Extrinsic intrinsic factors /certified fixed orthodontic courses by Indian dental academy

“ EXTRINSIC AND INTRINSIC
FACTORS IN THE ETIOLOGY OF
MALOCCLUSION & ITS ROLE IN
POST TREATMENT STABILITY ”
www.indiandentalacademy.com
INDIAN DENTAL ACADEMY
Leader in continuing dental education

W. K. Bridgman in 1859 states “the proper antagonism of the
teeth is of very utmost importance, for if any of the cusps be
out of place they disturb equal distribution of forces in
biting & tend to produce mischief at the points holding
those cusps in their assumed positions”
Normal occlusion of teeth is supposed to be requisite for
normal facial balance which is influenced by soft tissue,
underlying bone, occlusion, axial inclination of teeth. The
position of the teeth within the jaw and the mode of
occlusion are determined by developmental processes that
interact with the teeth and associated structures during the
periods of formations, growth and postnatal modifications.

NORMAL OCCLUSION
The word occlusion is derived from “clusion” i.e.
close & “oc” i.e. up.
Edward H. Angle in 1907 defined “occlusion as
being the normal relation of occlusal inclined
planes of teeth when the jaws are closed”
B.S.S.O in 1926 defined it as – “ that occlusion
which is within the standard deviation from the
ideal”

CONCEPTS AND EVOLUTION OF OCCLUSION
Initially concept was given by E. H. Angle in 1899.
Matthew Cryer questioned Angle’s concept.
Dr P.R. Beggs gave his concept in 1924 of attritional
occlusion.
To understand the normal occlusion & to differentiate it from
malocclusion Lawrence F. Andrews in 1960 - 64 gave the
six keys of normal occlusion.
1. Molar relationship
2. Crown angulations – mesiodistal tip
3. Crown inclination – labiolingual or buccolingual
4. Rotations
5. Spaces
6. Plane of occlusion www.indiandentalacademy.com

WHAT IS MALOCCLUSION
It is a condition where there is departure from the normal relation of the
teeth to other teeth in the same arch and to the teeth in the opposing
arch.
Salzmann says “diagnosis of malocclusion is not to be based on
subjective, arbitrarily, established criteria or “standards”, but must
take into consideration the genetic endowment, ontogenetic growth &
postnatal development of the individual patient.”
Carabelli in mid of 19th
century was the first to describe abnormal
relation of upper & lower dental arches.
Angle defined “malocclusion of the teeth is but the perversion of their
normal relation.”

INCIDENCE OF MALOCCLUSION
As per the various broad population studies done for the
prevalence of malocclusion
20 % of deciduous dentition had malocclusion
39 % of mixed dentition
58 % in permanent dentition
No difference noted according to sex.

REVIEW
First direct attempt of classification give by Fox in 1803.
Marjolin in 1823 gave direction of dental arches; prominence, recession,
inversion.
J.C.F.Mary in 1828 gave the inclination of the teeth; inward, outward,
laterally.
C.F. Delabarra in 1829 was first to indicate 4 types of bite; overbite,
underbite, edge to edge, cross bite
Blandid in 1836 & J.M.A.Schange in 1841 gave the classification as per
the number, form, direction & position.

M.S.Cartwright in 1864 gave irregularities of the teeth according to 3
forms of teeth, “heredity” “congenital” “mechanical”
Kingsley in 1872 classified the cause of irregularities first by
developmental & second as accidental
A.Ogston in 1974 classified congenital malformation of the lower jaw
- Non development of inferior maxilla.
- Excessive development
- Congenital smallness of the mandible either both halves / unilateral
- Congenital dislocation

Most universally used classification was introduced by
Edward. H. Angle in 1899, the basis of Angle’s classification
was his hypothesis that the first molar is the key of
occlusion.
Simon with suggestion made by Bennet in 1912 categorized
malocclusion in 3 planes of space:
Horizontal,
Vertical &
Transverse.
Ackermann – Proffit recognizing the sagittal orientation &
limitations of the angles classification; gave a method of
diagrammatic & categorizing malocclusion using the Venn
Symbolic Logic Daigram, known as SET THEORYwww.indiandentalacademy.com

THE ORTHODONTIC EQUATION
CAUSE TIME TISSUES RESULT
some predisposing prenatal primary following of the three
Some existing postnatal secondary or combination.
-Heredity -continuous/intermittent -neuromuscular -malfunction
-Developmental cause -may act at different age -teeth - malocclusion
of unknown origin levels -bone and cartilage -osseous dysplasia
-Trauma -soft tissue other than
-physical agents muscles
-Habits
-Diseases
-Malnutrition
In an article by Dockrell in 1952 “classification of etiology of
malocclusion”
Act at on produce

INTRINSIC FACTORS

HEREDITY
Offspring inherits few attributes from his parents which are
modified by environmental factor, physical entities,
pressure, habits, malnutrition, etc.
Definite genetic determinant influence dentofacial
morphology, thus growth & development has a strong
hereditary component.
Certain racial & familial characteristics tends to recur. There is
a possibility of recapitulation of a hereditary trait from
either parent or combination of both parents to produce a
characteristic modification.’

Heredity with racial influence: certain facial characteristics
show racial influence
Heredity with facial type: Hasen & Siversten pointed out
sex linked nature of facial width & dental arch shape.
Female demonstrates positive correlation wider the face
wider is the jaw.
Heredity influence on growth & development pattern:
Growth & development has a strong hereditary influence.
Environmental influence modify the hereditary determined
pattern.
Onset of puberty vary with different races & geographic
distribution.’ www.indiandentalacademy.com

Heredity & specific dentofacial morphology:
Lundstrum made an intensive analysis of these
characteristics in twin & concluded that heredity could be
considered significant in determining the following
characteristics:
Tooth size
- Width and length of arch
- Height of palate
- Crowding / spacing / rotation of teeth
- Tooth shape and number
- Overjet and overbite
- Inter arch variation in transverse/Sagittal/vertical plane

- Frenum
- Position and confirmation of perioral
musculature to tongue size and shape.
- Soft tissue peculiarities
- Congenital deformity
- Facial asymmetry
- Micrognathia / macrognathia
- Cleft palate and lip
- Mandibular prognathism / retrusion

Genetic aberrations make their appearance prenatally / may
not be seen until many years after birth. It can be
explained as follows as some primary etiological sites:
1. Neuromuscular system: the anomalies with inheriting
component are size, position, tonicity, contractility,
neuromuscular coordination pattern of facial, oral &
tongue musculature. It effects by reflex contraction on
bony skeleton & dentition leading to skeletal imbalance.
It is not possible to differentiate in the origin of certain habits.
There may be various reasons.’
Some malocclusion are associated with tongue size, lip length,
tonicity.
2. Soft tissue other than muscle:

3. Dentition:
- Size and shape of the teeth
- Number of the teeth
- Primary position of tooth germ and path of eruption.
- Shedding of deciduous teeth and sequence of eruption
- Mineralization of the tooth.
4. Skeletal structures:
Affected inherently as well as environmentally or acquired
congenital malformation.
Class III have strong familial tendency.
Any pathological condition affecting growth of the jaw affects
the dentition
Trauma
Infection during growing years can affect the jaw growthwww.indiandentalacademy.com

CONGENITAL
Can be identified as early as in 18 – 20 wks of pregnancy or
can be seen immediately after the birth. The aberrations are
both inherently & environmentally influenced.
The congenital abnormality that can cause malocclusion can
be classified as:
EXTRINSIC: abnormal state of mother during pregnancy
accidents during pregnancy or during birth
intra uterine pressure
accidental traumatization of the infant by external
forces

INTRINSIC:
clefts of face and palate
macroglossia / microglossia
cleidocranial dysostosis
malnutrition & endocrinopathies
infectious diseases
metabolic & nutritional deficiency

Cleft lip and palate:
- cicatricial bands restrict the horizontal maxillary anterior
segmental development
- Teeth on side of cleft are in lingual crossbites with
opposing lowers.
- Premaxilla displaced anteriorly or due to tight repaired lip
pushed posteriorly.
- Maxillary incisors badly malposed with bizarre axial
inclination and teeth frequently jumbled.
- Maxillary laterals are missing / twined / atypical in shape.
- Strong forces applied on teeth to correct the malocclusion
can lead to early loss of the teeth.
- Teeth are in good relation to basal bone but entire palatal &
alveolar structure is displaced medially.

Cerebral palsy: paralysis/lack of muscular co-ordination attributes to
intracranial lesions, considered to be a birth injury.
The tissue are normal but lack in motor control with abnormal
function in muscle of mastication, deglutition, respiration, speech.
Aberrant action upset the muscle balance producing abnormal
pressure habits leading to malocclusion.
Tortocollis: foreshortening of sterno cleido mastoid muscle change the
bony morphology of cranium and face with bizarre facial
asymmetry with uncorrective dental malocclusion.
Micrognathism : seen with either of jaw mainly associated with
congenital heart disease.
Maxillary deficiency is due to premaxillary deficiency
Mandibular deficiency due to chin with steep mandibular angle.

Cleido cranial dysostosis: its congenital and frequently
inheretent.
Features are: Absence of clavicle, delayed closure of sutures,
maxillary retrusion, mandibular protrusion, retarded
eruption of permanent teeth, retained deciduous teeth, roots
of permanent are short & thin, supernumerary present.
Syphillis: abnormal shaped teeth, malposed teeth like
hutchinson’s incisors, mulbery molars, enamel deficiency,
extensive dental decay, small maxilla, anterior cross bite.

Oligodontia : it is commonly inheriting and congenital
III molars are commonly involved.
Anodontia: associated with hereditary ectodermal dysplasia
Some common reasons of congenital absent teeth are :
- Heredity
- Ectodermal dysplasia
- Localized inflammation / infection
- Systemic conditions
- Evolutionary changes in the dentition.
Rubella : infection to mother during pregnancy can lead to dental
hypoplasia, retarded eruption, extensive caries.

ENDOCRINAL FACTOR
Prenatal influence show hypoplasia of tooth while postnatal can retard or
hasten the growth but do not distort the direction of the growth.
It affect the rate of ossification of bones, time of suture closure, time of
eruption of teeth, rate of resorption of roots.
Periodontal membrane and gingiva are extremely sensitive to endocrine
dysfunction thus affect teeth indirectly.

Features of the endocrinal imbalance are:
1. Hypo thyroidism:
- Retarded growth with decreased vertical growth of face
- Anterior open bite tendency
- Delayed eruption of teeth
- Maxillary protrusion
- Spacing of the teeth
- Over retained deciduous
- Narrowing of dental arch
- Abnormal resorption pattern
- Gingival disturbances

2. Hyper thyroidism:
- Accelerated skeletal growth with irregular eruption of teeth
- Increased vertical facial height
- Open bite tendency
- Premature eruption of deciduous
3. Hypo pitutarism:
- Retarded growth with decrease linear facial measurement and cranial
base measures
- Delayed tooth eruption
- Incomplete root formation with incomplete closure of apical foramen

4. Hyper pitutarism:
- Accelerated development seen in mandible
- Accelerated dental development and eruption
- Enlarged tongue
- Thick cortical plates
5. Parathyroidism :
- Accelerated skeletal growth with irregular eruption of teeth
- Increase vertical facial height
- Premature eruption of deciduous
- Mobility due to loss of cortical bone
- Interruption of tooth development

METABOIC DISEASE FACTOR
Febrile diseases not only affect health of
child but also the dentition and
surrounding hard and soft tissue.
They are able to show decrease growth and
delayed eruption of teeth.

EXTRINSIC FACTORS

ENVIRONMENTAL
PRENATAL INFLUENCE:
Cause of malocclusion is due to
- Uterine fetal posture, Fibroids of the mother cause facial
asymmetries apparent during birth & disappear till 1st
year of life.
- Micro mandible / pierre robin syndrome / treacher collin syndrome
have tremendous increment of growth largely eliminate the original
malformation.
- Amniotic lesions
- Maternal diet and metabolism
- Drug induced deformity e.g. thalidomide
- Infections like germen measles
- Injury and trauma

POSTNATAL INFLUENCE
- Cranial bone slide and mold more than the facial and dental
area
- High forceps delivery injure the infant with permanent
damage to TMJ due to Ankylosis patient show hypo plastic
mandible with retarded growth / vogelgesicht.
- Malocclusion associated with cerebral palsy attribute to
birth injury due to loss of muscle co-ordination
- Disabling accidents produce undue pressure on the
developing dentition.
- Falls lead to condylar fracture & facial asymmetry
- Extensive scar tissue restrict the mandibular growth.

DEFICIENCY DISEASE /
MALNUTRITION / DIETARY PROBLEMS
- Malnutrition affect quality of tissue being formed, the rate of
calcification
- Good nutrition plays an imp role in growth & maintenance of good
bodily health and hygiene
- Vitamin deficiency lead to malocclusion by upsetting the dental
developmental time table
- This leads to premature loss of teeth, prolonged retention of teeth,
poor tissue health, abnormal eruption pathways
- Its mainly due to faulty utilization of ingested food, hormonal /
enzymatic imbalance, chronic alcoholism.

Protein deficiency – delayed eruption
Vitamin A deficiency – retarded eruption
Vitamin B deficiency – retarded growth of the bones
Vitamin C deficiency – bleeding gums, loosening of the teeth
Vitamin D deficiency – retarded eruption and early loss of deciduous
Hyper vitaminosis, vitamin B 12 deficiency, folic acid deficiency – cleft
lip and palate

INFECTION AND DISEASES
Malocclusion can be secondary to some neuropathies or neuromuscular
disorders or it may be a sequel of treatment problem like scoliosis.
1. Systemic: febrile diseases upset the dentitional development time
table during infancy and early childhood. It mainly affects the
quality rather than the quantity of the dentitional development.
2. Local:
a) Gingival & periodontal diseases
b) Tumors
c) caries

d) Nasopharyngeal diseases and disturbed respiratory function:
There are 3 hypothesis to be considered:
- Adenoid enlargement leads to mouth breathing resulting in
particular type of facial form and dentition.
- Enlarged adenoids leads to mouth breathing but not influence facial
form and type of dentition.
- Enlarged adenoids in certain types of faces and dentition leads to
mouth breathing
The basic assumption is due to compression, tissue atrophy, altered
air pressure:
Enlarged adenoids obstruct the airway – mouth breathing – change in
tongue, lip and mandibular posture – upset the soft tissue balance –
lead to alter the craniofacial form & malocclusion – increase in the
anterior facial height – narrow & high palate – increased lower
facial height – anterior open bite, posterior cross bite tendency

PHYSICAL AGENTS
Nature of food :
In the primitive fibrous food stimulates their muscle to work thus
increasing the load of function on the teeth. This type of food
produces less caries, great mean arch width, increased wear of
occlusal surfaces
Now highly refined, soft, pappy modern food plays a role I etiology of
malocclusion, as lack of adequate function results in contraction of
dental arches, insufficient occlusal wear, absence of occlusal
adjustments

TRAUMA AND ACCIDEDNTS
1. Prenatal trauma / birth injury:
Hypoplasia of mandible is caused by intrauterine pressure /trauma
during delivery
Vegelgesicht: inhibited growth of mandible due to ankylosis in TMJ
2. Trauma at time of delivery : e.g. forcep delivery
3. Postnatal trauma :
Occur at any age and affect any region
Fracture of jaw and teeth, loss of vitality
Habits produce microtrauma if persists for a long time
Trauma to TMJ impair growth, function leads to asymmetry, TMJ
dysfunction
Frequent falls
Trauma leads to dilaceration, deformation, displacement, ankylosis.
Abnormal resorption pattern, deflect permanent tooth germ.www.indiandentalacademy.com

POSTURE
- poor posture accentuates existing malocclusion
- Those who hold their head straight & erect with head placed over the
spinal column will almost reflexly hold their chin forward in prefered
position
- Body posture is the summated expression of muscle reflexes & so
usually capable of change & correction
- E.g. abnormal tongue position usually cause open bite
a full fledged malocclusion seen in child resting his head on his
hands for long period each day, sleeping on his arm, or fist or
pillow.
a stoop shouldered child with head resting on his chest create his
own mandibular retrusion.

HABITS
All habits are functional abrasion producing forces that are abnormal as
produced repeatedly over time thus bring about permanent
deformation in musculoskeletal unit.
This deformity depends on intensity, duration and frequency of habit.
The muscular element is capable of retrained but underlying skeletal
structure goes to abnormal proportion.
Thus it follows the functional matrix theory.
Abnormal pattern interferes with regular pattern of facial growth.

Bone is a plaster tissue responsive to pressure that are continually acting
on it. Dynamic role of musculature is apparent.’
The dentist thinks muscles as a primary masticatory element. An average
person eats 3 meals per day, but swallows al the day long, breaths
constantly & talks a good part of time.
Premature occlusal contacts & compensatory muscle activity during
active function produces even greater departure from the normal,
which can even change the bony morphology thus accentuating the
malocclusion.

1.POSTURAL RESTING POSITION:
It is a sort of balance of extraoral & intraoral muscle forces with the
buccal & perioral musculature passively restraining the anterior
displacement of the teeth.
Lingual pressure are greater but hydraulic effect, tissue mass, cheek
elasticity & morphogenetic pattern contributes to a total balance.

BUCCINATOR MECHANISM:
It runs posteriorly to pterygomandibular raphe, decussating the fibers of
deep constrictor muscles that carry on a round & anchor at pharyngeal
tubercle of occipital bone.
All facial muscles are intimately related to postvertebral, prevertebral, &
cervical musculature, so that a change in one muscle would influence
relationship with other muscle.
e.g. pattern in class II
pattern in class III
Thus the musculature dose not create skeletal malocclusion but
accentuates the existing deformity by virtue of its adaptive functional
activity.

2. FINGER SUCKING HABIT:
According to William James: an acquired habit from psychological
point of view is nothing but a new pathway of discharged formed in
brain, by which certain incoming current even after tent to escape.
Habits is relation to malocclusion are classified into:
- Useful
- Harmful
According to Dr. E A Barton apart from effect of constantly sucking the
foul thumb there is another side which demands consideration. The
thumb is a hard body frequently in mouth tends to pull the growing
premaxilla forward with upper incisors which projects labially beyond
upper lip giving “ Dents Des Anglais Appearance ”

FINGER SUCKING FROM BIRTH TO 4 YEARS:
New born infant have a relatively well developed suckling mechanism
and receives not only nutriment but also a feeling of euphoria, we
being, sense of security, feeling of warmth, and being wanted.
Lips of infants are sensory organ & pathway to brain is relatively well
developed
PHILOSOPHY OF SUCKLING:
Gum pads are apart – tongue brought forward in plunger like fashion –
tongue & lower lip in constant contact – mandible move up & down
in rhythm & forward & backward by virtue of flat condylar path as
buccinator mechanism alternately contracts & relax.
Conventional nipple dose not duplicates the suckling and thus it becomes
sucking.

Breast fed babies have less abnormal perioral muscle habit & less
retained infantile swallow.
Habit continued to 3 years show a temporary damage confined to
anterior segment.
The damaging features of the habit are similar to characteristics of
typical hereditary pattern of class II Div 1 malocclusion. The
sequence of total maxillary protrusion to sucking habit with increased
pressure from buccinator mechanism activating the pterigomandibular
raphe just behind the dentition forcing the teeth anteriorly, with severe
openbite, buccal crossbite, protruding maxillary anteriors, mandibular
incisor crowding, tongue thrust retained infantile suckle swallow
pattern.

ACTIVE FINGER SUCKING HABIT AFTER THE AGE OF 4:
- Ineffectual badgering attempt to break the habit continues it.
- The finger sucking is associated with perioral musculature with
increased overjet & makes normal swallowing pattern difficult with a
class II tendency. As swallowing requires “closing off ”to create a
partial vacuum, the lip muscle aberration is assisted by compensatory
tongue thrust during swallowing thus retarding deglutition maturation.
- Finger sucking habit becomes innocuous (only at bed time) but tongue
thrust continues to adapt to the morphology. Tongue does not drops
back & spread out with abnormal mentalis muscle function while
lower lip activity flattens the anterior segment.
- Fore finger sucking is considered to cause more severe deformation

Effects of digit sucking :-
Maxilla :
- Proclination of maxillary incisors
- Increased arch length
- Increased anterior placement of apical base of maxilla with / without
midline diastema
- Increased SNA angle
- Increased clinical crown length of upper incisors
- Increased counter clockwise rotation of occlusal plane
- Decreased width of palate
- Atypical root resorption of primary central incisors
- Trauma to anteriors due to their prominence

Mandible:
- Proclination of mandibular incisors
- Increased mandibular intermolar width
- Mandible more distally placed than maxilla
- Mandibular incisors experience a lingual and apical force
Interarch relationship:
- Decreased interincisal angle
- Increased overjet & decreased overbite
- Posterior crossbite & anterior openbite
- Narrow nasal floor & high palatal vault
- Uni / bilateral class II occlusion
Other effects:
- Affect psychological health
- Risk of malpositioning of teeth &jaw
- lisping www.indiandentalacademy.com

“Digit sucking is not directly involved with production of malocclusion”
Freudian belief holds that an abrupt interference with such a basic
mechanism is likely to lead a substitution of such antisocial
tendencies.
Cook measured the forces of thumb sucking & found 3 distinctly
different pattern of force application during sucking utilizing force
sufficiently strong to displace the teeth & deform the growing bone.
Melson found digit sucking & pacifiers to increase the tendency towards
abnormal swallowing.

MUSCLE FACTOR:-
Teeth erupt in an environment of functional activity governed by the
muscle of mastication, tongue, face. The muscles of tongue, lip,
cheeks are important in guiding teeth into their final position,
variation in muscle for and function affect the position and occlusion
of the teeth.
All muscle exert their influence by virtue of their origin and insertion.
The muscles have their main origin on basal part of the jaw, so
position of jaw affect position and action of muscles which functions
on the teeth.

3. LIPS :
1. Vertical form of the lip: determine the amount of lip pressure on teeth
-ideal lip form
-lip competency
2. Sagittal form of the lip: determine the position of lip pressure on teeth
It is equally possible for the lip activity to produce class II / class III
relationships by altering the inclination of the incisor teeth during
eruption or to produce class I occlusion on class II / class III skeletal
relationship if the skeletal discrepancy is not severe.

Function of the lips:-
- Modify erupting tooth position
- Govern the position of incisor teeth
- Lower lips lead to retroclination of incisors in normal function of
swallow, speech, smiling activities
- The ultimate position of teeth before and after the orthodontic
treatment is very much dependent on the lips

In finger sucking the muscle activity accentuates the deformity.
Increase in overjet leads to lip incompetence & difficulty in creating
negative pressure for normal swallow.
Lower lip drops behind the upper incisors & thrust against it with
abnormal mentalis muscle activity to affect the closure.
Upper lip remains hypotonic, functionless, retracted, and short called as
“incompetent resting lip posture ”.
To create an anterior lip seal orbicularis oris mentalis muscle complex
contracts.
Thus the tongue thrust forward to aids in lower lip closing during
swallowing
Upper lip no longer serve as an effective restraining force, the lower lip
teaming with tongue exert a powerful upward & forward vector of
force against premaxilla thus enhancing the severity of malocclusion.

This leads to protrusion of maxillary incisors & anterior openbite
This cycle repeats during each swallow.
Spontaneous drop of finger sucking habit leads to tongue thrust habit.
LIP SUCKING:
It results due to excessive overjet & difficulty in closing the lips
properly during deglutition.
It leads to flattening & crowding of lower anteriors with retraction while
maxillary incisors forced up & forward.
Vermillion border hypotonic & red with flaccid lip & accentuated
mentolabial sulcus.

4. TONGUE
In conjugation with lips and cheeks it is the other major guiding force for
the erupting teeth. The muscles of the tongue are attached to the
inner aspect of the mandible, hyoid bone, palate, styloid process and
affect the teeth by virtue of size, resting posture and function.
Resting position of the tongue:- is completely with in the dental arches
filling the space enclosed by teeth, some times it takes up the
adaptive postural position protruded between the teeth to touch the
lower lip in order to seal the front of the mouth
The essential features of normal swallowing are:
- Closure of the lips
- Teeth in light occlusal contact
- Tongue elevated to the palate
- Momentary clenching of teeth as food passes into the pharynx

Adaptive swallowing involves tongue between teeth carried out with
buccal teeth apart or together.
1. Tooth apart adaptive swallow : tongue positioned between the
teeth so does not fill the upper arch – both muscle & air pressure in
upper arch reduced –narrowing of arch & buccal cross bite –full
vertical development of anterior dento alveolar segment prevented
by tongue – incomplete overbite.
2. Tooth together adaptive swallow : involves forward positioning of
teeth between incisors during swallowing – anterior open bite.s

Tongue thrust is a retention of infantile suckling swallow, with eruption
of deciduous the tongue does not drops back & continue to thrust
Etiology of tongue thrust is :
- genetically inherent
- Learned behavior due to improper bottle feeding, tenderness of gums,
tonsilitis, upper respiratory tract infection
- Macroglossia
Malocclusion caused by tongue thrust are:
- Openbite (anterior / posterior)
- Proclination of upper anterior segment with spacing in canines &
incisors.
- Posterior cross bite due to narrow & constricted maxillary arch.

Mechanism of action of malocclusion caused by tongue:
Tongue thrust forward continuously – increase in overjet and overbite –
peripheral position no longer lie on the lingual cusps of buccal
segment – posterior teeth erupt and gradually eliminate the inter
occlusal clearance – the postural resting vertical dimension and
occlusal vertical dimension becomes the same with posterior teeth in
contact all the time – leads to bruxism, bilateral narrowing of
maxillary arch, as the tongue drops down lower in the mouth –
providing less support to the maxillary arch – cross bites

MOUTH BREATHING:
Caused in nasal passage obstruction / inadequacy.
Nasal obstruction:
- Enlarged turbinates : infection leads to hypertrophy of the mucosa
causing obstruction
- Adenoid hypertrophy : blocks the posterior nares leads to mouth
breathing. In enlarged tonsils soft palate rest on their upper poles
instead of dorsum of tongue thus displace tongue downward &
forward causing an open bite posture.
- Intranasl defect deviate the septum

Altered respiratory pattern – mouth breathing – alter the posture of head,
jaw, tongue – alter the equilibrium of pressure of jaw teeth and growth
– lowers the mandible & tongue extends the face thus face height
increases – posterior teeth supra erupt – mandible rotate down and
back – increase in overjet and anterior open bite – narrow the
maxillary arch – adenoid face appearance – incompetent lips – short
upper lip – proclination and spacing in upper anterior teeth – lower lip
heavy and everted – mandible in distal rotation to maxilla – lower
anteriors elongate and touch the palatal tissue.

LOCAL FACTOR

ANOMALIES IN NUMBER OF TOOTH:
Heredity plays a strong part & some believe extra tooth as a left over
from the primitives.
High frequency of extra / missing tooth is associated with congenital
deformity e.g. clefts.
General pathosis also affect the number of teeth.
SUPERNUMERARY TOOTH :
- they vary in size, shape and location
- There is no definite time for its development may form prior to birth /
as late as at 10 – 12 years called as third set of teeth
- Commonly seen in maxilla in between central incisor
- Many a time they are well formed & so become difficult to identify
called as “supplementary teeth” in premolar region of near lateral
incisor www.indiandentalacademy.com

- Frequency seen is the mesiodens in midline palatal to maxillary
incisors, conical in shape with short root & crown, occasionally fused
with right / left central incisors
- Unerupted becomes generally cystic
- Some remain out of occlusion so have no deleterious effects & must
be left alone.
EFFECTS:
- Lead to deflection / noneruption of permanent central incisor or if
they erupt it is in malposed
- Permanent teeth fail to erupt due to presence of supernumerary teeth,
congenital absence, any mucosal barrier
- Delay the eruption of adjacent teeth
- Increase the arch perimeter (increase the overjet in maxillary arch &
decrease the overjet in mandibular arch )
- Crowding in dental arch

MISSING TEETH:
- Called as partial anodontia / hypodontia
- Congenitally missing more commonly found than supernumerary.
- Order of frequently missing tooth
Maxillary & mandibular III molars
Maxillary lateral incisors
Mandibular II premolar
Mandibular incisors
Maxillary II premolar
- In congenitally missing tooth size tooth shape deformity is quite
frequent
- Congenitally missing are many a times bilateral e.g. mandibular II
premolar
- Partial / complete anodontia is rare.

- Heredity plays a significant role
- Congenital absence seen commonly in permanent than deciduous
- When permanent missing roots of deciduous do not sorb
- In missing maxillary lateral incisor, permanent canine erupt mesial to
deciduous canine in space of missing teeth.
- Teeth are even lost in accidents
EFFECTS:
- Spacing
- Aberrant swallowing pattern
- Abnormal tilting & axial inclination
- The location of adjacent teeth
- Absence of permanent lead to over retained deciduous teethssssss

ANOMALIES IN TOOTH SISE:
- In order to have normal occlusion there must be harmony in tooth size
& arch length
- Called as micro / macrodontia. True microdontia is rarely seen.
- Largely determined by heredity
- Microdontia seen with pitutary drawfism while macrodontia with
gygantism
- Greatly vary from individual to individual also within same individual
- Crowding is major characteristic
- The width is greater in male than in female, mainly seen in permanent
than in deciduous
- Canine show greater difference than lateral incisors e.g. peg laterals
- Frequently seen in mandibular premolar region

- Developmental aberration are anomalous in shape / fused with
neighboring tooth
- Increase in tooth size lead to crowding
- decrease in tooth size leads to spacing.

ANOMALIES IN TOOTH SHAPE:
- Most commonly seen is the peg lateral, small size leads to spacing in
anterior segment.
- Laterals also deform in the congenital clefts
- Japanese show pronounced cingulum, sharp marginal ridges, well
defined boundary to lingual fossa, this all together force the involved
tooth labially & prevent normal overbite & overjet
- Mandibular II premolar show maximum variation with extra lingual
cusp thus increasing mesiodistal dimension which reduces the space
that the loss of II deciduous teeth provide.
- Other anomalies are gemination, fusion, concresence, talon cusp,
dilaceration, amelogenesis imperfecta, hypoplasia, dens in dente,
odontomas, mulberry molars, hutchinson’s inciors.

ABNORMAL LABIAL FRENUM
- labial frenum & midline diastema is a topic of controversy due to
incomplete understanding of role of heredity, tooth size, local habits,
process of growth & development
- Spacing in maxillary centrals & thick frenum is a chicken or egg
controversy.
- In the past frenum was needlessly clipped.’ thus in lack of
recognization of habit problems, tooth size discrepancy, congenitally
missing teeth, midline supernumerary tooth, clipping of frenum did a
little job.
- Now what exactly is normal?
- Faustin Waber noted some etiological factors like:
- Microdontia, macrognathia, supernumerary tooth, peg laterals,
missing laterals, heavy occlusal force against the lingual surface of
the maxillary incisors, habits, midline cyst.

- According to Taylor interincisal spacing close without any
interference
- Existence of heavy fibrous frenum dose mot always mean spacing,
during ortho treatment frenum get atrophy.
- Frenum migrates superiorly enough at the age of 10 – 12 years
- Heredity plays an important role.
Age Incedence
of daistema
6 97%
6 – 7 88%
10 – 11 48 %
12 – 18 7 %

PREMATURE LOSS OF PRIMARY TOOTH
- The primary are considered as space saver for permanent. If primary
tooth lost before crown formation completion & root formation begin
of permanent, bone reform atop it thus delay the eruption – adjacent
teeth drift in space.
- Caries play an important role in decreasing the arch length by
decreasing the mesiodistal dimension.
- Rate of loss of space is related to extraction age in maxilla but not in
mandible e.g. loss of first primary molars in maxilla block out
permanent cuspids while loss of maxillary II primary molar tends to
impact the II premolar.
- Molar & canine occlusal relationship is significantly affected by
premature loss of primary molars in either archeswww.indiandentalacademy.com

- Loss of PRIMARY INCISORS is of less concern but its loss before
permanent erupt – drifting of most distal teeth – malocclusion.
- Loss of PRIMARY CUSPIDS matter of great concern – as permanent
canine erupt late in maxilla & if lost before permanent central &
lateral erupt – permanent spacing seen in anterior segment with
labioversion of canine erupting due to no space.
- In mandible early loss – lingual tipping of anteriors with abnormal
mentalis muscle activity.
- Loss of FIRST PRIMARY MOLAR – permanent canine & I
permanent molar move mesially – I premolar not displaced as it is
narrow mesiodistally.
- In mandible – II primary molar shift forward at the time permanent
molar is erupting

- Loss of SECOND PRIAMRY MOLAR – first permanent molar drift
forward & rotates mesiolingually – II premolar, canine shift distally
as it is wider mesiodistally the space get occupied with permanent
canines – incisors alter midline – canine erupt with no space to
occupy.
- In mandible – II premolar is last to erupt – block out the teeth – loss
of tooth substance is more important than the whole teeth as it
establish occlusal relationship & in maintenance of arch perimeter
- Loss of ONE OR MORE PRIMARY TOOTH – drifting with loss of
posterior support when mandible held in position to provide some sort
of adaptive occlusal function – result in crossbite – affects TMJ,
musculature, growth of facial bone, final position of permanent teeth
- Loss of PERMANENT TOOTH – upset physiological functioning –
break mesiodistal contact – shift

According to Dewey after loss of primary molars the drifting of
permanent molar the factors related were
1. Leeway space – more drift occurred in arches with less leeway space.
2. Cusp height – high cusp height prevent drifting
3. Age when the primary teeth were lost – great loss occur when primary
molars lost before eruption of the permanent
Abnormal order lead to shift & loss of space
This will shorten the arch length, crowding, tip the contagious teeth,
over erupt the opposing teeth, cause further periodontal problem
Periapical pathology of primary teeth hasten the eruption of successors
due to loss of bone & increased vascularity

PROLONGED RETENTION & ABNORMAL
ERUPTION OF DECIDUOUS TEETH
ETIOLOGY :
- Absence of underlying permanent successor
- Hypothyroidism
- Ankylosed deciduous tooth that fail to resorb
- Non vital deciduous
EFFECTS:
- Deflection in path of eruption
- Cross bite due to palatal eruption
- Impaction of permanent as its last tooth to erupt, space occupied by
deciduous canine is less, premolar migrate mesially leaving limited
space for canine, longest path of eruption its the only tooth to erupt
after root completion.
- Prolong retention lead to break in contact, rotationswww.indiandentalacademy.com

Any mechanical interference deflect an erupting permanent tooth
If the roots of deciduous not resorbed, permanent successor withheld
from eruption & defect into malocclusion
Some children are precocious & loss teeth early while other very
slow, both the patterns are normal
Gonadotropis hormone accelerates the dental development
Early maturation lead to crowding
Medicines like cortisone, steroids, metabolic, climatic, endocrinal
balance alter the pattern.
Many a times fragments of root remain n alveolar process that do not
resorb but deflect the permanent tooth.

DELAYED ERUPTION OF PERMANENT TOOTH
- heredity plays an important role
- Hpothyroidism leads to absence of permanent, presence of
supernumerary, deciduous root pieces “road blockers”, mucosal
barrier, eruption force not vigorous, bony crypt, premature loss of
deciduous,
- early loss of deciduous lead to flaring & spacing which decrease the
space available for the permanent
- Odontomas, cyst, fibroma, tumor delay or malpose the teeth
- Ankylosed deciduous teeth
- Congenitally missing succedenous teeth

ANKYLOSIS
- Called as partial anodontia, with union of roots and bone, occur at the
age of 10 – 12 years
- Due to injury to periodontal membrane, or if it get perforated, any
bony bridge forms joining lamina dura & cementum.
- Occur at buccal or lingual aspect.
- If left can cover the mucosa deflect / block the tooth.
- Accidents, trauma, endocrinal conditions, congenital diseases,
cleidocranial dysostosis , certain infections, in case of apisectomy.

ABNORMAL ERUPTIVE PATHWAY
- Each tooth travel a distinct path till it erupts. But it can deviate due to
- Tooth bud displaced from its ideal location
- Presence of supernumerary odomtomas, cyst, tumors
- Unresorbed / retained deciduous tooth or root fragment
- True arch length discrepancy or excess tooth material
- Heredity cause crowding due to less space.
- A blow, mechanical interference by ortho treatment, early class II
treatment restrict the maxilla posteriorly so II molar erupt into
crossbite or impacted.
- Ectopic eruption mainly due to arch length deficiency e.g. maxillary
II deciduous molar
- Most commonly maxillary canine is in abnormal position.’

DENTAL CARIES:
Premature loss of deciduous or permanent – drifting of adjacent teeth –
abnormal axial inclination – over eruption – bone loss – loss of arch
length – crowding – tilting of teeth, supra eruption.
IMPROPER DENTAL RESTORATION:
Improper proximal restoration – gingival inflammation, loss of
periodontal membrane attachment, mobility in tooth
Tight contacts lead to elongation of teeth, tilting.
Cross bite occur due to poorly placed restorations
Mechanical separation, large restorations, unnecessarily increases the
arch length
Under contoured proximal restoration decreases arch length while over
contoured occupy the space left out by deciduous
Premature contact – functional shift of mandiblewww.indiandentalacademy.com

BRUXISM / CLENCHING:
It was described by Marie in 1907. Called as psychogenic or idiopathic
functional aberration
Contraction of masticatory muscle, rhythmic side to side grinding,
gnashing of teeth during sleep cause malocclusion
EFFECTS
- Deep bite
- Malposed dental unit, Tooth mobility
- Non functional pattern of occlusal wear
- Pulp exposure
- Fracture of crown & root
- Muscular facial pain, tired ness, hypertrophy, incordination
- Locking of jaw, deviation
- TMJ pain and dysfunction

ETIOLOGY:
GENERAL
- Psychogenic
- Environmental, heredity
- Nervous tension
- High strung person, excited children, athletes
- Nutritional deficiency, hyperthyroidism,
- Infections, GIT disturbances, enzymatic imbalance,
- Pubertal growth spurt
- Nocturnal : due to increased negative pressure in tympanic cavity from allergic
edema of Eustachian tube mucosa
- LOCAL
- Faulty restoration
- Traumatic occlusal relationship
- Functionally incorrect occlusion
- Cyst , faulty eruption of teeth
- “ Bruxism cause malocclusion or malocclusion cause bruxism is a chicken or egg
controversy ”

CLASSIFICATION OF ETIOLOGY OF
MALOCCLUSION
The proposed classifications are:-
1. Bennet’s classification
2. The Graber's classification.
3. The Moyer's classification
4. The White & Gardener’s classification
5. The Salzmann's classification
6. The McCoy and Shepard’s classification.
7. The Strang’s classification
8. Some other classification.

BENNETS’S CLASIFICATION
Sir Normal Bennet introduced a classification of abnormality of
occlusion based on their etiology;
Class I: abnormal position of one or more teeth due to local causes.
Class II: abnormal formation of a part of whole or either arch due to
developmental defects of bone.
Class III: abnormal relationship between upper and lower arches,
between either arch or facial contour and correlated abnormal
formation of the arch.

Graber's Classification
General
-Heredity
-Congenital
-Environmental
Prenatal
Postnatal
-Predisposing metabolic
climate & disease
Endocrine imbalance
Metabolic disturbances
Infectious disease
-Dietary problems
-Abnormal pressure habits
& functional
-Posture
-Trauma &accident.
Local
-Anomalies of no.
Supernumerary teeth
Missing teeth
-Anomalies of tooth size.
-Anomalies of tooth shape
-Abnormal labial frenum: mucosal barriers
-Premature loss of deciduous teeth
-Prolonged retention
-Delayed eruption of permanent teeth
-Abnormal eruptive path
-Ankylosis
-Dental caries
-Improper dental restorations

General factors will always be present producing ideal occlusion or same
occlusal variation & usually the major factors are interrelated.
The muscles are attached to the jaws & variation in jaw position
produces variation in muscle action. Variation in muscle activity alter
the relevance of variation in the size of dentition.
The local factors are present in isolation or in combination or may
superimpose on the adverse effect of one or more of the general factor
adding further complication to the occlusion of the teeth.
Final form of occlusion & position of teeth exhibit a wide range of
variation.

Moyer’s Classification (1972):- (causes and clinical entity)
1. Hereditary :
a) neuromuscular system
b) bone
c) teeth
d) soft part (other than nerve And muscle)
2. Developmental defects of unknown origin
3. Trauma :
a) prenatal / birth injuries- hypoplasia of mandible, position of fetus
b) postnatal – fracture of jaw, teeth, habits
4. Physical agents:
a) premature extraction of primary teeth
b) nature of food
5. Habits
6. Diseases :-
a) systemic
b) endocrinal
c) local
7. malnutrition

WHITE AND GARDINER’S CLASSIFICATION
A. Dental base abnormality: -AP malrelations
- Vertical / lateral malrelations
- Disproportion of size between teeth and basal bone
- Congenital abnormalities
B. Pre eruption abnormalities: -Abnormality in position of developing tooth germ
- Missing teeth
- Supernumerary teeth or teeth with abnormal form
- Prolonged retention of deciduous teeth
- Large labial frenum
- Traumatic injury
C. Post eruptive abnormalities: - premature loss of deciduous
- Extraction of permanent
- Active muscle force
- Resting position of musculature
- Suckling habits
- Abnormalities in path of closure

Salzmann’s diagrammatic representation:-
ETIOLOGICAL FACTOR OF MALOCCLUSION
PRENATAL AND POSTNATAL
GENETIC ENVIRONMENTAL
DEVELOPMENTAL
CONGENITAL FUNCTIONAL
DIFFRENTIATIVEDIFFRENTIATIVE

Genetic- transmitted by gene may / may not be present since birth.
Differentiative- engrafted on the body during the pre functional
embryonic developmental stage. May affect the whole body / only
teeth & jaw.
Congenital- may be hereditary / acquired, present since birth
Environmental-
General : diseases / radiation
Local : eruption anomalies
premature loss/ prolonged retention of deciduous
loss of permanent tooth
periodontal diseases & trauma, infections
harmful dentofacial pressure habits, TMJ disturbances

Developmental:
General-
abnormality in relative growth rate in dentofacial region
hypo / hyper tonicity of muscles
childhood diseases, nutritional, endocrine & metabolic
disturbances
radiation /radiotherapy to mother or fetus
Local-
birth injuries
macro or micrognathia
micro or macro glossia
abnormal labial frenum
facial hemi atrophy
anomaly of tooth development & eruption

Functional :
General:
hypo / hyper tonicity of muscles
neutrotropic disturbances
postual defects of tongue and jaw
masticatory disturbances
Local :
premature loss/ prolonged retention of deciduous
loss of proximal contacts
periodontal diseases & trauma, infections
harmful dentofacial pressure habits, TMJ disturbances

According to McCoy & Shepard (1956)
- Indirect / predisposing causes:-
hereditary
congenital defect
prenatal abnormalities
acute or chronic infections
deficiency disease
metabolic and endocrinal disturbances
- Direct / determining causes :-
missing tooth
supernumerary tooth
transposed teeth
malformed teeth
abnormal labial frenum

intrauterine pressure
sleeping habit
posture / pressure
abnormal muscular habit
malfunctioning muscles
premature shedding of deciduous teeth
tardy eruption of permanent teeth
prolonged retention of deciduous teeth
improper dental restoration
loss of permanent teeth

STRANG’S CLASSIFICATION
 Heredity
 Prenatal influence bearing upon malocclusion.
1. Condition of the mother
a. Faulty diet.
b. Diseases of serious character.
c. Traumatism
2. Conditions in Embryo
a. Faulty position in utero producing localized
Pressure & tissue displacement.
b. Injury during development.
c. Hare lip & Cleft lip.
d. Injury at time of delivery.

 Postnatal causes of malocclusion.
 Intrinsic
 Premature loss of deciduous
 The loss of permanent teeth.
 Prolonged retention of the deciduous teeth.
 Missing &supernumerary teeth
 Environmental.
 Systemic.

One classification refers to:-
- Inherited or congenital:-
inherited from parents,
problems of tooth number and size,
congenital deformities,
condition affecting the mother during pregnancy,
fetal environment.
- Acquired :-
premature loss and prolonged retention of deciduous teeth,
habit
abnormal function
diet
trauma
metabolic and endocrinal disturbances

TO SUMMARIZE THE
ETIOLOGY OF SOME
COMMON
MALOCCLUSIONS

ETIOLOGY OF CROWDING
1. Disproportion in arch size and tooth size or arch length discrepancy.
2. Prolonged retention of deciduous teeth.
3. Altered path of eruption.
4. Premature loss of deciduous teeth.
5. Delayed eruption of permanent teeth.
6. Presence of supernumerary teeth.
7. Trauma
8. Localized abnormal size and shape of the teeth e.g. fusion
9. Late horizontal growth of mandible
10. Mesial migration of buccal segment

CAUSES OF SPACING
GENERALISED:
 relative microdotia
 oligodontia / partial anadontia
 Large tongue
 Suckling habits
LOCALISED:
 Missing tooth
 Undue retention of primary teeth
 Deleterious sucking habit
 Premature loss of permanent teeth
 Localized soft tissue abnormalities

CAUSES OF MIDLINE DIASTEMA
- macrognathia - microdontia
- Hereditary - racial predisposition
- Mild gen. spacing - ugly-duckling stage
- Deciduous teeth - congenitally missing
- Supernumerary teeth - peg laterals
- Extraction - ectopic eruption
- Midline cystic lesions - RME
- Increased over jet - finger sucking
- Thumb sucking - tongue thrusting
- Abnormal labial frenum - retained deciduous
- Palatally erupted lateral incisors - trauma, fibromas
- Impacted tooth in midline

CAUSES OF ANTERIOR CROSS BITE
1. Trauma
2. Arch length discrepancy
3. Retained deciduous teeth
4. Failure of resorption of roots of deciduous upper anteriors.
5. Occlusal prematurities
6. Loss of upper deciduous molars
7. Asymmetric growth of maxilla and mandible

CAUSES OF POSTERIOR CROS BITE
1. Arch length discrepancy
2. Retained deciduous teeth
3. Thumb sucking
4. nasal obstruction
5. Mouth breathing
6. Narrow maxilla.

CAUSES OF ANTERIOR OPEN BITE
1. Occur during normal closure of development of dentition
2. Disturbances in eruption of teeth and alveolar process (Ankylosis)
3. Mechanical interference with eruption and alveolar growth (finger /
thumb sucking / lip sucking habit)
4. Gross osseous dysplasia (micrognathia, mandibular hypertrophy)
5. Soft tissue factor (tongue thrust)
6. Dental factor (failure of alveolar development)
7. Skeletal factor (increased lower facial height, decreased ramal
height, increased maxillo mandibular lane angle)

POSTERIOR OPEN BITE
1. lateral tongue thrust
2. ankylosed primary teeth
3. faulty orthodontic treatment
4. primary failure of eruption

CAUSES OF DEEP BITE
1. Skeletal factor:
- Decreased lower facial height
- Increased ramal height
- Low maxillo mandibular plane angle
2. Dental factor:
- Increased interincisal angle
- Supra eruption of anterior teeth
- Under eruption of posteriors
3. Soft tissue factor:
- Lateral spreading and low tongue posture interferes with nsormal
eruption of the posterior teeth
- High lip line

ETIOLOGY OF MALOCCLUSION
1. Class II Div 1:
- Hereditary
- Habits
2. Class II Div 2:
- Low tongue posture
- High lip line
3. Class III:
- True class III – hereditery
- Pseudo class III – occlusal prematurities
early loss of upper deciduous teeth

BIMAXILLARY PROTRUSION
its a skeletal problem in which both maxilla and mandible have a
relationship more forward than normal with respect to cranial base,
with large SNA and SNB angle .
In true bimaxillary protrusion axial inclination of teeth are normal.
While in bimaxillary dental protrusion there is procumbancy of both
upper and lower teeth on the basal bone.
It is genetically predetermined.
Arise from mesial drifting of teeth in both the arches.
Commonly seen in negroids, Keralites.

UNFAVORABLE SEQUELAE OF
MALOCCLUSION
Depending upon the severity of malocclusion and psychological frame of
the patient’s mind the sequelae can range from mild malocclusion to
severe psychological problems:
- Poor appearance of the patient
- Predisposition to periodontal disease, dental caries trauma
- Abnormal muscle function
- Abnormal oral function resulting from malocclusion
- Interference to normal growth and development
- TMJ problems
- Impacted / unerupted teeth

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