THE AETIOLOGY OF MALOCCLUSION
THE AETIOLOGY OF CLASS II MALOCCLUSION
CLASS II MALOCCLUSION
Class II malocclusion can be divided into two types:
Class II Div I
o the lower incisor edges lie posterior to the cingulum plateau of the upper incisors,
there is an increased overjet and the upper central incisors are proclined
Class II Div II
o the lower incisor edges lie posterior to the cingulum plateau of the upper incisors,
the overjet is minimal but may be increased and the upper central incisors are
There are four major factors which contribute to the aetiology of any malocclusion and to the
relationship between the maxilla and mandible:
Usually, a malocclusion is a result of the combination of all four of the above factors.2
AETIOLOGY OF CLASS II DIVISION I MALOCCLUSION
A class II skeletal pattern is usually present in patients with a class II division I malocclusion. This is
most commonly due to a retrognathic mandible. It is also possible for patients to present with a
protruded maxilla but this is less common. Size discrepancies between the mandible and maxilla may
also be the cause of the class II malocclusion and would be due to decreased mandibular size and
increased maxillary size. Vertical skeletal discrepancies are also common.3
The soft tissues exert forces on the teeth and can contribute to the malocclusion
Patients with class II division I malocclusion usually have incompetent lips due to the prominence of
the upper incisors. This can encourage upper incisor proclination and lower incisor retroclination as
the lower lip is drawn behind the upper incisors and therefore worsening the incisor relationship.
However, dentoalveolar compensation can occur to mask the skeletal problem if the patient
postures the mandible forwards or uses their circumoral muscles to achieve an oral seal.
A high lip line can cause protrusion of the upper incisors as it means the lip is no longer placing force
over the upper incisors to prevent them splaying outwards
Crowding in the upper arch can result in a lack of space for the upper incisors, pushing them labially
out of the arch and cause an increase in overjet.
Habits such as digit sucking can have a significant effect on a patient’s malocclusion4. Digit sucking
causes proclination of the upper incisors and retroclination of the lower incisors. This will cause an
increase in overjet and can exacerbate an existing class II malocclusion.
AETIOLOGY OF CLASS II DIVISION II MALOCCLUSION
Class II division II malocclusion is usually associated with a class II skeletal pattern. The vertical
skeletal pattern is also typically reduced which results in the over eruption of the lower incisors and
an increased overbite, due to an absence of an occlusal stop.
A high lower lip line is common in class II division II and this causes retroclination of the upper
A high lip line can also cause retroclination of the upper incisors due to forces being applied to the
Crowding is common in patients with a class II div II relationship. The retroclination of the upper
incisors leads to a smaller arc circumference creating a lack of space. Lower arch crowding can also
be seen as the retroclination of the upper incisors and increased overbite can cause the lower
incisors to tilt lingually and thus cause crowding.
In a few cases, the increased overbite can be traumatic and has been seen to cause ulceration of the
palatal tissues and stripping of the lower labial gingival tissues.
AETIOLOGY of Class III
Variation between and within populations can be observed almost until the nth degree and in terms
of occlusion and malocclusion the same rules apply. Before understanding how and why differences
occur between individuals it is important to clearly define what is a Class III malocclusion and how is
this different from so called normal occlusion. Once
we understand the difference then it will be possible
to draw up some conclusions as to why these
Angle described a Class III malocclusion as one
where the mandibular first molar is anteriorly placed
in relation to the maxillary first molar (Figure 1).
Normal occlusion, again described by angle is where
the mesiobuccal cusp of the upper first molar
Figure 1 showing anterior position of lower first molar, occludes with the buccal groove of the lower first
and also dento-alveolar compensation
molar. In simplest terms, the mandible is placed
further forward than the maxilla. The British Standards incisal classifies Class III as – the lower incisor
edge occludes anterior to the cingulum plateau of the upper incisors. However Angle’s classification
is more useful in defining this malocclusion as the soft tissues often mould the teeth and camouflage
a class III.6
Class III relationships are relatively uncommon in the UK, in the region of 5%, interestingly in
Scotland this figure is seen to rise to 8.8%, and in oriental populations they can be more common
with up to a 22% incidence. 7
The aetiology of the malocclusion can be looked at by considering 4 causative areas:
The soft tissues
It has been shown that a Class III malocclusion is largely hereditary, and skeletal pattern
discrepancies are most significant in causing the malocclusion. Environmental, dental and soft tissue
factors also play a role, however it is unusual that these alone cause a malocclusion without some
sort of skeletal involvement. Class III malocclusions are highly multi-factorial.
The majority of Class III malocclusions occur due to a discrepancy in the skeletal pattern. There are a
number of ways in which this may manifest, and is often a mixture of
Increased mandibular length
A more anteriorly placed glenoid fossa – leading to mandibular
Reduced maxillary length
A more retruded position of the maxilla leading to maxillary
A reduced cranial base angle (ANB <2o)
Class III malocclusions cannot be pinpointed to one discrepancy of the
Figure 2 showing
skeletal pattern and so is often a mixture of one of more of the above. mandibular prognathism
Most patients do however present with an increase in mandibular size and length with a more
anterior position in the glenoid fossa. The skeletal relationship discrepancies may work
synergistically together to enhance the malocclusion, or against each other to cancel out, or
Class III malocclusions are also associated with increased or reduced vertical skeletal relationships,
more so in male patients than female. The growth pattern of the mandible is very important in this.
A forward rotation growth pattern could cause an increased overbite and pronounced chin, whereas
a backward rotation growth pattern would cause a decreased overbite . The growth of the mandible
is very important to consider when treatment planning for a class III case, as further growth after
treatment could worsen the problem.
It is accepted that class III is largely an inherited trait. Often, a child with a Class III will have a sibling
or parent with the same malocclusion. Studies are now being carried out to determine the exact
genes which are involved and how they affect the trait – however these aren’t currently very
However studies have shown that although it is largely inherited, environmental factors also play a
role in influencing the growth of the cranial base.
In a class III malocclusion the maxillary incisors lie in a
similar plane to a normal occlusion, however can be
proclined due to soft tissue influences. The mandibular
incisors are often seen to be more anteriorly placed
than in normal occlusions – which confirms with the
theory that it is the size and position of the mandible
which is most influential in a class III malocclusion.10 Figure 3 showing a crowded upper arch
A narrow maxillary arch coupled with a broad, anteriorly placed mandibular arch can cause a class III
malocclusion. Crowding is subsequently commonly seen in the upper (Figure 3), and a well aligned or
even spaced lower leading to a buccal crossbite.
The soft tissues have a role to play in class III malocclusions. They do not tend to cause it, they tend
to mask the problem. The tongue tends to procline the upper incisors and the lips can retrocline the
lowers. This results in an incisal relationship which is much less severe than the underlying skeletal
relationship – this is known as dento-alveolar compensation. Dento-alveolar compensation tends to
be present in females more so than in males.
The environmental factors that have been discussed include the following,
Difficulty in nasal breathing
Congenital anatomic defects
Disease of the pituitary gland
Habit of protruding the mandible
Trauma and disease
Premature loss of 6
Irregular eruption of permanent incisors or loss of deciduous incisors.
The aetiology of Class III is very complex and multi-factorial. Baker reported a case in which
monozygotic twins were concordant for mandibular prognathism. The purpose was to assess the
variation of cranio-dento-facial complex. Both twins had similar dentition but their occlusion was
dissimilar to some extent. Both twins were given full assessments and from the recorded
information some conclusion were made. 11
Some findings were concluded to be due to environmental factors, e.g. The form of the cranial base
and the anterior position of the mandible. However the latter is up for debate as other journals
described this as a genetic factor. Other findings were concluded to be definitely influenced by
Another study looked at a pair of monozygotic twins. It was seen that the vertical relationships of
the twins were concordant with each other, however the relationship of the cranial base altered
slightly. This shows that the cranial base was least affected genetically and that some environmental
factors definitely had a role to play in the malocclusion. 12
Therefore from the twin studies it was concluded that genetics is not the sole reason for class III
malocclusion but there are other factors to be considered, namely environmental factors.
AETIOLOGY OF ANTERIOR OPENBITE
Dental open bite
Cases of AOB in which the vertical skeletal pattern is not contributory.
Open bite caused by digit sucking is characterised by an asymmetrical open bite, the greater extent
being on the side the digit is most commonly placed, and upper incisal proclination (effects on the
lower incisors are more variable), and often over eruption of posterior teeth as a result of the digit
acting as a barrier to eruption of the anteriors.
The incidence of digit sucking decreases with age, from around 30% at 1 year of age, dropping to
12% at 9 and 2% at 12, which is important because the influence made by this habit depends on the
age of the patient, the intensity, frequency and duration of the digit sucking. In younger patients
there need be less concern since open bites due to digit sucking in the primary dentition tend to
resolve spontaneously when the child gives up the habit.13
The extent of the displacement of the teeth is more effected by the duration of the habit than the
magnitude, children who digit suck for many hours a day especially those sleeping with a digit in the
mouth, can experience significant displacement, and some studies suggest there may even be mild
skeletal displacement as well as dental displacement.
Abnormal Tongue Function
Abnormal tongue thrusts are often noted in patients with AOB however it is believed that these are
often a result of the AOB or other factors, and Proffit suggests tongue thrusts are not likely to be the
causative factors in an AOB, more likely abnormal tongue resting positions may have an effect as the
durations involved in thrusts, whether endogenous or adaptive (adaptive being in an adaptive
response to an AOB, whereas endogenous cases are rare usually relating to excessive circumoral
amuscular activity on swallowing), is too short to cause any displacement but the durations involved
when the tongue is at rest are much greater. Often an abnormally large tongue (macroglossia) can
result in unusual tongue resting positions resulting in AOB, such cases will require tongue reduction
as part of their treatment.
SKELETAL OPEN BITE
The open bite is at least partly due to the vertical facial form, usually the AOB develops due to
excessive vertical growth. These are usually more severe than dental open bites, often with only the
most distal molars in contact. There is normally an increased lower facial height and there may be a
vertical maxillary excess. Characteristically the FMPA is increased, and there is often over eruption of
the incisors though insufficiently so to close the AOB. Skeletal open bites are normally also
associated with the development of the mandible, and there are signs that a patient may develop an
AOB such as backward inclination of the condylar head or a straight mandibular canal.
These can affect the oral and facial musculature giving rise to AOB, Gershater reported an incidence
of 32.3% in patients with learning disabilities
A major decrease in tonic muscle activity as a result of muscular dystrophy ( or other muscle
weakness syndromes/and some forms of cerebral palsy) allow the mandible to rotate downwards
from the rest of the facial skeleton, leading to posterior growth rotation of the mandible and
excessive posterior tooth eruption, narrowing of the maxillary arch and an AOB that gets worse with
grow (Figure 4).14
Figure 4 Lengthening of the lower face and accompanying anterior open bite in a 15 year old patient
resulting from muscle weakness due to muscular dystrophy.
Iatrogenic Open Bite
Failure to prevent over eruption of posterior teeth when biteplanes and functional appliances are
used may also give rise to AOB, as may extrusion of the molar teeth during fixed appliance treatment
if the mechanics of the appliance are poor.
Pathological Open Bite
Trauma to the facial skeleton, acromegaly and cleft palate are all associated with localised AOB.
The aetiology of malocclusion; 1982 British dental journal 152 (3), pp. 73
Aetiology of malocclusion of the teeth; Eskes, P.W.H., Leighton, B.C. 1992 Archives of Disease in Childhood 67
(3), pp. 352
The heritability of malocclusion: part 2. The influence of genetics in malocclusion. Mossey,
P.A. 1999 British journal of orthodontics 26 (3), pp. 195-203
Is digit sucking of significance?; Brenchley, M.L. 1991 British dental journal 171 (11-12), pp. 357-362
The role of soft tissues in the aetiology of malocclusion. Turner, S., Nattrass, C., Sandy, J.R.
1997 Dental update 24 (5), pp. 209-214
The aetiological factors in Class III malocclusion; Battegel JM; European Journal of Orthodontics; October
Treatment Planning in Class III Malocclusion; G.T. McIntyre; Dental Update 2004; 31:013-021
An Introduction to Orthodontics; Mitchell, Laura; 3 Edition 2007.
Evidence of Linkage in a Hispanic Cohort with a Class III Dentofacial Phenotype S. Frazier-Bowers, R. Rincon-
Rodriguez, J. Zhou1, K. Alexander, and E. Lange. Journal of Dental Research 88(1):56-60, January, 2009
Classification of Angle Class III malocclusion and its treatment modalities; JU. Park, SH. Baik; 2001, Int J Adult
Orthod Orthognath Surg; Vol. 16, No. 1, 19-29.
Similarity of malocclusion in families; Baker CR. 1924; International Journal of Orthodontics; 10:459-62
Class III Malocclusion: Genetics or Environment? A Twins Study. Jena AK, Duggal R, Mathur VP, Parkash H.
Indian Society of Pedodontics and Preventive Dentistry March 2005;23(1): 27-30
The Causes, Diagnosis and Treatment of Anterior Open Bite; Daniel Burford and Joe H. Noar; 2003, Dental
Update; 30: 235-241
Contemporary Orthodontics, 4 Edition; 2007; William R. Proffit, Henry W. Fields, David M. Sarver; Mosby