Download The effects of enlarged adenoids on a developing malocclusion

DENTAL TRIBUNE
Clinical 19
United Kingdom Edition · December 1–7, 2008
The effects of enlarged adenoids
on a developing malocclusion
By Dr Derek Mahony and Dr Kevin Williams
Abstract
This article reviews upper
airway obstruction caused by
hypertrophied adenoids and the
possibilities of a subsequent
malocclusion. Early diagnosis,
and treatment, of pathological
conditions that can lead to the
obstruction of the upper airways
is essential to anticipate and
prevent alterations in dental
arches, facial bones and muscle
function. Correct nasal breathing facilitates normal growth
and development of the craniofacial complex (Fig. 1). Important motor functions such as
chewing and swallowing depend largely on normal craniofacial development. Any restriction to the upper airway passages can cause nasal obstruction possibly resulting in various
dentofacial and skeletal alterations.1 Upper respiratory obstruction often leads to mouth
breathing (Fig. 2). Habitual
mouth breathing may result in
muscular and postural anomalies, which may in turn cause
dentoskeletal malocclusions 2
(Fig. 3). Hypertrophy of the adenoids, and palatine tonsils, are
one of the most frequent causes
of upper respiratory obstruction
(Fig. 4). Philosophies regarding
the treatment of adenoid hypertrophy range from dietary control and environmental modifi-
cations to dentofacial orthopaedics, change of breathing
exercises, and surgical procedures.
Introduction
The aims of this article are to
highlight the skills and tools
that assist the clinician in iden-
tifying upper airway obstruction; to improve the diagnosis of
adenoid hypertrophy; and to
improve the classification and
CHRONIC PERIODONTAL DISEASE?
WHAT HAVE
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Fig. 1a
treatment of associated malocclusions.
The methodology used in this
literature analysis consists of a
thorough review of narrowly tailored research and Journal articles. The paradigm explored in
each article involves upper airway obstruction, adenoid hypertrophy and malocclusion. The results and conclusions stemming
DT page 20
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J Clin. Periodontol, 2004; 31: 697-707.
References: 1. Preshaw P.M.
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DENTAL TRIBUNE
20 Clinical
United Kingdom Edition · December 1–7, 2008
common – that airway obstruction caused by adenoid hypertrophy and malocclusion are related. The degree of that relationship and what it affects is
still under debate. This paper
attempts only to highlight the
positive existence of this relationship and its possible effects
regarding dentofacial growth
and development.
DT page 19
from these articles generally fall
into three categories:
• That hypertrophied adenoids
have a definitive effect resulting in skeletal malocclusion3
• That hypertrophied adenoids,
coupled with other factors, may
aid in the development of skeletal anomalies4
• That adenoid hypertrophy has
no effect on airway obstruction
and malocclusion.
Fig. 3
The research in this area is
expansive, but largely inconsistent. Thus, the cause-and-effect
relationship of adenoid hypertrophy and malocclusion must
be carefully examined on a
Fig. 4
case-by-case basis.5 Regardless
of the various researchers’ conclusions, one theory remains
Basic facial growth and
development
Fig. 5
Developments in the understanding of human craniofacial
growth have stemmed from histological and embryologic studies, radiographic cephalometry,
correlation of growth and facial
anomalies analysis of surgical interventions, animal research
and other science fields.6 Despite
these studies, we are still waiting
for a definite consensus regarding the controlling mechanism of
craniofacial tissue.
Seasons Greetings to all our
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Postnatal facial growth is influenced by genetic and environmental factors.2 Most facial
growth and development occurs
during the two childhood growth
peaks. The first growth peak occurs during the change from primary to permanent dentition
(between five and 10 years of
age) and the second growth peak
occurs between 10 and 15 years
of age.2 The study of the early
years of life shows that by the
age of four, 60 per cent of
the craniofacial skeleton has
reached its adult size. By the age
of 12, 90 per cent of facial growth
has already occurred.7 By age
seven, the majority of the growth
and development of the maxilla
is complete and by age nine, the
majority of the growth and development of the mandible is complete. Proper facial growth is affected either positively or negatively, early in life, by the sequential occurrences of four major
factors:
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• The cranial base must develop
properly
• The naso-maxillary complex
must grow down and forward
from the cranial base
• The maxilla must develop in a
linear and lateral fashion
• A patent airway must develop
properly.
The relationship between
the naso-maxillary complex and
the cranial base is significant for
aesthetic reasons and proper facial bone, muscle and soft tissue
support. To allow proper downward and forward rotation of the
mandible, the maxilla must be
adequately developed, in width,
for acceptance of the mandible.
Any limitation on mandibular
rotation may affect the relationship of the condyle to the glennoid fossae (in the temporal
bone) resulting in multiple TMJ
problems. An improper airway
will affect the global individual
growth.8 The simultaneous
growth of these factors is not
nearly as significant as how
these factors interrelate during
facial growth and development.
For example, the basic design of
the face is established by a series
of interrelated factorial developments. The naso-maxillary
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complex is associated with the
anterior cranial fossae. The posterior boundary of the maxilla
determines the posterior limits
of the midface. This structural
plane is significant to facial and
cranium development. The basic structural format of facial
growth and development is dependent on, and governed by,
the interrelation of multiple
functional matrices. These
functional matrices include a
phenomenon of bone displacement and growth at the TMJ with
the maxillary forward and
downward movement equaling
mandibular growth upward and
downward. The displacement
and growth phenomenon is responsible for the spatial relationship necessary for functional joint movement resulting
in the final result of facial
growth.9 Additionally, muscle
adaptions affect dentoskeletal
development. The integration of
the musculoskeletal system affects respiration, mastication,
deglutition, and speech.2
This basic understanding of
facial growth and development
is relevant as adenoidal tissue
enlargement coincides with
major facial growth, for example, they occur simultaneously.
Facial growth may be restricted
by abnormal development of
adenoidal tissue resulting in abnormal swallowing and breathing patterns (Fig. 5).
Adenoidal growth and
development
Lymphoid tissue is normally
present as part of the
Waldeyer’s tonsillar ring in the
form of a nasopharyngeal tonsil
(Linder-Aronson 1970). The
Waldeyer’s ring is the system of
lymphoid tissue that surrounds
the pharynx. This system of tissue includes adenoids and
pharyngreal tonsils; lateral
pharyngeal tonsils; lateral pharyngeal bands; palatine tonsils
and lingual tonsils (Fig. 6). Tonsils and adenoids have disparate embryonic origins and
cytology even though they are
both part of Waldeyer’s ring.10
Bacteria may play a role in adenoid hyperplasia. Specifically,
different pathogens, such as
Haemophilus influenza and
Staphylococcus aureus, have
been associated with lymphoid
tissue hyperplasia. The adenoid lymphoid structures are
lined with ciliated respiratorytype epithelium which is normally distributed throughout
the upper and posterior nasopharynx walls. During the
presence of disease, the distribution of the dendritic cells
(antigen presenting cells) is altered. The result is that there is
Fig. 7
an increase in dendritic cells in
the crypts, and extrafollicular
areas, and a decrease in surface
epithelium dendritic cells.
Lymphoid tissue is normally
not apparent in the early infant
stage of life. Marked symptoms
of adenoid development are
most common in the childhood
age range of two to 12. During
adolescence, a decrease in adenoid size is noted as current with
the growth of the nasopharynx.
Rarely is adenoid tissue present
in adults and when it is noted it is
usually in an atrophic condition.
The cause of the involution of
the Waldeyer’s ring is still under
investigation.12 The imbalance
in the relationship between the
enlargement of the nasopharynx/nasopharyngeal
airway
and the concomitant growth of
adenoid tissue can result in reduced patent nasopharyngeal
airway and increased nasopharyngeal obstruction.10
The growth of adenoidal tissue as demonstrated by a bell
curve, peaks at or near age six6
and also begins involution at or
near this age as well (Fig. 7). Facial growth is coupled with adenoidal growth. As the cranial
base forms the roof of the nasopharynx, a close examination
of the growth and development
of the craniofacial complex becomes significant for evaluation
of the size and configuration of
the nasopharyngeal airway. Any
abnormal development regarding this craniofacial complex
may affect the nasopharyngeal
airway. Abnormal adenoidal
growth that occurs during
childhood, may consume the
nasopharnx
and
extend
through the posterior choanae
in the nose.13 This excessive
adenoidal growth usually interferes with normal facial growth
and can result in abnormal
breathing patterns, congestion,
snoring, mouth breathing, sleep
apnea.4 Eustachian tube dysfunction/otitis media, rhinosinusitis, facial growth abnormalities, swallowing problems, reduced ability to smell and taste,
and speech problems.12 Theoretically, many clinicians believe the blockage should be removed as soon as possible
through a surgical procedure
called adenoidectomy. However, according to a study conducted by Havas and Lowinger
one-third of child study patients, with traditional adenoidectomies, were ineffective
with intranasal extensions of
the adenoids obstructing the
posterior choanoe. For this segment of the study population the
“powdered-shaver adenoidectomy” was effective in the complete removal of the obstructive
Fig. 8
adenoid tissue ensuring postural patency.13
Upper airway obstruction
and mouth breathing
During normal nasal respiration, the nose filters, warms
and humidifies the air in preparation for its entry into the body’s
lungs and bronchi. This nasal
airway also provides a degree of
nasal resistance in order to assist the movements of the diaphragm and intercostals muscles by creating a negative intrathoracic pressure. This intrathoracic pressure promotes
airflow into the alveoli.7,15
Correct normal resistance is
2cm–3.5cm H2O/L/Sec and results in high tracheobronchial
airflow which enhances the oxygenation of the most peripheral
pulmonary alveoli. In contrast,
mouth breathing causes a lower
velocity of incoming air and
eliminates nasal resistance.
Low pulmonary compliance results.7 According to blood gas
studies, mouth breathers have
20 per cent higher partial pressure of carbon dioxide and 20
per cent lower partial pressures
of oxygen in the blood, linked to
their lower pulmonary compliance and reduced velocity.7,16.
Contributing factors in the
obstruction of upper airways include: anatomical airway constriction, developmental anomalies, macroglossia, enlarged
tonsils and adenoids, nasal
polyps and allergic rhinitis.5
However, for purposes of this
paper the focus shall be on enlarged adenoids as the major
contributing factor. There are
numerous studies that link adenoid hypertrophy with nasopharyngeal airway obstruction to
the development of skeletal and
dental abnormalities.14
Airway obstruction, resulting
from nasal cavity or pharynx
blockage, leads to mouth breathing which results in postural modifications such as open lips, lowered tongue position, anterior
and posteroinferior rotation of the
mandible, and a change in head
posture. These modifications
take place in an effort to stabilize
the airway. As previously discussed, facial structures are modified by postural alterations in soft
tissue that produce changes in the
equilibrium of pressure exerted
on teeth and the facial bones (Fig.
8). Additionally, during mouth
breathing, muscle alterations affect mastication, deglutition and
phonation because other muscles
are relied upon.2
DT page 22
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DENTAL TRIBUNE
22 Clinical
United Kingdom Edition · December 1–7, 2008
an added valuable diagnostic tool
for the orthodontist in the evaluation of children with upper airway obstructions14 (Fig. 13).
Treatment of nasal
obstruction
Fig. 9
DT page 21
Malocclusion – the issue still
in debate
Is there a cause and effect relationship between adenoids,
nasal obstruction and malocclusion?
Dentofacial changes associated with nasal airway blockage
have been described by CV
Tomes in 1872 as adenoid facies.
Tomes coined this term based on
his belief that enlarged adenoids
were the principle cause of airway obstruction and resulted in
noticeable dentofacial changes.7
Tomes reported that children,
who were mouth breathers, often exhibited narrow V-shaped
dental arches10 (Fig. 9). This narrow jaw is a result of mouth
breathers keeping their lips
apart and their tongue position
low. The imbalance between the
tongue pressure, and the muscles in the cheek, result in cheek
muscles compressing the alveolar process in the premolar region. Simultaneously, the lower
jaw postures back (Fig. 10).
These simultaneous actions
have been termed the compressor theory.11
Tomes’s views were supported in the 1930s by numerous
leading orthodontists. These
supporting clinicians reported
airway obstruction as an important aetiologic agent in malocclusion. Rubin advocated that in
order for these patients to fully be
assessed they must be thoroughly evaluated by both a rhinologist and orthodontist.7 Malocclusion is the departure from
the normal relation of the teeth in
the same dental arch or to teeth in
the opposing arch.3
Airway obstruction, coupled
with loss of lingual and palatal
pressure of the tongue, produces
alterations in the maxilla. The positioning of the tongue also plays
an important role in mandibular
development. The tongue displaced downward can lead to a
retrognathic mandible; and an
interposed tongue can lead to anterior occlusal anomalies.
Additionally,
maxillary
changes can be viewed in the
transverse direction, producing
a narrow face and palate often
linked with cross bite; in the anteroposterior direction, producing maxillary retrusion; and in
the vertical direction causing an
increase in palatal inclination as
related to the cranial base and
excessive increases of the lower
anterior face height. The most
commonly found occlusal alterations are cross bite (posterior
and/or anterior), open bite, increased over jet, and retroclination of the maxillary and
mandibular incisors.2 Mahony
Fig. 10
and Linder-Aronson’s findings
were in agreement with the significant correlation between
changed mode of breathing and
diminished mandibular / palatal
plane angle (ML/NL) found in
adenodectomised children.22
Several authors have taken
the position that alleged faces are
not consistently found to be associated with adenoids, mouth
breathing, nor a particular type
of malocclusion; and that there is
no cause and effect relationship
between adenoids, nasal obstruction/mouth breathing and
malocclusion.
Proponents of this position
believe that the V-shaped palate
was inherited and not acquired
through mouth breathing. Hartsooh (1946), on a review of literature related to mouth breathing,
concluded that mouth breathing
is not a primary etiological factor
in malocclusion. Additionally,
Whitaker (1911) found that in a
study of 800 children, who underwent adenoidectomy or tonsillectomy only 30 per cent had dental anomalies that needed orthodontic intervention. There is
some suggestion that adenoids
and hypertrophic tonsils are a
consequence of a thyroid hormone deficiency. This hormone
deficiency acts as a catalyst for
activating the organism’s de-
Fig. 11
fense mechanisms, which include hypertrophy of lymphoid
tissue.11 Another orthodontic clinician, Vig, took the position that
without documented total nasal
obstruction, any surgery or other
treatment to improve nasal respiration is empirical and difficult
to justify from an orthodontic
point of view.7,17
Nasal respiratory evaluation
The relationship of airway
obstruction and dentofacial
structures/malocclusion is still
the subject of investigation and
controversy amongst orthodontists. The correlation between
functional problems and morphologic characteristics is yet to
be solidified. Regardless of varied opinion in this area practitioners should observe each patient carefully.
Suggested protocol
As the patient enters the
room, facial and head posture
should be noted to see if the lips
are closed during respiration.
Signs of allergic rhinitis should
be noted, as well as histories of
frequent colds or sinusitis. Assessment of family history for allergies is important. Sleep history should be evaluated: sleep
apnoea, loud snoring, openmouth posture while asleep.
Patient is asked to seal their
lips – difficulty breathing
through nose should be noted.
One nostril can be occluded and
the response noted – same procedure on the other side. (Fig. 11)
Fig. 12
The evaluation of nasal airway patency is complicated, especially when the possibility exists that airways may clinically
appear inadequate but be quite
functional physiologically. Lip
separating or an open-mouth
habit is not an infallible indicator
of mouth breathing. Often complete nasal respiration is coupled
with dental conditions that cause
open-mouth posture.10
Adenoid evaluation
Nasopharyngeal space and
the size of adenoids have been
evaluated using different methods of assessment:
Fig. 13
Fig. 14
1. Determination of the roentgenographic adenoid/nasopharyngeal ratio (a lateral
cephalometric xray)
2. Flexible optic endoscopes (Fig.
12)
3. Acoustic rhinometry
4. Direct measurements during
surgery.
Direct measurements are
considered to be the most accurate because space can be assessed in three directions.12 A lateral cephalometic radiograph is
Adenoidectomy with or without tonsillectomy is indicated if
hypertrophied adenoids (and
tonsils) are the cause of upper
airway obstruction.7
Powered-Shaver Adenoidectomy – Adenoidectomy coupled
with Endoscopic Visualization
will assist in achieving adequate
removal of adenoids particularly high in the nasopharnx.
Use of the powered-shaver technique allows for better clearance of obstructive adenoids.
The end result is more reliable
restoration of nasal patency.13
Septal surgery (rarely indicated
in the child) but may be considered in the presence of a marked
nasal septal deflection with impaction. Conservative septal
surgery in growing patients will
not have an adverse effect in
dentofacial growth.7,18,19,20
– Maxillary expansion (RME or
SAME) – an orthodontic procedure that widens the nasal
vault7,18 (Fig. 14).
– Cryosurgery or electrosurgery
– this is a viable option for patients with vasomotor rhinitis.7
– Bipolar Radiofrequency Ablation (allergic rhinitis) – performed under local anesthetic
– Inferior turbinectomy – Using
powered instrumentation
– Use of nasal sprays.
Fig. 15a
Fig. 15b
Fig. 15c
Fig. 15d
Conclusion
The effect of adenoids on facial expression, malocclusion
and mode of breathing has been
a topic of debate and investigation by practitioners in the field
for the last one hundred years. A
review of the literature exposes
several theories.
A healthcare provider, with a
practice philosophy based on
prevention of malocclusion development, cannot ignore the
early years of the patient’s
growth cycle. By age twelve, 90
per cent of facial growth has already occurred. This is the age
when many practitioners begin
orthodontic treatment.7 This is
the age when 80–90 per cent of
craniofacial growth is complete,
so most formation and/or deformation has occurred.21 To wait
until 90 per cent of the abnormality has occurred, before beginning treatment, is not consistent
with a preventive philosophy. Interceptive measures must be initiated sooner. Early intervention
requires an acceptance of a multidisciplinary approach to total
patient health. An integrated approach to patient evaluation, diagnosis and treatment is most effective. Primary care physicians,
dentists, allergists, otorhinolaryngologists, and orthodontists
must all work together for early
prevention and management of
young patients with increased
nasal airway resistance.
After diagnosis, a comprehensive risk benefit analysis re-
Fig. 15e
Fig. 15f
garding early intervention must
be considered. Although hereditary and environmental factors
must be considered, the universal goal is the promotion of
proper
nasal
respiration
throughout a child’s early years
of facial growth.
Figure 15 (a–f) shows the before-and-after treatment results
of a young girl who had her adenoids removed, and then underwent maxillary expansion before
full-fixed braces. She was treated
as a second opinion against the
removal of four premolar teeth to
relieve dental crowding. DT
References
1. Mattar, SE, Anselmo-Lima, WT,
Valera, FC and Matsumoto, MA,
Skeletal and Occlusal Characteristics in Mouth-Breathing Pre-
DENTAL TRIBUNE
School Children, J Clin Pediatr
Dent 2004 28(4):315-318.
2. Valera, FC, Travitzk, LV, Mattar, SE,
Matsumoto, MA, Elias, AM,
Anselmo-Lima, WT, Muscular,
Functional
and
Orthodontic
Changes in Pre-School Children
with Enlarged Adenoids and Tonsils, Int J Pediatr Otorhinolaryngal
2003, Jul; 67(7):761-70.
3. Khurana, AS, Arora, MM, Gajinder
S., Relationship Between Adenoids
and Malocclusion, J Indian Dental
Ass., April 1986; 58:143-145.
4. Pellan, P., Naso-Respiratory Impairment and Development of
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Clinical 23
United Kingdom Edition · December 1–7, 2008
About the author
About the author
Dr Kevin Williams
manages two general dentistry practices in
Greenville and Spartanburg, South Carolina,
with an emphasis on facial driven orthodontics
and oral surgery. He received his dental degree
from the Medical University of South Carolina
in 1993. His interest in airway and malocclusion developed from his children’s airway issues. Dr Williams is a Fellow in the Academy of
General Dentistry and a Certified Senior Instructor in the International Association of
Orthodontics. Email [email protected].
Dr Derek Mahony
is a graduate of the University of Sydney,
Faculty of Dentistry, and an Alumnus of the
University of London, masters programme
in orthodontics. He is a Fellow of the International College of Dentists and is considered a pioneer, throughout the world, in
raising dentist’s awareness of the need for
early interceptive orthodontic treatment.
Email [email protected].
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1.5Hour
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AOJ; 20:93-98,2004.
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