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1 Anterior open-bite malocclusion is defi ned as the absence of contact
between the maxillary and mandibular incisor edges consequently present-
ing a negative overbite ( Nielsen 1991 ; Ngan and Fields 1997 ). Generally, it
deteriorates the facial aspect, impairs mastication and speech, subjecting
the patient to uncomfortable situations ( Janson et al. 2003 ). The frequency
of this malocclusion in the mixed dentition is high (17% [ Worms et al.
1971 ]), and the prognosis for correction varies from good to defi cient,
depending on its severity and on the patient ’ s age. Before undertaking any
treatment alternative, knowledge of the etiology of this malocclusion is
important because in many instances, not only the morphological charac-
teristics have to be corrected, but also the etiological factors have to be
eliminated not only to assure treatment success, but also to provide long-
lasting stability. Therefore, this chapter covers the most common etiological
factors of anterior open-bite to help in managing the correction of this
malocclusion in the different stages of the dentition it may present.
The etiologic factors of the malocclusions can be divided into environ-
mental and genetic factors. However, all malocclusions are multifactorial
and result from interactions of environment and genetics ( Mossey 1999a ,
1999b ). The face and the dentition are infl uenced by the complex interac-
tion of both. It can be stated that the etiology of a particular malocclusion
is predominantly environmental or genetic, and this will determine how
much this malocclusion can be corrected by therapeutic intervention, that
is, the prognosis of orthodontic correction. The greater the infl uence of
Open-Bite Malocclusion: Treatment and Stability, First Edition.
Edited by Guilherme Janson and Fabrício Valarelli.
© 2014 John Wiley & Sons, Inc. Published 2014 by John Wiley & Sons, Inc.
Etiology of o pen- b ite m alocclusion Karina Freitas and Rodrigo Cançado
COPYRIG
HTED M
ATERIAL
2 Open-Bite Malocclusion: Treatment and Stability
environmental factors in the etiology of a malocclusion, the better the
orthodontic treatment prognosis, as long as the causative factor is elimi-
nated. When there is a strong genetic etiologic factor, most likely the best
approach would consist in an orthodontic-surgical approach ( Beane 1999 ).
Because environmental open bites are more amenable to an orthodontic
approach, this chapter will fi rst cover the environmental etiologic factors
and secondly the genetic factors.
ENVIRONMENTAL FACTORS
Anterior open bite can be considered as functional consequent to its func-
tional etiologic factors. The most important functional factors are deleteri-
ous oral habits, ( Popovich and Thompson 1973 ; Mahalski and Stanton
1992 ; Johnson and Larson 1993 ) and oral breathing ( Proffi t and Mason
1975 ; Lowe and Johnston 1979 ; Harvold et al. 1981 ; Linder-Aronson et al.
1986 ; Nagahara et al. 1996 ; Yashiro and Takada 1999 ). Some other factors
may contribute in the environmental etiology such as traumatisms and
pathologies ( Prosterman et al. 1995 ).
Deleterious h abits In a normal occlusion, there is a balanced relationship among the oral
structures, basal bones, teeth, and intra and extraoral musculature, refl ect-
ing in a correct function of the stomatognathic system ( Moyers 1988 ). This
is denominated the buccinator mechanism. Thus, the teeth are in a bal-
anced position receiving opposing forces arising internally by the tongue
and externally by the lips and cheeks (Figure 1.1 ) ( Graber 1966 ).
The solution of this muscular balance for some abnormal function of
the oral muscles has a negative impact on the teeth position and occlusion.
Nonnutritive sucking habits, such as pacifi er and thumb-sucking, atypical
tongue thrust, and anterior tongue posture, all considered deleterious oral
habits, can break this muscular balance.
Pacifi er and t humb- s ucking
Humans start sucking fi ngers, tongue, and lips during fetal life, in the
maternal womb (Figure 1.2 ). At birth, the infant has a well-developed func-
tion of sucking to receive the nutrients essential for life. It is during suction
developed in breastfeeding that the children not only get the nutrients that
need to meet the physiological demands, as well as feelings of security,
warmth, and acceptance necessary for their welfare and for their proper
emotional development. At this stage, suction is a mean of communication
of the infant with the environment ( Newman 1990 ).
The early well-developed oral perception provides a sense of comfort,
safety, and emotional satisfaction during sucking. When breastfeeding is
Etiology of open-bite malocclusion 3
Figure 1.1 Balanced forces between the tongue, lips, and cheeks on the teeth and bone structures.
Figure 1.2 Prenatal thumb-sucking seen in a ultrasonographic examination.
not possible, the use of bottles with orthodontic nipples that resemble the
anatomy of a woman ’ s breasts is recommended, because they allow better
contact of the tongue with the palate, as necessary for normal swallowing
( Graber 1966 ) (Figure 1.3 ).
When a child is bottle-fed, his physiological demand is met, but the
natural need to suck is not supplied in the few minutes spent in the
mother ’ s lap. Thus, the child can begin the compensating thumb or pacifi er
sucking ( Graber 1966 ).
4 Open-Bite Malocclusion: Treatment and Stability
Figure 1.3 Breastfeeding provides the natural need to suck to the child.
Pacifi er or thumb-sucking are considered as mechanisms of emotional
supply of the child. Consequently, pacifi er or thumb-sucking in the early
child development is considered normal. Through these habits, the child
releases the emotional tensions from lack of affective care resulting from
confl icting relationship between child and parents, which becomes a way
to draw attention from people close to them ( Moyers 1988 ). Parental oppo-
sition to these habits can determine negative psychological consequences.
When children grow and develop other means of communication with
the external environment, they usually spontaneously abandon the sucking
habit. Interruption of sucking habits during the deciduous dentition can
provide self-correction of the anterior open bite. However, persistence of
the habit until the mixed dentition represents a deviation from normality,
because these habits are potent etiologic malocclusion factors, particularly
for anterior open bite ( Ogaard et al. 1994 ; Bishara et al. 2006 ).
Pacifi er or thumb-sucking act as mechanical obstacles, preventing erup-
tion of the anterior teeth and establishing an open bite ( Moyers 1988 ; Proffi t
et al. 2007 ) (Figure 1.4 ). Anterior open-bite malocclusion due to pacifi er use
is characteristically restricted to the anterior teeth and circular (Figure 1.5 ).
Anterior open bite consequent to thumb-sucking is characterized by labial
inclination of spaced maxillary incisors and lingual inclination of the man-
dibular incisors (Figure 1.6 ). Anterior open bite may be associated to maxil-
lary constriction and uni- or bilateral posterior crossbite, because, during
sucking, the tongue is lowered, without contact with the maxillary poste-
rior teeth ( Moore 1996 ).
However, a deleterious oral habit does not always necessarily results
in an open bite. First, it depends on how the habit is exercised, that is, it
Etiology of open-bite malocclusion 5
Figure 1.4 Pacifi er and thumb-sucking are strong etiologic factors for open-bite malocclusion.
depends on the duration (for how long it is exercised, e.g., for how long
the child keeps the pacifi er in position), on the frequency (number of times
per day it is exercised), and on the intensity (the amount of force developed
by the habit) of the habit. These factors are important in the etiology of
this malocclusion and are known as Graber ’ s Trident ( Graber 1958 ). Besides
its mode of action, another important factor in the onset of an anterior
open bite is the facial growth pattern. In the presence of deleterious habits,
patients with vertical growth pattern have a greater tendency to manifest
anterior open bite than patients with horizontal growth pattern ( Schendel
et al. 1976 ; Nielsen 1991 ). Therefore, the manifestation of an open bite
depends on the association of environmental (Graber ’ s Trident) and genetic
factors (facial growth pattern). This explains why there are children with
habits but without an open bite (Figure 1.7 ).
Figure 1.5 Anterior open bite caused by the use of pacifi er is characterized by being restricted to the anterior region of the dental arches and circular.
Figure 1.6 Thumb-sucking characteristically causes labial inclination of the maxil-lary incisors and lingual inclination of the mandibular incisors.
6
Etiology of open-bite malocclusion 7
Prevention requires that intervention of thumb-sucking habit is started
as soon as possible. Several studies ( Graber 1966 ; Moore 1996 ; Vadiakas
et al. 1998 ) have suggested the use of orthodontic pacifi ers as a preventive
step in thumb-sucking habit, based on fi ndings that pacifi er habit tends to
be discontinued earlier than thumb-sucking habit.
Anterior t ongue p osture and t ongue t hrust
Atypical tongue posture and atypical tongue thrust is present in 100% of
cases with anterior open bite ( Fujiki et al. 2004 ). The tongue is considered
to have a secondary role in the etiology of anterior open bite because it can
maintain or aggravate the existing open bite when placed between the
anterior teeth ( Speidel et al. 1972 ; Subtelny 1973 ; Proffi t and Mason 1975 ;
Nielsen 1991 ; Proffi t et al. 2007 ). This abnormal tongue placement may
occur at rest, during speech, and swallowing. Incorrect tongue posture at
rest has the greatest deleterious potential because, although the force is
low, it remains during a large period of time between the teeth ( Ingervall
and Janson 1981 ) (Figure 1.8 ). On the other hand, during swallowing, in
Figure 1.7 Child with thumb-sucking habit, but without open bite, demonstrating that the malocclusion is dependent on Graber ’ s trident and on patients growth pattern.
Figure 1.8 Anterior tongue posture is also a contributing factor for open bite.
8 Open-Bite Malocclusion: Treatment and Stability
which the force is much greater, the mean period of tongue thrust is
between an hour ( Straub 1951 ) to an hour and a half ( Graber 1963 ) within
24 hours, and therefore presents a very small potential of maintaining or
accentuating the open bite ( Subtelny 1973 ; Moyers 1988 ; Proffi t et al. 2007 ).
Tongue thrust during swallowing is considered to be consequent to a
previously established anterior open bite caused by deleterious oral habits.
This is explained by the physiologic maturation of swallowing. The child
without irrupted deciduous teeth presents an infantile swallowing, which
is normal at this stage. The characteristics of an infantile swallowing are
separated jaws, active contractions of the musculature of the lips, tongue
placed between the gum ridges, in contact with the lower lip, and little
activity of the posterior tongue or pharyngeal musculature. When the
deciduous teeth are completely erupted, around 3 years of age, there is
maturation of the facial and masticatory muscles, and the child develops
the mature swallowing pattern. During mature swallowing, the teeth
occlude, the mandible is stabilized by the muscles supplied by the trigemi-
nal nerve, the tip of the tongue should contact the incisive papilla, and the
labial muscles are passive ( Subtelny 1973 ; Moyers 1988 ; Proffi t et al. 2007 ).
In order to swallow, negative pressure must be obtained by sealing the
mouth. Therefore, the child with an open bite thrusts the tongue between
the teeth and strains the lips to seal the mouth ( Proffi t et al. 2007 ) (Figure
1.9 ). With an open bite, maturation of the masticatory musculature occurs
Figure 1.9 Lips strain in an open-bite child in order to seal the mouth.
Etiology of open-bite malocclusion 9
differently, changing the normal pattern to an atypical swallowing pattern
or tongue thrust swallow. In this type of swallowing, there is atypical
tongue thrust, absence of masseter contraction, and activity of the perioral
muscles. Therefore, tongue thrust during swallowing is considered to be
a secondary factor in open-bite etiology: fi rst, there is development of
the open bite, and posteriorly, tongue adaptation through its placement
between the anterior teeth ( Proffi t et al. 2007 ).
Mouth b reathing Normal breathing consists in the air fl ow through the nasal cavity
where the nostrils promote purifi cation, heating, and humidifi cation of
the inhaled air before reaching the lungs. Patients with nasal obstruction
do not have these benefi ts when breathing through the mouth. In the pres-
ence of some nasal obstruction, the air fl ow is impaired or obstructed, and
the child begins to breathe through the mouth. The etiology of nasal
obstruction can be divided into upper and lower breathing obstacles. The
upper obstacles are hypertrophied adenoids, allergic rhinitis, nasal turbi-
nates hypertrophy, and nasal septum deviation. The lower obstacles are
hypertrophied tonsils or frequent tonsillitis ( Watson 1981 ; Linder-Aronson
et al. 1986 ).
In the primary dentition, the prevalence of anterior open bite in mouth-
breathing children is similar to the general population (30%), whereas in
the mixed and permanent dentition, this prevalence remains almost the
same in mouth-breathing individuals, but decreases in the population
(between 12% and 20%) ( Souki et al. 2009 ).
Upper r espiratory o bstacles
Hypertrophied a denoids
Adenoid hypertrophy is the abnormal growth of the adenoids, and in some
situations, this growth is so exacerbated that can cause a complete blockage
of the air passage through the upper airways. Even in situations that do
not lead to a complete blockage of the air passage through the upper
airways, hypertrophy of the adenoids can promote a partial blockage of
the air passage through the nostrils and cause great discomfort to the
patient in an attempt to breathe through the nose. Thus, the patient begins
to breathe through the mouth ( Gates 1996 ). There are two main ways
to assess adenoid size: (1) indirect assessment with the nasopharyngeal
mirror and (2) lateral headfi lm. The use of the nasopharyngeal mirror is
sometimes not possible in the young child, and in these cases, the lateral
headfi lm represents the best way to assess adenoid size (Figure 1.10 )
( Weimert 1986 ).
10 Open-Bite Malocclusion: Treatment and Stability
Although the abnormal growth of adenoids can cause some pediatric
sleep-disordered breathing, multiple anatomic obstructions should also
be considered ( Guilleminault et al. 2005 ; Huynh et al. 2011 ). Children with
increased sleep-disordered breathing and obstructive sleep apnea symp-
toms seems to share some common characteristics in the vertical plane,
such as long faces, retropositioned mandibles, and lip incompetence ( Pirila-
Parkkinen et al. 2009 ; Huynh et al. 2011 ). Some characteristics of these
patients could also be observed in the transverse plane, such as maxillary
constriction, which usually occurs simultaneously with reduced transverse
dimension of the upper airways, and increased nasal resistance, which
consequently increases mouth breathing.
Enlarged adenoids can contribute to the worsening of mouth breathing,
causing an imbalance of lingual, labial, and cheek muscles ( Linder-Aronson
et al. 1993 ). This imbalance might be associated with unfavorable changes
in the development of occlusion and anomalies of dental position. Although
there is no clear understanding of the relationship between observed skel-
etal and dental changes with airway obstruction, some disruption in the
normal functional environment may be responsible for these unfavorable
changes. Considering the assumption that upper airway obstruction,
regardless of cause, infl uences negatively normal facial development, the
young child with airway obstruction has to be carefully handled during
growth ( Bresolin et al. 1983 ).
Two factors are crucial for the occurrence of blockage of the upper airways: (1) the size of the adenoids, and (2) the size of the nasal pharynx passageway. The size of adenoids and the age at which this structure atrophies present great variability between individuals. Generally, the adenoid reaches its largest size at 5 years of age, and then the growth is interrupted and adenoid atrophies in late childhood at about 7 years of age ( Gates 1996 ).
Figure 1.10 (A): Normal adenoid; (B) and (C): hypertrophied adenoid.
Etiology of open-bite malocclusion 11
When the blockage of the upper airway is in the nasal cavity, treatment
may be more diffi cult when compared with hypertrophied adenoids. Nasal
obstruction can occur anywhere in the upper airways, and identifi cation
of the causative agent can be diffi cult to diagnose ( Bresolin et al. 1983 ). If
allergic rhinitis is the causative agent, removal of inciting allergens should
be helpful. Antihistamines and decongestants frequently cause an improve-
ment in the clinical condition of patients because they shrink the nasal
mucosa ( Bresolin et al. 1983 ).
Nasal s eptum d eviation
The nasal septum is the part of the nose that separates the two airways
and the nostrils. A deviated septum is when there is a shift from the midline
or center position. In normal conditions, the nasal septum is centralized,
and the air passages in the nasal cavity are symmetric. The nasal septum
deviation is an abnormality in which a portion of the cartilaginous tissue
deviates to one side of the nostril causing an obstruction for the airway
passage on the side on which the deviation occurred. These deviations are
common, and for most patients, cause no symptoms, and no treatment is
required. Many people with a deviation are unaware they have it until their
health is affected or discomfort is large enough. By itself, a deviated septum
can go undetected for years, and thus be without any need for correction
( Metson and Mardon 2013 ). However, the septal deviation may be severe
enough to adversely affect the patient and can commonly obstruct the
passage of air through the nostrils (Figure 1.11 ).
Allergic r hinitis
Rhinitis is a medical term describing irritation and acute or chronic infl ammation of the nasal mucosa. The infl ammation caused by allergic rhinitis results in exces-sive mucus production, generated by the accumulation of histamine, which causes nasal bleeding, the typical symptom of rhinitis. Allergic rhinitis occurs when an allergen, such as pollen or dust, is inhaled by an individual whose his immune system has been previously sensitized to these agents ( May and Smith 2008 ).
Allergic rhinitis can be classifi ed as seasonal or perennial. Seasonal allergic rhinitis occurs rarely before 6 years of age and has its signs and symptoms exacerbated in times of pollen. The perennial allergic rhinitis can occur at any time during the year and occurs more frequently in younger children. The main symptoms of allergic rhinitis are rhinorrhea (excess nasal secretion), itching, and nasal congestion and obstruction ( Sur and Scandale 2010 ). Allergic rhinitis is one of the main causes of nasal airway obstruction in the young child ( Rubin 1980 ).
12 Open-Bite Malocclusion: Treatment and Stability
The main etiological factors of nasal septum deviation are impact
trauma, such as by a blow to the face and a congenital disorder, caused by
compression of the nose during childbirth ( Metson and Mardon 2013 ). The
main symptoms of a deviated septum are infections of the sinus and sleep
apnea, snoring, repetitive sneezing, facial pain, nosebleeds, and breathing
diffi culty.
Some differences can be highlighted when comparing skeletal and
dental features in children with chronic nasal-breathing obstruction sec-
ondary to nasal septum deviation and nose breathing. Regarding linear
dimensions in the vertical plane, children with chronic nasal-breathing
obstruction due to nasal septum deviations usually present increase of
upper anterior facial height (N-palatal plane) and total anterior facial
height (N-Me) in comparison with nose-breathing subjects. Considering
the angular relationships of the horizontal planes of the face, such as sella-
nasion, palatal plane, and occlusal planes to the mandibular plane, these
angles are usually greater in mouth breathing due to nasal septum devia-
tions in comparison with nose-breathing subjects. Additionally, the gonial
angle (Ar-Go-Me), palatal height, and overjet are signifi cantly higher in
mouth-breathing subjects. Regarding the anteroposterior position of the
jaws, a retrognatic maxilla and mandible is frequently observed in mouth-
breathing patients due to nasal septum deviations in comparison with
nose-breathing subjects. Some differences can also be observed in the
occlusal aspect. Mouth-breathing children due to nasal septum deviations
usually present Class II malocclusion, whereas most of nose-breathing
subjects present normal occlusion ( D ’ Ascanio et al. 2010 )
However, the association between nasal resistance and open bite is of
only 8.2% when evaluating children from 7 to 15 years of age ( Lopatiene
and Babarskas 2002 ).
Figure 1.11 Nasal septum deviation obstructing the airway passage through the nostrils seen in a computed tomography examination.
Etiology of open-bite malocclusion 13
Lower r espiratory o bstacles
Hypertrophied p alatine t onsils
The tonsils are two structures forming part of the lymphatic system that
are located at the entrance of the upper airway and which has as main
function to help the body ’ s defense against respiratory infections or pre-
venting the entry of organisms through the mucosal respiratory system.
Because it represents one of the fi rst sources of defense against microorgan-
isms, it is a region potentially subject to infections and is one of the major
immunocompetent tissues of the oropharynx. It is a part of Waldeyer ’ s
ring, which is also formed by the nasopharyngeal tonsil or adenoid ( NT ),
the paired tubal tonsils ( TT ), the paired palatine tonsils ( PT ), and the
lingual tonsil ( LT ) ( Merati and Rieder 2003 ).
Tonsillitis is an infection of the tonsils that causes infl ammation and
represents the most common acute manifestation of tonsillar pathology
(Figure 1.12 ). The main symptom of tonsillitis is sore throat, and the pain
is usually worse when swallowing. Other symptoms can include fever,
general ill feeling, headaches, and vomiting. In a clinical view, the tonsils
may present with normal size or enlarged and often with the presence of
erythematous areas. The presence of exudates and secretions is common
but does not occur in all clinical situations. In fact, not all of these signs
and symptoms are present in all patients diagnosed with tonsillitis ( Merati
and Rieder 2003 ).
Tonsillar hypertrophy is the enlargement of the tonsils, but without
the presence of infl ammation. The obstructive tonsillar hypertrophy is the
Figure 1.12 Tonsillitis causing lower airway obstruction due to enlarged palatine tonsils.
14 Open-Bite Malocclusion: Treatment and Stability
main indication for tonsillectomy, which is the surgical removal of the
tonsils. The main signs and symptoms that may be observed in patients
with tonsillar hypertrophy are sleep disturbances in a wide spectrum of
severity, loud snoring, irregular breathing, coughing, night choking, inter-
rupted sleep apnea, dysphagia, and excessive daytime sleepiness ( Merati
and Rieder 2003 ).
Radiographs are not particularly useful in evaluating tonsil size. Direct
visualization is far more useful when compared with lateral cephalograms
that gives a rough impression of tonsil size (Figure 1.13 ) ( Weimert 1986 ).
A large variation in tonsil size is frequently common.
Nowadays, there are specifi c indications for surgical removal of tonsils,
and the most common indication is recurrent infection (Figure 1.14 )
( Weimert 1986 ).
To be able to breathe, the mouth-breathing child remains most of the
time with the mandible in a lowered position to keep the mouth open. The
tongue follows the mandible and consequently will not establish contact
with the palate in the rest position, as usual, during nose breathing ( Proffi t
et al. 2007 ). The absence of lateral contact of the tongue with the palate
results in predominance of lingual forces of the bucinator muscle, and this
consequently will result in smaller transverse development of the palate,
which can cause posterior crossbite (Figure 1.15 ). Concurrently, there will
be greater posterior vertical development of the palate. Besides, the tongue
can rest over the anterior teeth, restricting their vertical development and
contributing to anterior open bite. Notice that mouth breathing is a common
etiologic factor for posterior crossbite and anterior open bite. That is the
reason why many times, these malocclusions are associated. The associa-
Figure 1.13 Lateral cephalogram showing enlargement of palatine tonsils.
Etiology of open-bite malocclusion 15
tion between mouth breathing and open bite is 35.5% in children from 3
to 6 years of age ( Gois et al. 2008 ).
Hypertrophied tonsils are also considered as a contributing factor for
anterior open bite because it causes mouth breathing and anterior tongue
posture. Increase in tonsil size impairs the air fl ow through the lower
respiratory airway ( Moyers 1988 ; Proffi t et al. 2007 ). Therefore, to free the
lower airway and breathe normally, the child has to open his/her mouth
to be able to project the tongue anteriorly, and since the mouth is open,
there will be also mouth breathing. The anteriorly projected tongue can be
placed between the teeth, preventing the normal vertical development of
the incisors and maintaining and/or aggravating the open bite ( Subtelny
1973 ; Harvold et al. 1981 ).
Figure 1.14 Surgical procedure for the removal of hypertrophied palatine tonsils.
Figure 1.15 (A): Normal tongue position. (B): Lowered tongue position during mouth breathing.
16 Open-Bite Malocclusion: Treatment and Stability
Tongue thrust due to tonsillar hypertrophy can also occur in the premo-
lars and molars region, causing a posterior open bite. This condition
usually occurs when there is early loss of posterior deciduous teeth during
the stage of occlusal development. Thus, the tongue loses its lateral shield
and ends up placed in spaces between the posterior teeth during swallow-
ing, limiting eruption of permanent teeth.
Traumatisms Dental traumatisms can cause ankylosis—which possibly comes from
some kind of injury—which causes changes in the periodontal ligament,
forming a bone bridge joining the cementum and the lamina dura. Anky-
losis of any primary tooth may cause, beyond its retention, a delay or even
an ectopic eruption of the permanent successor and may cause open-bite
malocclusion ( Mandava and Kumar 2009 ) (Figure 1.16 ).
GENETIC FACTORS
Growth p attern In orthodontics, patients can be classifi ed into three groups according
to their growth pattern: horizontal, normal, or vertical growth pattern
Figure 1.16 A blow to the deciduous maxillary central incisor caused its ankylosis that is producing an anterior open bite.
Etiology of open-bite malocclusion 17
(Figure 1.17 ). Patients with horizontal growth pattern usually present
low mandibular plane and gonial angles, decreased lower anterior face
height, deep overbite, increased free-way space, decreased molar and
incisor dentoalveolar heights, and greater biting forces than patients with
vertical growth pattern ( Isaacson et al. 1971 ; Peterson et al. 1983 ; Trouten
et al. 1983 ; Dung and Smith 1988 ; Nanda 1988 , 1990 ; Janson et al. 1994 ).
Patients with normal growth pattern have balanced characteristics between
these extreme growth patterns. Consequent to these characteristics, patients
with vertical growth pattern are also more susceptible to the environmental
infl uences predisposing to open bite, and consequently present this maloc-
clusion most frequently ( Schudy 1964 ; Dung and Smith 1988 ; Nanda 1988 ,
1990 ). This does not mean that every subject with a vertical growth pattern
will present an open bite because there may be a compensatory eruption
mechanism ( Dung and Smith 1988 ; Betzenberger et al. 1999 ). However,
subjects with an open bite usually will present more vertical characteristics
than subjects with a balanced or horizontal growth patterns ( Trouten et al.
1983 ; Nanda 1988 , 1990 ).
Generally, when the growth pattern causes severe skeletal deformities
either in the vertical and/or in the anteroposterior planes, the best treat-
ment consists in an orthodontic-surgical approach ( Beane 1999 ).
Pathologies Craniofacial a nomalies
Some congenital deformities and syndromes can cause malocclusion,
including anterior open bite. Cleidocranial dysostosis is a congenital defor-
mity usually associated with heredity, which may be associated with the
presence of anterior open bite ( Daskalogiannakis et al. 2006 ).
Figure 1.17 (A), (B), and (C) show horizontal, balanced, and vertical growth patterns. A vertical growth pattern is more likely to present anterior open bite.
18 Open-Bite Malocclusion: Treatment and Stability
Treacher Collins syndrome involves hypoplastic mandible, glossoptosis,
small size of the pharynx and nasopharynx, and occasionally choanal
atresia can cause severe breathing problems, and consequently, open-bite
malocclusion ( Shete et al. 2011 ) (Figure 1.18 ).
Excessive activity of the tongue, in the act of swallowing or even at rest,
can change the incisors axial inclinations and cause an open bite. In patients
with some degree of neurologic impairment, this is observed quite fre-
quently ( Pedrazzi 1997 ) The compensatory coordination of the tongue
movement, the movement of the soft palate and the pharyngeal constrictor
muscle activity, still occur during swallowing in these patients ( Fujiki et al.
2000 ).
Juvenile rheumatoid arthritis is a disease with oral involvement with
anterior open bite, limited mouth opening, and in most of the cases, com-
promises the temporomandibular joint ( Savioli et al. 2004 ; Carvalho et al.
2012 )
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Etiology of open-bite malocclusion 19
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