Aetiology of malocclusion / for orthodontists by Almuzian

Mohammed Almuzian, University of Glasgow, 2013 Page 1
UNIVERSITY OF GLASGOW
Aetiology of malocclusion
Personal notes
Mohammed Almuzian
2013

Contents
Definition.................................................................................................................................4
History.....................................................................................................................................4
Prevalence................................................................................................................................ 4
The etiological factors .............................................................................................................. 5
Certain terms in genetics ...........................................................................................................6
Evidences of genetic roles in development of malocclusion: ........................................................ 6
Environmental factors ............................................................................................................... 8
Modern theory of the environment influence on malocclusion...................................................... 9
Epi-Genetic Theory................................................................................................................... 9
Soft tissues theory................................................................................................................... 10
Developmental pathology influencing facial development ......................................................... 10
Postnatal factors..................................................................................................................... 11
Physiological soft tissue factors (see soft tissue factors)............................................................. 12
Soft tissue factors.................................................................................................................... 12
Introduction............................................................................................................................ 12
Soft tissue factors.................................................................................................................... 12
Muscles of facial expression, Sandy 1997................................................................................. 13
Lips at rest (Position, lip line & competence)........................................................................... 13
Skeletal AP & vertical relationship as determinant factors for lip position, line and competency.
Three examples of patients with different skeletal discrepancies: ............................................... 13
Lips at function....................................................................................................................... 13
Tongue at rest......................................................................................................................... 15
Tongue in function.................................................................................................................. 15
Muscle of mastication ............................................................................................................. 16
Adenoid & Soft tissues stretching ............................................................................................ 16
Methods of Measuring Airflow (Rhinomanometry) ......................... Error! Bookmark not defined.
Periodontal ligament & Zone of soft tissue balance................................................................... 17
Examples of when soft tissue integrity is lost:........................................................................... 18
AP position of the LLS is fixed within this narrow zone of balance .. Error! Bookmark not defined.
……………………………………….

To sum up the roles of soft tissue on orthodontics treatment , please remember these: ................. 19
1. The effect of ST on the treatment plan Ackerman & Proffit, 1997....................................... 19
2. Role on the orthodontic mechanics ................................................................................... 21
3. Effect of soft tissue on age related changes in the occlusion................................................ 23
4. Effect of soft tissue on orthodontics stability ..................................................................... 22
5. Roles of Soft Tissues in the development of different types of malocclusion........................ 19
Local factors........................................................................................................................... 23

Aetiology of malocclusion
Definition
Malocclusion can be defined as an appreciable deviation from the ideal that
may be considered aesthetically or functionally unsatisfactory (Andrews 1973).
History
 When we talk about the aetiology of malocclusion it is fair to say that the
pendulum has swung backwards and forwards over the last hundred years
between principally malocclusion being due to genetic factors or being due to
environmental factors.
 If you go back to the days of Edward Angle, he would say that virtually all of
the malocclusion is due to environmental and if you change the environment
then you will correct the malocclusion.
 Clearly this is far from the truth as we know all now and over the more recent
years most people would agree that its due to a combination of genetics and
environment
Prevalence
1. Within the UK, the last Child Dental Health Survey found around 35% of 12
year olds with a definite need for orthodontic treatment on dental health or
aesthetic grounds, which increased to 43% when those started their treatment
(Chestnutt et al, 2006).
2. Proffit (2002) notes that from the results obtained from U.S Public Health
Service Surveys (Kelly et al, 1973) & (Kelly and Harvey 1977) that the
incidence of malocclusion in US children between the ages of 6-17 years of age
was approximately 75% with around 35% requiring some kind of orthodontic
treatment. (Poffit 2000)
3. Ethnicity also has a significant bearing on malocclusion.

 Class II problems are commoner in white populations of northern European
descent.
 Class III malocclusion is a common trait amongst Chinese and Japanese
societies.
 Amongst African-Caribbean populations, anterior open bite is more common
than in Caucasians who, in turn, have a greater proportion of deep bite.
The etiological factors can be classified into
A. Genetics
B. Environment
Or
A. Skeletal factors
B. Soft tissue factors
C. Dentoalveolar disproportions (local factors)
D. Habit
In details
A. Genetics
This theory says that from the moment of fertilisation, genes contain all the
necessary information to regulate cells and tissue. All the genetic information is
in the neural crest cells. In general there are two types of genes involved
1. Regulatory genes: Gene called “homeobox gene” and this is thought to be
responsible for the whole development of the craniofacial complex

2. Intercellular regulatory genes: These are molecules which are further divided into 2
groups:
I. Growth factors, TGFa TGFb, NGF, FGF & PDGF
II. Steroid-Thyroxine Retinoic Acid (STRA) “super family”, it is thought that a
variation in these contributes to craniofacial malformations.
Certain terms in genetics
 Genotype is defined as the genetic constitution of an individual, and may refer
to specified gene loci or to all loci in general.
 Phenotype is the final product of a combination of genetic and environmental
influences.
 Polygenic means many genes.
 Epigenetic transmission, when the interaction of genes with each other and the
environment during development determine the phenotypic variation of the trait.
 Multifactorial inheritance, the trait is determined by the interaction of a
number of genes at different loci, each with a small, but additive effect, together
with environmental factors
 Discontinuous multifactorial traits, is Multifactorial trait but it need to reach
specific level or threshold to express itself.
 Dominant it is the mode of inheritance when one copy of the effective gene are
required for expression of the trait.
 Recessive, it is the mode of inheritance when two copies of the effective gene
are required for expression of the trait.
Evidences of genetic roles in development of malocclusion:
1. Society studies: Genetically homogenous societies exhibit similar levels of
malocclusion. Begg, 1964
2. Twin studies: Monozygotic twins are genetically identical and share a similar
trait of malocclusion Lundstroem (1949-1983) Twin Studies.

3. Genetic roles in the development of specific occlusal trait
Many developmental dental anomalies have been shown to occur together and
have a strong familial trend.
 Genetic influence in CLP,Between 2 -20 genes are thought to be
responsible for the development of CLAP eg. TGFa.
 Genetic influence on tooth size, number, form, shape, position and
eruption:
i. Supernumerary teeth genetically related Brooke 1974
ii. Ectopic canine genetically related Peck and Peck 1994
iii. Submerged primary teeth genetically related Kurol 1981
 Arch length, crowding, spacing, cross bite and OB: Lundstroem
(1949-1983) Twin Studies
 Vertical problems: Hunter 1968, Vertical growth pattern more
genetically correlated than horizontal one, if you had the long face in one
generation then chances are that you would have a long face in the next.
 Cl2 D1 problems Harris 1969 showed a higher correlation between the
patient and the immediate family.
 Cl2 D2 problems Familial occurrence has been shown in twin studies.
(Peck et al, 1998).
 Cl3 problems Twin studies have shown concordance of mandibular
prognathism to be six times higher in twins than siblings (Downs, 1928;
Litton et al 1970; Lundstroem (1949-1983) Twin Studies.
4. Genetic roles in the development of soft tissue matrix: Van der Linden 1969
concludes that heredity control the shape and behaviour of soft tissue matrix
which is important in the development of certain type of malocclusion like class
II D2.

Notes:
 These studies have also shown that malocclusion does not follow simple
Mendelian inheritance, but rather polygenetic or epigenetic transmission
 May be one will ask why the sibling have the same crowding trait to their
parents? The answer is that they have the same skeletal and facial pattern
which are genetically determined and might face the same environment.
 So what is the importance of determine the aetiology of malocclusion? As
we know the malocclusion is multifactorial inheritance and if the genetic has
more influence than environmental, then treatment will be difficult, but if the
environment factors are more expressive then the orthodontic prognosis is
better. However this is not easy since the diagnostic tools available to
differentiate between genetic and environmental are suggestive, blunt and not
precise.
B. Environmental factors
Revolutionary theory
Comparison of large population studies with archaeological records confirms
that malocclusion has become more common over the past 1000 years. It has
been hypothesized that dietary changes in modern societies, with increased
consumption of soft, energy-rich food, has resulted in less interproximal wear
between the teeth. (Begg, 1954). Additionally, hard diet requires vigorous
mastication, stimulating the growth of facial bones, particularly in the transverse
dimension of the maxilla and mandible.
However, the tooth wear is merely a by-product, brought about by diet-related
attrition and high masticatory activity, and has only a minor effect on tooth
alignment (Varrela, 2006).

Modern theory
The environment exerts its influence mainly through change on the soft tissue
matrix which has an influence on the skeletal and dental development leading to
malocclusion.
1. Functional matrix effect (Epi-Genetic theory)
2. Soft tissues stretching theory
In details
1. Epi-Genetic Theory
This is basically the functional matrix theory revised by Moss in 1997, he
divided the original functional matrix theory into two groups:
1. Capsular matrix
It acts indirectly and alters volume of capsule; it is further subdivided into 2
components
 Neurocranial capsule, Responsible for growth of cranium
 Orofacial matrix, Responsible for growth of maxilla and mandible
2. Periosteal matrix
 Moss noted that when CHICLID fish are fed a soft diet they respond by
forming conical, non-moliform teeth and when they are fed a hard diet they
respond by forming moliform teeth, and so he uses this analogy that growth is
in some way related to function.
 The skeletal muscles regulate the active growth process eg coroniod process
does not develop in the absence of the temporalis muscle. It acts directly on the
skeletal unit. However, it is not just the muscles involved, but also nerves,
blood vessels, glands etc.

2. Soft tissues theory
It is a change in the skeletal relationship which has arisen because of the need to
change the functional requirements of the body.
Environmental factors could be classified into:
1. Intra-uterine developmental pathology influencing facial
development
Disturbances in utero due to:
 Teratogen like asprin or smoking causing CLP,
 Alcohol causing Foetal Alcohol Syndrome.
 Foetal moulding conditions or amnioitic band syndrome caused by low
aminiotic fluid or positional abnormality of the foetus during
development (Pier Robin syndrome)
 Hemifacial Microsomia: Abnormality of 1st
arch caused by the rupture
of stapedial artery during intauterine life at the stage when the branchial
arches are developing with gross cellular distruction. this is an example
of a developmental pathology which is not genetic but which is an
illustration of something which could be an environmental factor
influencing growth and development of the face and jaws. The structures
which could be damaged include:
1. External ear – underdevelopment / accessory ear tags
2. Middle ear – deafness
3. Ramus – lack of vertical dimension
4. Soft tissue – masticatory muscle, skin + fascia
5. Occlusal cant due to facial assymetry

2. Postnatal factors
Possible causes may be physiological, habitual or pathological soft tissue
factors.
a. Habitual (Sucking habits) factors (see soft tissue factors)
Thumb sucking
 Thumb-sucking is a habit (local factor) sucking of the digits will
create an AOB.
 Secondary to the habit will be a tongue thrust to create an anterior
oral seal; therefore the tongue thrust is associated with the habit.
 If habit stops before 7-9yrs old there will be reduction of AOB &
adaptive change in tongue thrust (stops).
 But if habit remains beyond 7-9yrs then tongue becomes in-bred
and even if stop sucking digits the tongue thrust will maintain the
AOB unless you orthodontically change the environment.
b. Pathology
I. Traumatic:
 The condyle is the commonest site of fracture in the mandible during childhood
and many go undiagnosed. In severe cases with bilateral fracture and dislocation
from the glenoid fossa, an anterior open bite can be one of the presenting
features due to a loss in ramus height.
 A long-term sequelae of early trauma to the mandibular condyle can be
asymmetry, with an ipsilateral decrease in ramus height and deviation of the
chin point to the affected side
 The severity of outcome is in part related to the age at the time of injury.
 However, a high percentage of children sustaining a condylar fracture have
normal mandibular growth due to the reparative capacity of the condyle, even
when displaced from the glenoid fossa.

II. Inflammatory: Juvenile rheumatoid arthritis is an inflammatory arthritis
occurring before the age of 16 years and involving the temporomandibular
joints can result in the development of a severe class II malocclusion due to
restricted growth of the mandible
III. Hormonal: Excessive growth hormone resulting in overproduction of growth
hormone from an anterior pituitary tumour causes gigantism in children and
acromegaly in adults. In both circumstances, the patient presents with a
worsening class III malocclusion characterized by mandibular excess
c. Physiological soft tissue factors (see soft tissue factors below)
Soft tissue factors
Introduction
 In orthodontic terminology means all non-calcified structures which are
relevant to tooth position and orthodontic treatment.
 Soft tissues exert a variety of forces in multiple directions
 Final tooth position is a position of equilibrium
 Moving teeth against un-favourable soft tissue will result in relapse or
instability
 Soft tissue can be a 1o aetiological factor or they can be a 2o aetiological
factor, secondary to the underlying 1o skeletal discrepancy
Soft tissue factors
1. Muscles of Facial Expression
2. Muscles of Mastication
3. Adenoids (mentioned before)
4. Fraenum (local soft tissue factor in diastema)
5. PDL (for neutral zone balance)

Muscles of facial expression, Sandy 1997
1. LIPS
a. At rest
b. In function
2. TONGUE
a. At rest
b. In function
Lips at rest (Position, lip line & competence)
Skeletal AP & vertical relationship as determinant factors for lip position, line
and competency. Three examples of patients with different skeletal
discrepancies:
1. Class II discrepancy with the skeletal relationship as primary aetiology with
lip trap as secondary aetiology
2. Increased vertical dimension with the skeletal relationship as primary
aetiology with lip incompetence as secondary aetiology causing increasing in
the proclination of the upper incisors.
3. Class II discrepancy with reduced vertical dimension with skeletal
relationship as primary aetiology & the high lower lip line as secondary
aetiology will result in the chin being closer to nose than it should be so the
lower lip covers more of upper incisors with greater restraining effect on upper
incisors leading to that the upper incisors become retroclined. However, the
upper lateral incisors are at a higher level therefore sometimes they get less
restraining effect and they become trapped outside the lip & become proclined.
Lips at function
A. Anterior oral seal
 The causes of incompetent lip are:
1. AP & vertical skeletal discrepancy

2. Short lips
3. VME
4. Increase VH
5. Posterior growth rotation
6. Functional problem of the lip like scra as a result of trauma or CLP
 The method of achieving an AOS is based upon: “The principle of least
physiological effort” by Prof Ballard, i.e. if you have an overjet of 10mm on
severe skeletal Class II, then the lower lip will, in trying to achieve an AOS,
meet the palatal mucosa because it is easier.
 The types of anterior oral seal is achieved depends upon AP & vertical skeletal
relationship and include:
1. Circum-oral contraction in mild class II and AOB
2. Mandibular posturing in mild class II
3. Lower lip to maxillary incisor cingulum in moderate class II (lower lip trap)
4. Lower lip to palatal mucosa in sever class II (lower lip trap)
5. Lower lip to tongue in very sever class II
6. Upper lip to tongue in sever class III
B. Hyperactive or “strap- like” lower lip
 It mainly cause retroclination of the lower incisor with associated LLS
crowding
 It might cause increase in the OJ and OB.
 Hyperactive lip bashes the lower incisors and the giggling forces leads to bone
loss and periodontal breakdown with loss of attachment
 Methods of treatment tried with hyperactive lip:
1. Mentalis myotomy
2. Lip bumpers to stretch muscle fibres

3. If the lower incisors moved forward the using a permanent rigid retainer is
mandatory
Tongue at rest
Size
 Very difficult to quantify.
 The relative size of tongue reduces with age & adapts to the lower position
within arch i.e. less tendency to “thrust” with aging.
 It can result in loss of vitality of incisors due to giggling forces of the tongue
bashing against upper incisors
Position
 Tongue may be normal in size but be anteriorly placed to produce spacing and
AOB.
 Partial glossotomy can result in spontaneous space closure and reduction of
AOB
Tongue in function
Tongue thrust
1. Adaptive (secondary) thrust
 Thrust occurs in an attempt to achieve an oral seal when the lips are
incompetent or an AOB is already present from a digit sucking habit
 Thrust may maintain an AOB but adapts if the AOB is corrected
2. Endogenous (primary) thrust
 Very rare & affects 1% of population
 Usually associated with lack of neuromuscular control e.g. Downs syndrome or
cerebral palsy.
 May cause AOB which is difficult to close

 Usually associated with a lisp, bimaxillary proclination, reverse COS in the
lower and deep COS in the upper.
 The diagnosis is therapeutic which means the high tendency to relapse after
treatment.
Muscle of mastication
 Hunt 1992 & 2006 found that long face syndrome has predominantly collage
fiber type 1 which is weak and long acting while short face syndrome has more
type 2 collagen fibres which is heavier and short acting.
 Conditions associated with a loss of muscle tone, such as muscular dystrophy
and certain types of cerebral palsy, result in a downward and backward rotation
of the mandible, an increased lower face height and an anterior open bite
 However (Proffit & Fields, 1983) believe that this muscle change is a result
from malocclusion.
Adenoid & Soft tissues stretching
 It is a change in the skeletal relationship which has arisen because of the need to
change the functional requirements of the body.
 Soft tissues stretching theory of Solow & Tallgren 1976, showed that:
airway obstruction lead to some sort of neuromuscular feedback mechanism
where the patient can't breathe through nose, so adopt a head up posture with
extension, In so doing, you now stretch the superhyoid muscles, skin + fascia.
This in turn imparts a force on the mandible and in turn means that the mandible
adopts a downward posture ( LAFH + MM angle) this will allow the tongue
to drop and imparts less force on maxillary arch in the lateral dimension which
with the unopposed action of the cheeks pushes the dentition into a narrower
arch which leads to cross bite situation
 It was proposed that the “Adenoids” were the most important “soft tissue”
responsible for the difficulty in breathing through your nose then the adenoids

enlarged causing chronic constriction in the nasopharyx followed by the now
same pathway as “soft tissue stretch theory”. ARONSON (1979). The study
was:
1. looked at 81 pre-pubertal children who were obligate mouth breathers needing
adenoidectomy, 81% had features of adenoid face, 4% looked normal,
2. Features of the Adenoidal Face include
 Flat middle 1/3rd
of face  due to functional requirement of antrum which
are underdeveloped
 Long Face due to neuromuscular feedback ie “head up + downward mandibular
posture”
 Over eruption in mandibular arch  over eruption due to lowered
mandibular posture
 Narrow, High - arched Palate  due to lowered tongue unopposed pressure
from cheeks
3. He measured the SN angle to the true vertical (angle “a”)
4. He looked at the size of this angle pre and 5yrs post adenoidectomy
5. He found that “normalisation” of this angle occurred ie it increased at the follow
up suggesting that head-up posture was not present
6. However, Vig (1985) that “ the magnitude of the morphological difference
attributed to adenoid removal was far too small to be of any clinical
significance”
Periodontal ligament & Zone of soft tissue balance
The equilibrium theory was described first by Weinstein in 1963 and hen
popularized by Proffit 1979, he divided the force of equilibrium into:
1. Primary factors are:
 Intrinsic forces by tongue and lips
 Forces from dental occlusion

 Forces from the periodontal membrane.
 Extrinsic forces: habits (thumb sucking, etc.), orthodontic appliances
2. Secondary factors in equilibrium
 Postural relationships in the stomatognathic system
 Secondary factors relating to eruption forces like failure of eruption
This chap also looked at the zone of balance by putting inducers on the labial &
lingual surfaces of the incisors and measuring the forces of soft tissues pushing
against the inducers over a 24hr period. He noted that the tongue forces always
exceeded that of the lips & cheeks both at rest and in function. So why aren’t
the teeth migrating and splaying out? The reasons:
A. AP forces
1. Size & duration of force, teeth won’t respond to short, sharp shock force.
2. Atmospheric pressure, every time you swallow you create negative pressure
inside the oral cavity
3. Contraction of periodontal transeptal ligament fibres.
4. Forces of occlusion
Examples of when soft tissue integrity is lost:
1. Afro-carribeans due to flaccid everted lip structures
2. Cancrum oris
3. Haemangiomas swelling of the lips/tongue/cheeks produces a “new” zone of
balance.
4. Bilateral cleft pre-maxilla swings forwards
5. Pd diseases

To sum up the roles of soft tissue on orthodontics treatment, please
remember these:
1. Roles ofSoft Tissues in the development of different types of malocclusion,
Mossey 1999, Turner & Sandy 1997
A. Class II division 1
 Lip seal: lower lip to tongue seal can cause class II D 1 incisor relationship.
 Lip trap and activity: lower lip trap may procline the upper incisors further.
Lip hyperactivity can retroclined teeth.
 Habit: Digit habits can produce a Class II division 1 malocclusion even with
an underlying Class 1 skeletal pattern due to effects on the dentition.
B. Class II division 2
 High lower lip line can retrocline the upper incisors with the development of a
Class II division 2 malocclusion.
 Strap like lower lip cause retroclination of lower incisors
 Hyperactivity of the massteric muscle can produce low facial height. Mills
(1982)
C. Class III
I. Soft tissues do not generally play a part; however, there is a tendency for the
lips and tongue to contribute towards dentoalveolar compensation.
II. Enlarged tonsils and mandibular forward posture due to nasal obstruction can
cause class III.
D. Bimaxillary proclination
 Large tongue plays a significant part in the position of the incisors.
 Flaccid and everted lips
 Incompetent lips
E. Vertical anomalies

 Habit: digit separates the jaws, the vertical equilibrium on the posterior teeth is
altered and a greater eruption of posterior teeth occurs, contributing to the
anterior open bite
 Breathing: increased overjet and over-eruption of posterior teeth may occur also
as a result of altered head posture secondary to chronic nasal obstruction.
 Tongue: A large tongue may encroach on the dental arch, impeding tooth
eruption anteriorly or laterally, depending on tongue position
 Weak muscle of mastication
F. Transverse anomalies
 Digit sucking can result in a transverse discrepancy between the jaws.
 Chronic nasal obstruction can cause cross bite due to lower tongue position
 Soft tissue lesions such as fibro-epithelial polyps and haemangiomas are
relatively uncommon causes of transverse anomalies but their effects can be
dramatic
G. Crowding
 Changes in lip and tongue pressures may affect the development of the alveolus
and if the dental arch form is 'moulded' to a smaller arch size, then crowding
and malalignment may occur.
H. Spacing
 Localized spacing may occur with a large 'fleshy' labial or lingual fraenum,
I. Tooth rotations and relapse
 Contraction of these distorted supracrestal fibres may cause relapse of the
rotation if insufficient retention time is allowed for the reorganization of these
fibres
J. Soft tissue scarring in cleft lip and palate

 Facial growth has been shown to be inhibited in patients with surgically
repaired cleft lip and palate anomalies compared with unrepaired clefts." This
effect is mediated by soft tissue scarring
2. The effect of ST on the treatment aims Ackerman & Proffit, 1997
This should be analysed according to aesthetic guidelines and the treatment
should be aimed to address the underlying malocclusion without compromising
the aesthetic zone or indeed, improving the aesthetic balance.
3. Role on the orthodontic biomechanics
A. Muscle of mastication
 In treatment of class II malocclusion, "TB" appliances posture the mandible
forwards, stretching the elevator muscles of mastication and applying an
anteriorly directed force to the lower arch and a posteriorly directed force to the
upper arch.
 The activator was designed to be a loose appliance, which dropped down in the
mouth, activating the tongue to cause the mandible to be brought forwards into
an improved occlusal position (Lee, 1984).
 The Harvold appliance was intended to stretch the facial and the muscles of
mastication.
 The Frankel functional impede activity of the lips, cheeks and tongue, thus
allowing normal facial growth (Lee, 1984).
 Bite planes: They stretch the muscles of mastication vertically and allow any
teeth left unopposed to erupt.
B. The lips
 Functional appliances posture the mandible forwards and bring the lower lip
forwards in relation to the upper incisors. An anterior oral seal should then be
possible which may assist retraction of the upper incisors in class II, div 1 cases
as well as improving lip tone where the lips are incompetent.

 Lip bumpers utilise the musculature of the lips to apply a distal force to the
dental arch.
4. Effect of soft tissue on stability
1. Lips:
 Lip incompetence reduces the of stability of OJ correction.
 In cl2 d2, Successful treatment must therefore position the upper incisors
correctly in relation to lower lip.
 Cases of corrected bimaxillary proclination tend to relapse due to the
weak tone of the lips.
2. Cheeks and tongue
 Stability of arch dimensions: The equilibrium theory suggests that the opposing
forces of the tongue and lips and cheeks will render arch lengthening treatments
 If the position of the tongue is low in the mouth, relapse may occur after
crossbite correction.
 Tongue reduction has been mentioned previously in the stability of anterior
open bite.
3. Periodontal fiber; The supracrestal fibres of the PDL reorganise more slowly
than the rest of the ligament fibres and are stretched by rotational tooth
movements. A residual elastic rotational force is thus exerted on the tooth after
rotation. Edwards (1988) reported that circumferential fibrotomy (pericision)
reduced rotational relapse by 50%.
4. Stability of Corrective Jaw Surgery: Surgical correction of vertical dysplasias
are prone to relapse and Hunt (1992) has suggested that the proportion of
intermediate (IM) fibres in masseter and temporalis muscle may provide a
predictor of the likely degree of post-surgical stability. Intermediate fibres are
unique to masticatory muscles (Rinquist, 1973) and are thought to have the
ability to change into type I or type II fibres according to functional demands. A

corrected jaw relationship may induce these IM fibres to transform as required
and maintain the altered vertical dimension.
5. Effect of soft tissue on age related changes in the occlusion
1. Physiological mesial drift: the transeptal fibres that run between the teeth, as
shown by Moss and Picton (1974) has shown to be capable of causing tooth
movement. These fibres may play a role in late lower incisor crowding by
bunching the teeth progressively towards the front of the arch.
2. Migration: Migration is observed of anterior teeth whose periodontal support
has broken down. It has been suggested by Proffit(1979) that this-may be due to
the greater pressure of the tongue over the opposing force of the lips; the
stabilising role of the PDL having been lost.
Local factors
Local factors alone may cause a malocclusion or they may occur in any
combination of the factors listed above. Local factors include:
1. Abnormalities of tooth number
i) Anadontia
a) Rare condition
b) Total failure of development due to aplasia of dental lamina
c) Associated with ectodermal dysplasia (hereditary). This is characterized by:
 Anadontia
 Absence/reduced sweat glands leading to dry coarse skin
 Sparse thin eye-brows
 Defects of the nails
 Skeletal deformities  depressed bridge of nose/frontal bossing

 Absence of alveolar processes of max.& mand.(since no teeth)
ii) Oligodontia
Severe hypodontia associated with systemic manifestations (ectodermal dysplasia)
iii) Hypodontia see hypodontia notes
iv) Supernumery teeth. The type are:
 Conical supernumeries
 Tuberculate supernumeries
 Odontomes
 Supplemental supernumeries
2. Early loss of primary teeth: the effects depend on:
 Presence of crowding
 Which Tooth lost
 Timing / Age of loss
 Which Arch
 Eruption Sequence
3. Retained primary teeth
 Retained incisors (A`s + B`s)
 Retained molars
 Ankylosed molars (submerged)
4. 5. Delayed eruption of permanent teeth
 Impaction
 Ectopic Crypt Position
 Dilaceration
5. Loss of permanent teeth
 Loss of 6`s (FPM)
 Loss of 4s
 Loss of 1s

6. Abnormalities of tooth form
 Double tooth (Fusion / Gemination): Fusion between a lateral incisor and
a canine does not occur in the maxilla. The different nerve paths in the
maxillary and mandibular regions might explain this malformation
pattern
 Macrodontia
 Microdontia
 Additional Cusps
 Invaginated teeth
7. Habits
8. Abnormal Labial Freanum

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