“síndrome”. Os genes envolvidos sequer foram identificados e localizados no genoma humano, e nem mesmo presumiu-se
em qual cromossomo se localizaria o gene responsável. O deslocamento palatino do canino superior em casos de anodontia
parcial do incisivo lateral superior está potencialmente associado às mudanças ambientais provocadas pela sua ausência no
local de formação e erupção, o que caracterizaria uma etiologia epigenética para essa associação. A falta do incisivo lateral
superior na região canina implica em tirar um dos guias referenciais da trajetória eruptiva do canino superior, que ficaria,
assim, não irrompido e/ou impactado no palato. Como consequência, e em sequência, promove-se uma má oclusão, atresia
maxilar, transposição, retenção prolongada do canino decíduo e reabsorções nos dentes vizinhos. Dessa forma, pode-se
afirmar que estamos frente a um conjunto de anomalias e alterações múltiplas sequenciais conhecido como anomalias de desenvolvimento sequencial ou, simplesmente, sequência. Uma vez aceita a condição epigenética e sequencial para esse quadro
clínico, ele poderia ser chamado de “Sequência da Anodontia Parcial do Incisivo Lateral Superior”.
Palavras-chave: Anodontia parcial. Dentes conoides. Caninos impactados. Dentes não irrompidos.
1
Universidade de São Paulo, Faculdade de Odontologia de Bauru (Bauru/SP, Brazil).
Universidade de São Paulo, Faculdade de Odontologia de Ribeirão Preto, Programa
de Pós-graduação em Odontopediatria (Ribeirão Preto/SP, Brazil).
3
Faculdade de Medicina e Odontologia São Leopoldo Mandic, Disciplina de
Ortodontia (Campinas/SP, Brazil).
4
Faculdades Integradas de Adamantina, Disciplina de Patologia Bucal
(Adamantina/SP, Brazil).
How to cite: Consolaro A, Cardoso MA, Consolaro RB. “Maxillary lateral incisor partial anodontia sequence”: a clinical entity with epigenetic origin. Dental
Press J Orthod. 2017 Nov-Dec;22(6):28-34.
DOI: https://doi.org/10.1590/2177-6709.22.6.028-034.oin
Contact address: Alberto Consolaro
E-mail: consolaro@uol.com.br
» The authors report no commercial, proprietary or financial interest in the products
or companies described in this article.
2
© 2017 Dental Press Journal of Orthodontics
Submitted: September 20, 2017 - Revised and accepted: October 09, 2017
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Consolaro A, Cardoso MA, Consolaro RB
orthodontic insight
Partial anodontia is hereditary in nature, and
the most associated genes are MSX1, PAX9, and
AXIN2.10,20,25,40,41 In the Mendelian pattern of heredity,
family cases are mainly autosomal dominant; but there
are the recessive ones and even those related to the sex
chromosome.13-18
The gene associated with partial anodontia has an
incomplete penetrance and varied expressivity. When
the partial anodontia gene acts, it can lead to the complete absence of the tooth, but may also to its microdontia, with or without its associated conical shape (Fig 1
to 4). Conical teeth as a manifestation of the anodontic
gene also affects the shape of roots, leaving them triangular, tapered, and shorter.42 The tendency to conical
teeth explains the more convergent crowns and simpler
or less complex occlusal surfaces. It can be said that microdontic conical teeth are incomplete manifestations of
the partial anodontia gene, due to its incomplete penetrance and variable expression.
In patients with partial anodontia, the existing teeth
present the phenomenon of morphological simplification,8,22,26,37 characterized by:
» reduction of the mesiodistal distance of their
crowns;
» lower cusps in a less complex occlusal surface;
» absence or sharp reduction of the cingulum;
» absence or sharp decrease of cups of Carabelli;
Partial anodontia, known as hypodontia by Europeans, is a tooth disorder characterized by the absence of
one or more teeth and has hereditary etiology. It is not
terminologically appropriate to call partial anodontia as
congenital, once “congenital” is a quality of what appeared or was possible to be diagnosed at birth. Partial
anodontia, especially of permanent teeth, manifests itself only later, with the establishment of dental germs
and the formation of odontogenic tissues, not at birth.
Partial anodontia is part of the tooth agenesis group,
along with total anodontia. In fact, these terms, although
used as synonyms in some situations, are not. The most
affected tooth by partial anodontia varies with ethnicity.
In Europeans and their descendants, the most evolved teeth
are the mandibular and maxillary premolars; in the Japanese,
the mandibular central incisors; and in the United States,
the maxillary lateral incisors. In Brazil, the prevalence varies
with the migratory predominance in each region.8,9
The biggest prevalence of partial anodontia are the third
molars either the four or only one of them, in all ethnic
groups, with variations between 25 and 35% in frequency.
In addition to its high prevalence, partial third molar anodontia is associated with a great morphological variety as to
their position and number. This apparent instability often
leads to the non-inclusion of third molar partial anodontia
in the various studies on the subject: it would be very unpredictable and could affect the results.
A
C
B
Figure 1 - White 13.7 years old patient, Class II (1/4) on the right side and Class I on the left side, with the maxillary middle line slightly shifted to the left. Retention is noted in teeth #52, #53, #55, #63, #65 and #75 with morphological simplification of tooth #22 of conical shape, and diastema between teeth # 11
and #21. There was family report of partial anodontia in the maternal grandmother; parents and brother had no partial anodontia.
A
© 2017 Dental Press Journal of Orthodontics
Figure 2 - The maxillary deciduous canines did
not present mobility and the permanent successors did not present palpable areas in the
palatal region. The second molars had already
erupted, except for tooth # 17.
B
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orthodontic insight
“Maxillary lateral incisor partial anodontia sequence”: a clinical entity with epigenetic origin
» second molars with only three cusps;
» more convergent crowns; and
» shorter and conical roots, compared to
normal ones.
anodontic gene expression with unerupted canines displaced palatally and also with transposition, especially
between maxillary and first premolars. These authors
have sought to establish this gene relationship, but there
is little published work29 superficially mentioning external factors, polygenic and multifactorial aspects, without mentioning details or explanations of such phenomena. In 2016, Garib et al12 reported an increased risk of
children with dental anomalies diagnosed during mixed
dentition to develop palatally displaced canines, when
compared to children without these anomalies.
Partial anodontia and unerupted palatally
displaced canines and transposition: historical
and interesting findings
The impaction of canines was observed in prehistor19
ic, medieval39 skulls, and a few centuries’ old skulls.7
The current prevalence varies from 1 to 3% of cases reported4. Newcomb24 (1959) reported through clinical
observations, without any experimentation, that there
was a relationship between the canine shifted to the palatal area, dentition development and other anomalies.
The pioneers in establishing a direct relationship between maxillary partial anodontia and palatal maxillary canines impaction were Miller in 1963;
followed by Bass in 1967; and Weise in 1969.1,23,43
Only in 1981, Becker et al2-5 drew new attention and
reported the possibility of lateral incisors reduced in
size being associated with unerupted palatal canines.
Similar results were obtained by Brin et al6 in 1986 on
the analysis of 2,440 students (1,173 boys and 1,267
girls) aged between 14 and 18 years; further concluding that patients from families with palatally displaced
canines were more likely to have the same palatally
displaced maxillary canines, small, conical or absent
maxillary laterals and late dentition development.
In the 1990s, several authors have published studies
relating11,21,27-36,38 partial anodontia and varied forms of
Three theories or mechanisms that would
explain the relationship between partial
anodontia of the maxillary lateral incisors,
unerupted maxillary canines and other
alterations
In tooth formation there is not yet an accurate explanation of the mechanisms and genes that determine
their morphology, color, number, size and position, and
much less of the genes and mechanisms associated with
their eruption. Many papers published over the last 70
years have shown that partial anodontia involves a series
of dental morphological changes, which is called morphological simplification. Three phenomena or theories
(referred to as hypotheses, thoughts, philosophies, theses, schools, currents, etc.) explain why when the number of teeth is modified, morphology, size and other
teeth characteristics also change.
These three theories or phenomena, when quoted in
articles, are not explained in detail from a clinical point
of view, although researchers are also clinicians, and this
has caused confusion. In order to be clearly understood,
three fundamental concepts, described below, must be
explained very well.
Our body has 25,000 filed and biochemically available data in the nucleus of each of our 10 trillion cells.
This set of information is known as genome. In the past,
it was thought that our morphology was determined by
this set of genes or data received from our parents.
1st concept and theory: Epigenetics
Genes probably account for about 50% of our
characteristics. The other half is determined by environmental factors, that is, where we live and our
internal tissue environment, which is where our cells
live and develop.
Figure 3 - In the panoramic radiograph, the bad positioning of the teeth #13
and # 23 stands out, with absence of the teeth #12 and #18. Note the retention of teeth #52, # 53, # 55, #63, #65 and #75. The permanent maxillary
canines were mesially angulated. Tooth #13 was in a more critical situation,
erupting in the position of tooth #12 and in close contact with the root of
tooth #11. Tooth #23 was erupting towards the midline, superimposed by
the roots of teeth #21 and #22.
© 2017 Dental Press Journal of Orthodontics
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Dental Press J Orthod. 2017 Nov-Dec;22(6):28-34
Consolaro A, Cardoso MA, Consolaro RB
A
C
orthodontic insight
B
Figure 4 - Three-dimensional tomographic reconstructions, with greater precision regarding
the spatial location of unerupted canines in
the maxillary bone and their relationships with
neighboring permanent teeth and the retained
deciduous teeth in the dental arch. The conical
shape affects crown and tooth root in most of
the affected teeth.
D
The internal or external environmental factors
strongly influence gene functioning without mutating
them, which would configure a mutation. When mutations occur, developmental disorders arise in their most
varied forms and levels of complexity.
Environmental factors account for approximately
half of our final characteristics, including teeth and dentitions. The science that studies environmental factors
is known as Epigenetics. Such factors are metabolism,
hormones, nutrition, temperature, forces and many
others. In teeth and dentition, we have all these epigenetic factors acting until its final formation, and this includes growth forces or vectors, occlusion, addictions,
use of braces, etc. The number, color, shape, position,
size and time of tooth formation are therefore result of
gene action and epigenetic factors.
Explaining unerupted teeth, partial anodontia or its
position based only on information provided by genes is
to ignore the great importance of epigenetic factors, as
important as genetics in the formation and functioning
of our body (50 / 50).
The absence of the lateral incisor and its change in
shape and size might be epigenetic factors involved in the
various forms of canine displacement to the palatal region.
Tooth transposition probably also has a strong epigenetic
connotation, and this may be one of the aspects that explain some the studies associating it with partial anodontia
and unerupted canines. It is hard to imagine human dentition without the influence of epigenetic factors.
© 2017 Dental Press Journal of Orthodontics
The space where adjacent teeth to the maxillary canine are formed may be one of the key epigenetic factors. Two aspects should be noted:
1) An important factor, almost completely disregarded in the lack of space and displacement of the
maxillary canines, relates to the 3D space the canine
occupies in the same region where the central incisors, laterals and first premolars are. This “maxillary
canine region” space is larger or smaller, and more or
less malleable, according to the mineralization time
of these teeth: of the four, the laterals are the ones
that take the most time in mineralization from the
crown to the root, as shown in Figure 5. Without the
laterals, the canines lose one of the delimiters of this
space, as if it were a guide, and they “get lost” in the
eruptive trajectory, and might be located palatally.
Lateral incisors may be one of the eruption guides for
maxillary canines.
2) In the canine region, we have cores of differentiated bone formation, as the growth center of the
premaxilla, alveolar process and palatine process.
The absence of the maxillary lateral incisor affects the
resultant of the forces generated by the growth centers, being able to change these resultants, sometimes
referred to as growth vectors. These changes, coupled
with the previously mentioned factors can greatly influence the position of the palatally displaced canine,
which would primarily be much more associated
with epigenetic factors than genetic ones.
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orthodontic insight
“Maxillary lateral incisor partial anodontia sequence”: a clinical entity with epigenetic origin
Similarly, the position of the maxillary canine may
facilitate the sequential occurrence of transposition, rotation, resorption of adjacent teeth, as well as maxillary
atresia and malocclusion (Fig 6).
other to cause the disease in question. When a disease
has many causes, it is not multifactorial due to this;
it only has several causes.
By using the term “multifactorial in heredity”, one
must have greater precision on the concept of what is a
multifactorial heredity. The most suitable examples of
diseases transmitted by parents by multifactorial inheritance are diabetes mellitus and cleft lip and palate.
In multifactorial heredity, the gene has been transmitted from parents to children, but it will only work
actively producing the disease, if in association with an
environmental or epigenetic factor. In the case of diabetes mellitus, the gene will only induce the transmitted
disease if there is obesity, sedentary lifestyle and other
epigenetic factors. In the case of cleft lip and palate, the
gene will lead to cleft formation if there are environmental factors during pregnancy, such as stress, alcoholism, drugs, nutritional disorders and others. If there is
no such association, the disease will not manifest itself.
There is no evidence, however small, that palatal
canine impaction is of multifactorial hereditary nature,
and it may even be demonstrated in future works, but it
is not in the face of the present knowledge.
2nd concept and theory: Pleiotropic Gene, or
Pleiotropy
Pleiotropy is the characteristic of some genes functioning in our body, and the gene associated with the
human dentition may be one of them. A pleiotropic
gene is one that influences or determines various phenotypic characteristics at the same time.
Pleiotropy derives from the Greek pleion (“more
numerous”) and tropos (“affinity”). Together they form
the word pleiotropic, which represents the phenomenon
in which a pair of alleles determines the occurrence of
various characteristics in the same organism.
In other words, only one gene can determine the various characteristics of human dentition, such as number,
shape, size, color, and position. By changing this gene,
various features of the teeth would change, thus justifying the morphological simplification presented in anodontic patients. Among these, there would also be the
palatal impaction of canines and transposition.
3rd concept and theory: “Polygenic System”
The concept of “polygenic system” implies the organization of several smaller genes, acting in a synchronized way, being responsible for several characteristics.
By altering one of these genes, such as the one responsible for the number of teeth, other characteristics such
as shape, size and even position, would also change.
The relationship between partial anodontia and dental
position changes only based on clinical and epidemiological findings may be explained as follows, based on
the polygenic system: altering the gene responsible for
number may alter the adjacent gene responsible for position and time of eruption.
On multifactorial heredity and partial anodontia
versus maxillary unerupted canines
When explaining the palatal impaction of maxillary canines, it is fundamental to know the meaning
of the term “multifactorial”. When a multifactorial
nature is attributed to an illness, it implies that for it
to exist or to happen, the causes must act synergistically, simultaneously, one potentiating or causing the
© 2017 Dental Press Journal of Orthodontics
Figure 5 - The maxillary lateral incisor is surrounded anteriorly by the central incisor; later, by the canine and first premolar. The canine tends to
be located buccally to the lateral incisor; and the first premolar, palatally.
The absence of the maxillary lateral incisor, or its diminished size causes the
canine to lose one of its references in the eruptive trajectory, even moving
to the palatal region.
32
Dental Press J Orthod. 2017 Nov-Dec;22(6):28-34
Consolaro A, Cardoso MA, Consolaro RB
orthodontic insight
quential developmental anomaly, as in the Pierre Robin
Sequence, which causes the lack of upward movement
of the cephalic portion of the fetus. Without this movement, the jaw is prevented from growing because it is
caught by the cardiac prominence. Without the full
mandibular growth, the tongue does not come down
and does not develop normally, remaining between the
two secondary palatal processes, preventing the formation of the palate or causing it to assume a high arched
form, causing severe occlusal problems.
The names of multiple anomalies
Multiple anomalies may characterize repetitive clinical pictures in patients and thus receive names and concepts widely used in scientific communication.
» Syndrome: it is a set of multiple anomalies related
to each other and produced by the action of a single genetic cause, without presenting a sequence of cascade effects. In other words, a syndrome is a clinical picture of
multiple anomalies and developmental changes induced
by a single cause. As an example, we have the Gorlin
and Goltz syndrome, consisting of multiple maxillary
keratocysts, nevoid basal cell carcinomas on the skin,
and skeletal anomalies induced by the mutation of a tumor suppressor gene on human chromosome 9 (9q22).
» Association: is the set of changes or multiple
anomalies of a repetitive occurrence in many people,
non-occasionally and non-identifiable as a syndrome
because it has no known genetic cause. Often, there is
an association from which the gene defect is eventually
identified, thus failing to be an association and becoming a syndrome. It can also be called syntropy.
» Sequence: are multiple defects induced by a sequence of events initially promoted by a known or
presumed cause. The sequence may also be called se-
1st
Maxillary lateral incisor anodontia
2nd
Unerupted or impacted canine
3rd
Persistence of the deciduous canine
4th
Maxillary atresia
5th
Malocclusion - Transposition
6th
Radicular resorption of neighboring teeth
Considerations and final concept
The relationship between the partial anodontia of
the lateral incisor and the palatal displacement of the
unerupted maxillary canine, as well as other possible
anomalies of position and shape cannot be regarded as a
set of anomalies and changes of defined genetic etiology
as to be considered a “syndrome”.
There is clinically an “association” between lateral incisor anodontia, palatal displacement of maxillary canines
and other anomalies and disorders (Figs 1 to 4) without
the involved genes being identified and located in the human genome — its gene was not even presumed.
The palatal displacement of maxillary canines in
cases of partial anodontia of the maxillary lateral incisor is potentially associated with environmental changes caused by its absence in the place of formation and
eruption, which characterizes an epigenetic etiology for
this association (Fig 5).
The lack of the maxillary lateral incisor in the canine
region may mean taking one of the anatomical “guides”
of reference for the eruptive trajectory of the maxillary canine. Without this point of reference, the canine
would not erupt and remain in intraosseous position,
impacted on the palate. Or, it may erupt outside the
normal arch, displaced to the palatal region (Figs 1 to 4).
As a result and in sequence, it would promote malocclusion, maxillary atresia, transposition, prolonged
retention of the deciduous canine and resorption in
neighboring teeth. In this way, one can say that we are
facing a set of multiple anomalies and multiple sequential changes known as sequence developmental anomalies or simply sequence (Fig 6). Once the epigenetics
and sequential condition for this clinical picture is accepted, it could be called “Maxillary Lateral Incisive
Partial Anodontia Sequence” as a new clinical entity to
be identified in orthodontic planning.
Figure 6 - Sequence of anomalies and changes that may be initially induced by anodontia of the lateral incisor, and can be labeled “Maxillary Lateral Incisive Partial Anodontia Sequence.”
© 2017 Dental Press Journal of Orthodontics
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“Maxillary lateral incisor partial anodontia sequence”: a clinical entity with epigenetic origin
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