Etiology of o pen- b ite m alocclusion€¦ · provide self-correction of the anterior open bite....

1

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 ).


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


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


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.


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.


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 ).


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.


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 ).


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.


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.


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.


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.


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.


(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.


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 o pen- b ite m alocclusion€¦ · provide self-correction of the anterior open bite....

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