Malocclusion general factors /certified fixed orthodontic courses by Indian dental academy

Etiology Of Malocclusion –
General Factors

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Introduction
Malocclusion may be defined as
a significant deviation from what is defined as
normal or ideal occlusion (Andrews,1972) *.
The term ‘normal occlusion' is arbitrary,
but is generally accepted to be class I molar
relationship with good alignment of all teeth *.
*(The heritability of malocclusion:part 2. P.A. Mossey, British journal of orthodontics/vol.
26/1999)

Classification
Graber’s
Moyer’s
White

& Gardiner’s
Salzmann’s

Moyer’s









Heredity
Developmental defects of unknown
origin
Trauma
Physical agents
Habits
Diseases
Malnutrition

White & Gardiner’s




Dental base abnormalities
Pre-eruption abnormalities
Post-eruption abnormalities


Salzmann’s
GENETIC

ENVIRONMENTA
L

DEVELOPMENT
AL

CONGENITAL

FUNCTIONA
L

Graber’s



General Factors
Local Factors


General Factors











Heredity
Congenital Defects
Environment
Predisposing Metabolic Climate and
Disease
Dietary Problems
Abnormal Pressure Habits and Functional
Aberrations
Posture
Trauma and Accidents

Local Factors












Anomalies of Number of teeth
Anomalies of Tooth Size
Anomalies of Tooth Shape
Abnormal Labial Frenum; mucosal barriers
Pre mature Loss
Prolonged Retention
Delayed eruption of Permanent Teeth
Abnormal Eruptive Path
Ankylosis
Dental Caries
Improper Dental Restorations

Orthodontic Equation


Dockrell.R



Cause

acts for specific period of

Results

Time

on a particular


Tissue

produces

Heredity




Genetically homogenous population tend to
have normal occlusion as the Melanesians
of the Philippine islands, in whom the
malocclusion is almost non-existent.
In heterogenous population , the incidence
of jaw discrepancies and occlusal
disharmonies is significantly greater.


Role of homeobox genes
These genes are known to play a role in patterning the embryonic
development.

These are master genes of head and face controlling
patterning , induction, programmed cell death and epithelial
mesenchymal interactions.
Important genes in craniofacial development include Hox
group, Msx1 & Msx2, Dlx, Otx, Gsc and Shh.
Two major groups of regulatory proteins including
mesenchymal growth factors, BMPs and steroids/ thyroid/
retinoid group are the vehicles through which Hox genes
information is expressed.
(The heritability of malocclusion:part1; P.A. MOSSEY, British
Journal of orthodontics/vol.26/1999/103-113)

Horowitz etal.(1960) studied fraternal and identical adult twin pairs
using only linear cephalometric measurements, and he demonstrated
highly significant hereditary variations in the anterior cranial base,
mandibular body length, lower face height, and total face height..
( P.A. Mossey, British journal of orthodontics, vol. 26/1999/195-203).



Primary sites affected by genetically
transferred dentofacial deformities
–
–
–
–

Neuromuscular system
Dentition
Bone & Cartilage
Soft Tissues (except muscles)

Neuromuscular system


Consist anomalies in
– size, position, tonicity, contractility and
neuromuscular coordination pattern of
facial, oral & tongue musculature


Lip deformities





The lower lip plays more
important role than the
upper lip in function
movements and in
governing the position of
lower incisors in normal
function during swallowing,
speech & smiling.
The inherited pattern of lips
can result in malocclusion.
Abnormalities in lip form
and lip line can cause
malocclusion.


Tongue deformities
Tongue Size : Macroglossia
Microglossia
Tongues Positions
In case of
incompetent lips, tongue
protrudes between the teeth to
touch the lower lips. This
allows nasal breathing n
prevents full vertical
development of incisors
leading to open bite.

Dentition
Heredity is the main cause of abnormality in dentition.Twin studies
have shown that tooth crown dimensions are strongly determined
by heredity (Osborne etal, 1958)*.
The molecular genetics of tooth morphogenesis with the
homeostatic Hox 7 and Hox 8 (now referred to as MSX1 and
MSX2) genes being responsible for stability in dental patterning is
confirmation of Butler’s field theory (1963)*.
(The heritability of malocclusion:part 2;P.A. Mossey, British Journal of Orthodontics/vol.26/
1999/195-203)



Abnormalities
–
–
–
–

Size, shape, number of teeth
Mineralization of teeth
Path of eruption in primary position of tooth germ
Sequence of eruption www.indiandentalacademy.com

Size


Microdontia



Macrodontia

Shape

Gemination

Twinning

Fusion


Number
Hypodontia
MSX1 & PAX9 genes are found
to be involved in some families
with non-syndromic autosomal
dominant hypodontia .

1

Hyperodontia
Supernumary teeth,most frequently
seen in premaxillary region with male
sex predilection, are also genetically
determined
2

Mineralisation


Inherited defects differ from exogenic
induced disturbances
– present in both deciduous & permanent
teeth
– localized in either enamel or dentin
– arranged irregularly or as vertical ridges
& grooves

Bones & Cartilage



Bone morphology or growth alter occlusal relation &
functioning
Factors
–
–
–
–



Bone size
Shape of jaw bases
Bone location
Number of bones present

Inherited skeletal malocclusions
–
–
–
–
–

Class II, division 2
Mandibular Prognathism
Bimaxillay protrusion
Skeletal open bites
Mandibular retrognathism



…rotational growth of mandible resulted from the condylar
growth pattern and this would be under genetic control..*
…forwardly rotated mandible is largely responsible for
strong chin, hypodivergent angular relationship of mandible
with cranial base and deep, restrictive over bite.*



…atleast three hard-tissue anatomic features with
generally accepted hereditary bases: small tooth size,
abundant mandibular basal growth, strong chin.*



Inheritance of a complex occlusal variation in Angle’s class
II division 2 malocclussion may actually be polygenic and
additive in nature , through combined expression of
genetically determined anatomical components, rather than
being the effect of a single controlling gene for the entire
occlusal malformation.*

*(classII division 2 malocclusion: A heritable pattern of small teeth in welldeveloped jaws. Sheldon peck, Angle 0rthodontist vol.1;9-20;1998)

Bone size



Macrognathism
Micrognathism
– Hypolasia of jaws occurs with craniofacial
dysostosis, cleidocranial, dysostosis &
crouzon’s diseases


Bone Location


Prognathism
– Mandibular prognathism and class
II division 2 are attributed to
dominant inheritance.
– Best known example of familial
mandibular prognathism is referred
to as the Hapsburg jaw.



Retrognathism

Soft Tissues

Anomalies of Frenum

Hemifacial
microsomia

Ankyloglossia


Genetic Syndromes










Achondroplasia
Pierre Robin syndrome
Craniofacial dysostosis
Treacher Collins syndrome
Down’s syndrome
Gardner’s syndrome
Marfan syndrome
Heredity ectodermal dysplasia
Cleidocranial dysplasia



Achondroplasia

Autosomal dominant characterstics.
Failure of synchondrosis leads to
underdevelopment of midface because the upper
jaw is not translated forward by normal lengthening
of the cranial base.
This results in Class III malocclusion.


Pierre Robins syndrome
Triad of features are:
Glossoptosis
Cleft palate
Micrognathia
This results in Class II malocclusion.



Craniofacial dysostosis
Transmitted as autosomal dominant trait.
Premature craniosynostosis with or without
syndactyly.
Hypoplasia of maxilla with mandibular
prognathism and a high arched palate,
parrot’s beak nose



Treacher Collins syndrome
Hypoplasia of facial bones
Macrostomia, high palate, abnormal position of
teeth
Bird like or fish like facies.



Down syndrome
Features include:
- Macroglossia, fissured tongue, or pebbly
tongue.
- High arched palate.
- Enamel hypoplasia, microdontia.
- Severe periodontitis



Gardner’s syndrome
- Multiple impacted supernumerary teeth
- Multiple Polyposis of large intestine
- Osteoma of bones
- Multiple Epidermoid cysts
- Desmoid tumors



Marfan syndrome

–
–
–
–


Autosomal dominant trait
Defective organization of collagen.

Long and narrow face
Hyperextensibility of joints
High arched palatal vault
Multiple odontogenic cysts

Hereditary ectodermal dysplasia
X-linked recessive
– Hypohidrosis
– Hypotrichosis
– Hypodontia

Cleidocranial dysostosis






Unilateral or bilateral , partial or
complete absence of clavicle.
Delayed closure of cranial suture,
maxillary retrusion, Mandibular
protrusion , retarded eruption of
permanent teeth, retained deciduous
teeth & supernumary teeth.
Mutations have been found in core
binding factor 1 gene(CBFA1).

2

1

3


4

Congenital Deformities


Caused by developmental damage
during fetal period (Moss 1967, Enlow 1982)
–
–
–
–

Cleft lip & Palate
Cerebral palsy
Torticollis
Congenital syphilis

Cleft lip & Palate








Most frequent congenital
deformity
Incidence 1:700 live births
Can be caused by the use of
teratogens like , aspirin, dilantin,
6-mercaptopurine, valium and
cigarette smoke.
In Unilateral cleft, teeth on the
affected site are in lingual cross
bite
Teeth are frequently crowded in
cleft


1.a

2.a

1.b


2.b

Cerebral palsy





Paralysis or lack of muscular
coordination attributed to intracranial
lesion
Commonly result of birth injury
Lack of motor control causes
abnormal function in mastication
,deglutition ,respiration & speech.
Thus affects normal occlusion .

Torticollis or Wry neck


Malocclusion &
alteration in
morphology of
cranium & face is
caused due to
foreshortening of
sternomastoid muscle.

Congenital syphilis







Peg shaped laterals
Mulberry molars
Notched incisors
Enamel hypoplasia
Delayed eruption
Narrow maxillary arch

Environment





Phenotypes are products of genotypes
and the ultimate product is blend of
inheritance potential as it has been
modified by a dynamic environment.
Prenatal influence
Postnatal influence


Prenatal influence




Uterine posture , fibroids of mother ,
amniotic lesions
German measles , maternal diet ,
metabolism , drug like thalidomide
induced deformities






‘ Vogelgesicht’ ,
inhibited growth of
mandible due to
ankylosis of TMJ
Intrauterine pressure
or trauma cause
hypoplasia of
mandible

Postnatal influence




Forceps delivery can injure
the TMJ
Disabling accidents
produces malocclusion
Milwaukee braces wear
produces malocclusion
– Maxillary incisors are tipped
labially
– Mandibular incisors fit into
deep palatal grooves


Predisposing metabolic
climate & disease





Exanthematous fever
disturbs developmental
time table and often
leave permanent
marks on surfaces of
teeth.
Endocrine disorders
Infectious diseases

Endocrine disorders




Prenatally , manifest as hypoplasia of
teeth.
Postnatally , retard or hasten , but do
not disrupt the direction of facial
growth. May affect the rate of
ossification of bone , eruption of teeth
& resorption of primary teeth.

Hyperpituitarism

Hypopituitarism

Accelerated development of mandible
Accelerated development & eruption
Enlarged tongue and facial structure
Hypercementosis

Retarded growth
Decreased linear facial measurement
Decreased cranial base measurement
Open bite
Delayed tooth eruption
Incomplete root formation

Hyperthyroidism

Hypothyroidism

Heat intolerance
Accelerated skeletal growth
Increased vertical face height
Open bite
Mild prognathism

Growth retardation
Decreased vertical growth of face
Decreased cranial base length
Anterior open bite
Delayed eruption
Maxillary protrusion
Spacing between teeth

Hyperparathyroidism

Demineralisation
Mobility of teeth

Hypoparathyroidism

Retarded eruption
Early exfoliation
Enamel defects


Infectious diseases



Nasopharyngeal diseases & impeded nasal
breathing.
Enlarged adenoids causes
–
–
–
–
–



Increased anterior facial height
narrow and high palate
Retroclined incisors
Increased lower facial height
Open bite & cross bite

Gingival and periodontal diseases
– Causes loss of teeth
– Ankylosis of teeth

Nutritional deficiency
Malocclusion caused by
disturbed developmental time
table in :
- Rickets – Vit. D deficiency
- Scurvy – Vit. C deficiency
- Beri beri – Vit. B1 deficiency
 Malocclusion is caused due
to


– Premature loss of teeth
– Prolonged retention
– Poor tissue health

1

2

Protein deficiency

Delayed eruption
Decreased radicular
osteocementum

Vitamin A deficiency Calcification of

teeth is affected

Retarded eruption
General growth is slow

Vitamin C deficiency

Disturbed collagen
formation
Bleeding gums
Loosening of teeth

Atrophy and
disorganisation of odontoblasts

Vitamin D deficiency

Hypophosphatemia
Disturbed calcification


Abnormal pressure
habits


Habits are learned patterns of
muscle contraction.
–
–
–
–

Thumb & digit sucking
Tongue thrusting
Lip biting & sucking
Nail biting


Thumb and digit sucking




Habit is considered normal till 3 ½ to 4
years of age.
Triad of factors
–
–
–

Duration of habit
Frequency of habit
Intensity of habit


Thumb and digit sucking


Effects of thumb sucking
– Proclination of maxillary
anteriors
– Increased overjet
– Lingual tipping of
Mandibular incisors
– Anterior open bite
– Narrow maxillary arch
– Upper lip is hypotonic
– Hyperactive mentalis
activity

Tongue thrusting




Condition in which tongue
makes contact with any
teeth anterior to molars
during swallowing.
Effects :
–
–
–
–

Proclination of anterior teeth
Anterior open bite
Bimaxillary protrusion
Posterior open bite in case of
lateral thrust
– Posterior cross bite

Lip biting & sucking




Lower lip is turned inward and
pressure s exerted on lingual
surfaces of maxillary anterior
teeth .
Effects :
–
–
–
–

Proclined maxillary anteriors
Retroclined mandibular anteriors
Hypertonic lower lip
Cracking of lips

Nail biting


Causes minor local tooth
irregularity

Posture






Stoop shouldered child with head hung so
that the chin rests on chest may have
mandibular retrusion.
Child resting his head on his hands or
sleeping on his arms , fists can have
malocclusion
Poor posture accentuates an existent
malocclusion

Trauma or accidents




Idiopathic eruptive
abnormalities can be
caused due to the
blows on face and
dental areas.
Non vital deciduous
teeth have abnormal
resorption patterns.

References
1.Handbook of orthodontics
by Robert E. Moyers
2.Orthodontic diagnosis
by T. Rakosi
Irmtrud Jonas
T.M Graber
3.Orthodontics principles and practice
by T.M. Graber
4.Contemporary orthodontics
by W.R. Proffit
5.Orthodontics current principles and techniques
by T.M Graber
R.L Vanarsdall
6.Oral pathology
by Shafer

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Malocclusion general factors /certified fixed orthodontic courses by Indian dental academy

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