Etiology of malocclusion local factors

ETIOLOGY OF
MALOCCLUSION
www.indiandentalacademy.com

INTRODUCTION:
Certain original causes act for a time at a site and
produce a result. This an expression of Koch’s
postulates, but it is an oversimplification to
assume that Koch’s logic applies to developmental
problems eg. Malocclusion as it does to diseases,
for there are few specific causes of precise
malocclusions.

For eg. Tuberculosis may always be caused by
Mycobacterium tuberculosis, but open bite is not
always caused by thumb-sucking. Also there is no
virus that produces Class II div 1 malocclusion or an
organism that specifically causes cross-bite. Thus
rather than having “causes” as do some diseases,
malocclusions are usually clinically significant
variations from the normal range of growth and
morphology. Etiologic factors contribute to the
variance more often than they simply “cause” it.

LOCAL FACTORS:
1. Anomalies of number
a. Supernumerary teeth
b. Missing teeth
2. Anomalies of tooth size
3. Anomalies of tooth shape
4. Abnormal labial frenum
5. Premature loss
6. Prolonged retention of deciduous teeth
7. Delayed eruption of permanent teeth
8. Abnormal eruptive path
9. Ankylosis
10. Dental caries
11. Improper dental restorationswww.indiandentalacademy.com

ANOMALIES IN NUMBER OF TEETH:
In order to achieve good occlusion, normal number
of teeth should be present. Presence of extra teeth or
absence of one or more teeth predisposes to
malocclusion.
Heredity plays a strong part in anomalies in number
of teeth. According to some authors appearance of
extra teeth is merely a left over from the primitive
anthropoids who had a dozen more teeth than
Homosapiens.

There is a relatively high frequency of extra or
missing teeth associated with congenital deformities
such as cleft lip and cleft palate. Generalized
pathoses such as ectodermal dysplasia, cleidocranial
dysostosis and others may also affect the number of
teeth in dental arches.

SUPERNUMERARY TEETH:
Teeth that are extra to the normal complement are
termed supernumerary teeth. These teeth have
abnormal morphology and do not resemble normal
teeth. Extra teeth that resemble normal teeth are
called supplemental teeth.

They result from disturbances during the initiation
and proliferation stages of dental development.
There is no definitive time when supernumerary teeth
may develop. They may form prior to birth or as late
as 10- 12 years of age. They usually develop from a
3rd
tooth bud arising from the dental lamina near the
permanent tooth bud.

Supernumerary teeth may be found in any location;
but the most common is the “mesiodens”. It is
situated between the maxillary central incisors and
occurs singly or paired, erupted or impacted, and
occasionally even inverted.

Of major concern is the deflection or non-eruption
of maxillary central incisors as a result of
supernumerary teeth.
In any patient who shows a marked difference in
times of eruption of permanent maxillary central
incisors, this condition should be considered suspect
and investigated radiographically.
The careful removal of a supernumerary tooth
allows the permanent tooth to erupt though it may be
malposed. However, this is not always true; surgical
and orthodontic intervention may be necessary.

The maxillary 4th
molar* is the 2nd
most common
supernumerary tooth and is situated distal to the 3rd
molar. It is a small rudimentary tooth but may be of
normal size. A mandibular 4th
molar is also seen
occasionally, but this is much less common than the
maxillary molar.
Other supernumerary teeth seen with some
frequency are mandibular premolars and maxillary
lateral incisors*.
* Textbook of oral pathology – Shafer, Hine, Levywww.indiandentalacademy.com

Supernumerary teeth in the deciduous dentition
are less common than in the permanent dentition.
When this situation does occur in the deciduous
dentition, it is usually maxillary lateral incisor.
Supernumerary teeth may be erupted or
impacted. Impacted teeth pose a risk of cystic
formation.

Supernumerary teeth can cause:
1. Non-eruption of adjacent teeth
2. Delay the eruption of adjacent teeth
3. Deflect the erupting teeth into abnormal locations
4. Crowding in the dental arches.

MISSING TEETH:
Congenitally missing teeth are by far more common
than supernumerary teeth. Whereas supernumerary
teeth are usually found in maxilla, missing teeth are
frequent in both jaws. Also, missing teeth are more
likely to be bilateral than supernumerary teeth.

The following are some of the commonly missing
teeth in decreasing order of frequency*:
1. Maxillary and mandibular 3rd
molars
2. Maxillary lateral incisors
3. Mandibular 2nd
premolars
4. Mandibular incisors
5. Maxillary 2nd
premolars

Congenitally missing teeth are uncommon in
deciduous dentition, but when they occur they usually
involve maxillary lateral incisors.
Since primary teeth give rise to the permanent tooth
buds, usually there will be no permanent tooth if the
primary predecessor is missing.
Congenital absence of teeth result from disturbances
during the initial stages of dental development- initiation
and proliferation.

Anodontia, the total absence of teeth, is the
extreme form. The term oligodontia or partial
anodontia refers to congenital absence of many but
not all teeth, whereas the term hypodontia implies
the absence of only a few teeth.
Total or partial anodontia is seen rarely but the
patient should be carefully checked if there is any
history of missing teeth in the family.

Although the etiology of missing teeth is
unknown, heredity seems to play more significant
role for missing teeth than supernumerary teeth.
Hereditary ectodermal dysplasia may be associated
with total or partial anodontia and in these instances
the few teeth that are present may be deformed or
misshapen, frequently cone shaped.
Missing 3rd
molars may be evidence of an
evolutionary trend towards fewer teeth.

As a general rule, if only one or few teeth are
missing, the absent tooth will be the most distal tooth
of any given type. If a molar tooth is congenitally
missing, it is almost always the 3rd
molar; if an incisor
is missing, it is nearly always the lateral; if a premolar
is missing, it is almost always the 2nd
premolar.
Rarely is a canine the only missing tooth.

Congenitally missing teeth can cause:
1. Spacing in the dental arches
2. Aberrant swallowing patterns
3. Abnormal tilting / axial inclination or location of teeth
4. Absence of permanent teeth may result in over-
retained deciduous teeth.

ANOMALIES OF TOOTH SIZE:
There should be harmony between the tooth size
and the arch length, and also between the maxillary
and mandibular tooth size, in order to have normal
occlusion. An increase in size of teeth results in
crowding while, smaller sized teeth predispose to
spacing.

Abnormalities in tooth size result from disturbance
during the morphodifferentiation stage of tooth
development.
The size of teeth is largely determined genetically.
Thus most of these conditions show a positive family
history.
Anomalies of size of teeth can be of 2 types:
1.Microdontia
2. Macrodontia

1.MICRODONTIA:
This term is used to describe teeth which are
smaller than normal.
3 types are microdontia are recognized:
a. True generalized microdontia
b. Relative generalized microdontia
c. Microdontia involving a single tooth

a. True generalized microdontia:
All teeth are smaller than normal. Aside from its
occurrence in cases of pituitary dwarfism,
this condition is exceedingly rare.
b. Relative generalized microdontia:
Normal or slightly smaller than normal teeth are
present in jaws that are somewhat larger than
normal. Since it is well
recognized that a person
may inherit jaw size from
one parent and tooth size
from the other parent, the
role of hereditary factors
in producing such a condition
is obvious.www.indiandentalacademy.com

c. Microdontia involving a single tooth:
This is a rather common condition. It affects the
(in decreasing order of frequency) maxillary lateral
incisors, 3rd
molars, mandibular premolars*.

2. MACRODONTIA:
This term is used to describe teeth which are
larger than normal.
3 types of macrodontia are recognized:
a. True generalized macrodontia
b. Relative generalized macrodontia
c. Macrodontia involving single tooth

b. Relative generalized macrodontia:
Normal or slightly larger than normal teeth are
present in jaws that are somewhat smaller than
normal.
c. Macrodontia involving single tooth:
This condition is relatively uncommon. The
tooth may appear normal in every aspect except
for its size.
a. True generalized macrodontia:
This condition in which all teeth are larger than
normal has been associated with pituitary
gigantism, but is extremely rare.

ANOMALIES OF TOOTH SHAPE:
Anomalies of tooth size and shape are often
interrelated. Abnormally shaped teeth predispose to
malocclusion.
Anomalies of tooth shape include:
1. The presence of peg shaped maxillary lateral
incisors is often accompanied by spacing and
migration of teeth.

2. Abnormally large cingulum on maxillary incisors-
Prevent establishment of normal overbite and
overjet. The involved tooth is usually in labioversion
due to the forces of occlusion.
3. Additional lingual cusp of mandibular 2nd
premolars-
Increase the mesiodistal dimension of tooth

4. Fusion-
Fused teeth arise through the union of 2 normally
separated tooth germs. Fusion may be either
complete or incomplete. Some physical force or
pressure produces contact of the developing teeth
and their subsequent fusion.

Fusion may lead to –
1. Spacing in the dental arches
2. Affect aesthetics
3. Sometimes may complicate its movement by
orthodontic means

5. Gemination –
Results from attempt at division of single tooth
germ, leading to the formation of 2 incomplete
teeth.
May lead to:
1. Crowding
2. Affect occlusion
3. Aesthetics affected

6. Talon cusp –
An anomalous structure projecting lingually from
the cingulum area of a maxillary or mandibular
permanent incisor. It poses problems to the patient
in terms of caries control and interferes with proper
occlusion.

7. Congenital syphilis –
It is often associated with hypoplasia of maxillary
and mandibular anteriors. Characteristics of
congenital syphilis are “Hutchinson’s incisors”
and “mulberry molars”.

8. Dilaceration –
Characterized by an abnormal angulation
between the crown and root of a tooth, or angulation
within the root. Usually occurs due to trauma during
the period in which the tooth is forming with the result
that the position of the calcified portion of the tooth is
changed and the remainder of the tooth is formed at
an angle.

Dilacerated tooth often fails to erupt to proper
level and can thus interfere with normal occlusion.
They may also complicate extraction of teeth and
may interfere with tooth movement and
alignment.

9. Dens evaginatus –
A developmental condition that appears
clinically as an accessory cusp or a globule of
enamel on the occlusal surface between the
buccal and lingual cusps mainly of premolars.

Dens evaginatus results because of proliferation
and evagination of an area of inner enamel
epithelium and subjacent odontogenic mesenchyme
into the dental organ during early tooth development.
It may result in incomplete eruption, displacement
of teeth and may interfere with normal occlusion.

10. Supernumerary roots –
This developmental condition is not
uncommon and may involve any tooth. Teeth
with supernumerary roots may provide more
resistance to tooth movement and may also
complicate extraction.

ABNORMAL LABIAL FRENUM:
Spacing between the maxillary central incisors
and the presence of the fibrous tissue attachment
such as the labial frenum provides an excellent
“chicken and egg” routine for controversy.
Which came first?

At birth the frenum is attached to the alveolar
ridge, with fibers actually running into the lingual
interdental papilla. As the teeth erupt and as the
alveolar bone is deposited, the frenum attachment
migrates superiorly with respect to the alveolar
ridge. Fibers may persist between the maxillary
central incisors and in the V-shaped intermaxillary
suture, attaching to the outer layer of periosteum
and connective tissue of the suture.

Some of the other causes of midline diastema:
1. Ugly duckling stage
2. Microdontia
3. Macrognathia
4. Congenitally missing lateral incisors
5. Supernumerary tooth in the midline
6. Peg laterals
7. Abnormal pressure habits eg. Digit sucking,
tongue thrusting, lip biting or sucking
8. Midline cysts
9. Heredity

Thus a thorough examination and differential
diagnosis are imperative before an orthodontist plans
frenectomy for a patient.
One diagnostic adjunct that helps to determine
the role of the frenum is the “blanche test”. Ordinarily,
the frenum has migrated sufficiently superiorly by 10-
12 years of age that a tug on the upper lip (lip pulled
superiorly and anteriorly) causes no demonstrable
change at the maxillary central interdental papilla.

Where there is a heavy fibrous frenum that
may be contributory, however, a “blanching” of
the tissue just lingual to the maxillary central
incisors can be noted. This usually means that a
fibrous attachment still remains in this area and
may interfere with the normal developmental
closure of spacing.

Existence of a heavy fibrous frenum does not
always mean that spacing may be present.
Frequently, during the closure of diastema with
orthodontic therapy, the interposed fibers may
atrophy, making a frenectomy unnecessary.
It is an error to surgically remove the frenum
and then delay orthodontic treatment in the hope
that the diastema will close spontaneously.

If the frenum is removed while there is still a
space between the central incisors, scar tissue
forms between the teeth as healing progresses
and a long delay may result in a space that is more
difficult to close than it was previously.
It is better to align the teeth before frenectomy.
If the diastema is relatively small ( < 2mm), it is
usually possible to bring the central incisors
completely together before surgery.

If the space is large ( > 2mm), and the frenal
attachment is thick, it may not be possible to
completely close the space before surgical
intervention. The space should be closed atleast
partially and the orthodontic tooth movement to
bring the teeth together should be resumed
immediately after the frenectomy, so that the teeth
are brought together quickly after the procedure.

When this is done, healing occurs with the teeth
together, and the inevitable postsurgical scar
tissue stabilizes the teeth in their correct position
instead of creating obstacles to final closure of
space.

PREMATURE LOSS OF DECIDUOUS TEETH:
In this instance, the word “premature” refers to
the child’s own dental development, not to
population standards. Specifically, it refers to
the stage of development of the permanent
tooth that will succeed the lost primary tooth.
Premature loss can occur due to:
1. Caries
2. Trauma
3. Endocrinal disturbances like
hyperthyroidism
4. Metabolic disturbances like
hypophosphotasia

When a primary tooth is lost before the permanent
successor has started to erupt, bone may reform
atop the permanent tooth, delaying its eruption.
When its eruption is delayed, more time is available
for other teeth to drift into space that would have
been occupied by the permanent tooth.

1. The loss of primary incisors, ordinarily is not a
matter of concern; however if a primary incisor is lost
well before the eruption time of permanent incisors or
in cases of arch length deficiency or overjet problems,
the spaces tend to close rapidly. Therefore if a primary
incisor is lost before age 4, radiographs should be
taken of the developing permanent incisors and the
space observed regularly.

2. Primary cuspids, when lost prematurely may be
a matter of great concern. When there is a
generalized lack of arch length in both maxillary
and mandibular dental arches, the deciduous
canines are frequently shed prematurely and nature
attempts to provide more space to align the
permanent incisors that have already erupted. This
type of premature loss is often a clue for further
guided extraction of deciduous teeth and possible
removal of the 1st
premolars later.

In the maxilla, the permanent cuspid erupts so
late that if the primary cuspid is lost before the
central and lateral incisors have moved together, it
may permit permanent spacing of the anterior
teeth.
Strange as it may seem, incisor spacing and
labioversion of cuspid may occur in the same
patient.
Primary cuspid loss in the mandible is more
frequent and is more serious. The untimely loss of
these teeth may result in lingual tipping of the four
mandibular incisors.

3. The loss of primary 1st
and 2nd
molars is almost
always a matter of concern, even when occlusion
is normal.
In the mandibular arch, the leeway space is
1.7mm on each side, whereas, in the maxillary
arch it averages only 0.9mm on each side because
of greater size of the permanent canines, 1st
and
2nd
premolars. Leeway space is necessary for the
final alignment of the incisors and a “settling in” of
the occlusion as the terminal plane relation is
corrected.

Premature loss of 2nd
deciduous molars will very
likely lead to mesial drift of the 1st
permanent
molars and blocking the eruption of 2nd
premolars. Even when the premolar erupts, it is
deflected buccally or lingually into a position of
malocclusion.

When 2 or more primary molars are lost
prematurely, there is, in addition to drifting – loss of
posterior dental support and the mandible may be
held in a position to provide some sort of adaptive
occlusal function and a resulting accommodative
posterior crossbite. These positional crossbites
have far reaching effects on the TMJ, the
musculature, the growth of the facial bones and the
final position of permanent teeth.

Davey in a study of loss of maxillary primary molars,
concluded that the factors related to the migration
of the 1st
permanent molars were –
1. Age when the primary teeth are lost :-
the earlier the deciduous teeth are lost before
the permanent teeth are ready to erupt, the
greater is the possibility of malocclusion.
2. Arch length deficiency or crowding :-
the early loss of deciduous teeth may worsen
the malocclusion.
3. Cusp height :-
high permanent molar cusps inhibit drifting of
teeth.

PROLONGED RETENTION OF DECIDUOUS TEETH:
This refers to a condition where there is undue
retention of deciduous teeth beyond the usual eruption
age of their permanent successors. A deciduous tooth
that fails to undergo resorption will prevent the normal
eruption of its permanent successor.

Prolonged tooth retention versus Abnormal eruption
Which is primary?
Still a controversy
But, the important thing to recognize departure from
the normal. Regardless of the primary or secondary
status of deciduous versus permanent tooth, the
method of control is usually the same – removal of
the primary tooth according to the timetable
established by the same tooth in the remaining
quadrants of the mouth.

Prolonged retention of deciduous teeth can occur
because of :-
1. Absence of underlying permanent teeth
2. Endocrinal disturbances such as
hypothyroidism and hypopituitarism
3. Ankylosed deciduous teeth that fail to resorb
4. Malposition of erupting permanent teeth

Prolonged retention of deciduous anteriors
usually results in lingual or palatal eruption of their
permanent successor whereas prolonged retention
of buccal teeth results in eruption of the permanent
teeth either buccally or lingually or may remain
impacted within the jaws.

A palatal deflection in maxillary arch might lead
to the permanent tooth erupting in a crossbite.
Prolonged retention of a tooth may also lead to
impaction of the succedaneous tooth.

Quite often, certain parts of the deciduous roots
which are away from the path of eruption of the
permanent teeth fail to resorb, thereby leaving
small fragments of the deciduous roots retained in
the alveolar process. These fragments may deflect
the permanent tooth in its eruptive path or may
prevent the closure of
contacts of permanent
teeth. They are usually
asymptomatic but
occasionally do serve
as foci for infection or
cysts. Such fragments
should be removed.

DELAYED ERUPTION OF PERMANENT TEETH:
Nature has provided for a particular sequence for
the eruption of individual teeth in each arch. But if
one of the teeth does not occupy its designated
place in this sequence, there is a likelihood of
migration of other teeth into the available space. As
a result the tooth whose eruption has been delayed
might get displaced or impacted.

Probable causes for delayed eruption of permanent
teeth :-
1. Early loss of a primary tooth might cause
formation of a bony crypt over the succedaneous
tooth.
2. Presence of supernumerary tooth can block the
eruption of permanent tooth.
3. Presence of a heavy mucosal barrier can prevent
the permanent tooth from emerging into the oral
cavity.

4. Presence of odontomas or other cysts and tumors
might prevent the permanent tooth from erupting.
5. Presence of deciduous root fragments that have
not resorbed may block the erupting permanent tooth.
6. Presence of ankylosed deciduous teeth may cause
delay in eruption of permanent teeth.
7. Congenital absence of permanent teeth.

8. In certain endocrine disorders like hypothyroidism
and hypopituitarism, the eruption of permanent teeth
is delayed.
9. Delayed eruption of permanent teeth is also seen
in certain systemic disorders like ricketts.
10. Hereditary – In certain children tooth eruption
occurs much later than established norms.

ABNORMAL ERUPTIVE PATH:
This is usually a secondary manifestation of a
primary disturbance.
Some causes of abnormal eruptive pathway are:
1. In cases of arch length deficiency, deflection of
the erupting tooth may be merely an adaptive
response to the condition present.

2. Presence of supernumerary teeth, retained
deciduous teeth, root fragments, bony barrier or
mucosal barrier may result in abnormal eruptive
pathway.
3. Traumatic displacement of tooth buds. –
A deciduous tooth may be driven into the alveolar
process, and though it may erupt later, it may
displace the developing successor in an abnormal
direction.

4. Mechanical interference by orthodontic treatment
also can cause a change in eruptive path. eg. Early
Class II therapy against the maxillary arch to “move”
the maxillary dentition posteriorly can cause the
upper 2nd
molars to erupt into crossbite or can
impact the developing 3rd
molars.
5. Some abnormal eruptive pathways may be of
idiopathic (unknown) origin eg. A canine or premolar
may erupt buccally or lingually or may be transposed
with no apparent cause

6. 1st
and 2nd
permanent molars are occasionally
impacted; 3rd
are frequently impacted by an
abnormal path of eruption.
7. Coronal cysts can also cause abnormal eruptive
paths.

Another form of abnormal eruption is referred to
as ectopic eruption – In its most common form, a
permanent tooth erupting through the alveolar
process causes resorption of a contiguous tooth or
permanent tooth, rather than its predecessor.
Frequently the maxillary 1st
permanent molar
is the offending tooth,
causing abnormal
resorption of the
maxillary 2nd
deciduous
molar as it erupts
beneath the distal
convexity of this tooth.

ANKYLOSIS:
Ankylosis is encountered relatively frequently
during the 6 –12 year age period. It may result due
to an injury of some sort as a result of which a part
of the periodontal membrane is perforated and a
bony “bridge” forms joining the lamina dura and
cementum. The “bridge”
need not be large to
stop the normal eruptive
force of a tooth. The
most commonly affected
tooth is mandibular 2nd
deciduous molar.

Accidents or trauma, infections, certain congenital
disorders like cleidocranial dysostosis predispose to
ankylosis of teeth.
Clinically the ankylosed appears to be
“submerging” but in actuality, the other teeth are
erupting and the ankylosed tooth is not. The affected
tooth lacks mobility even though root resorption is far
advanced.

If left, ankylosed tooth can actually be covered
over again by the ever-growing mucosa and the
contiguous teeth often migrate into the space,
effectively locking the tooth in the process.
The permanent successors may be deflected to
have an abnormal eruptive path or may become
impacted.

DENTAL CARIES:
Caries can lead to premature loss of
deciduous or permanent teeth thereby causing
migration of contiguous teeth, abnormal axial
inclination and supraeruption of opposing teeth.

Proximal caries that has not
been restored can cause
migration of adjacent teeth
into the space leading to a
reduction in arch length. A
substantial reduction in arch
length can be expected if
several adjacent teeth involved
by proximal caries are left
unrestored.

IMPROPER DENTAL RESTORATIONS:
Malocclusion can be caused due to improper
dental restorations. Undercontoured proximal
restorations result in loss of arch length due to
drifting of adjacent teeth to occupy the space.
Overcontoured proximal restorations might bulge
into the space to be occupied by a succedaneous
tooth and result in a reduction in this space.

Overhang or poor proximal contacts may
predispose to periodontal breakdown around
these teeth.
Premature contacts on an overcontoured
occlusal restoration can cause a functional shift
of the mandible during jaw closure, whereas,
undercontoured occlusal restorations can lead
to the supra-eruption of the opposing teeth.

CONCLUSION:
Frequently, associated characteristics of
malocclusion have been blamed for a specific
condition when they belong to the “effect” end of
the “cause and effect” relationship. The paucity of
our present knowledge of etiology in orthodontics
compels us to attack the cause and effect
relationship from the wrong end – that of effect.
How nice it would be to approach it from the other
end…

No longer can conscientious orthodontists look at
a child’s mouth, observe a space deficiency and
then glibly attribute it to the premature loss of teeth
or prolonged retention of teeth. In the past, local
“causes” were stressed but today we know the
importance of general factors in etiology of
malocclusion along with the local causes.
Also as more knowledge is accumulated, many of
the answers in the future may come from scientists
in other fields.

As the philosopher Frederick Jensen has said,
“What we think we know today shatters the errors and
blunders of yesterday and is tomorrow discarded as
worthless. So we go from larger mistakes to smaller
mistakes – so long as we do not lose courage. This is
true of all therapy; no method is final.”

REFERENCES:
1. Orthodontics- Principles and Practice
T.M.Graber
2. Contemporary Orthodontics –
William R. Profitt
3. Textbook of Orthodontics –
Salzmann
4. Textbook of Oral pathology –
Shafer, Hine, Levy
5. Orthodontic Diagnosis –
Thomas Rakosi, Irmtrud Jonas, Thomas M. Graber

6. Handbook of Orthodontics –
Robert E. Moyers
7. The maxillary interincisal diastema and its
relationship to the superior labial frenum –
F. Popovich, G. W. Thompson, P. A. Main
Angle orthodontics, Oct 1977, Vol 47:4
8. The hereditability of malocclusion –
P. A. Mossey,
BJO, Jun & Sep 1999, Vol 26:2

Etiology of malocclusion local factors

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