Role of Muscles in Malocclusion Etiology and Treatment

Muscling in on Malocclusions: current
concepts on the role of Muscles in the
aetiology and treatMent of
Malocclusion
hunt n,shah r,sinanan a,lewis M.
Jr of orthodontics,Vol 33;pg 187-97;2006
www.indiandentalacademy.com

Contents
• Introduction
• Classification of muscles
• Function of muscles
• Comparission of short and long face syndrome
• The role of muscles in the aetiology of vertical facial
deformity
• Muscle proteins
• The role of muscles in response to treatment
• Conclussion
• References

Introduction
• Although Bones provide leverage and form the framework of
the body, they cannot move body parts by themselves.
Motion result from the alternating contraction and relaxation
of muscles.
• Muscles constitute 40-50% of total body weight. Muscular
strength reflects the prime function of muscle i.e changing
chemical energy into mechanical energy to generate force,
perform works and produce movement.
• In addition, muscle tissue stabilizes the body’s position,
regulates organ volume and it also generates heat.

CLASSIFICATION OF MUSCLES
• The basis of these classifications is as
follows:
1. DEPENDING UPON THE PRESENCE OR ABSENCE
OF STRIATIONS.
2. DEPENDING UPON THE CONTROL AND
3. DEPENDING UPON THE FUNCTION.

DEPENDING UPON STRIATIONS
Under this the muscles are divided into two groups namely
STRIATED MUSCLE AND
NON STRIATED MUSCLE
STRIATED MUSCLE:
Under light microscope, in each muscle cell, a large number of
cross striations (transverse lines) are seen at regular interval.
Eg.Skeletal and cardiac muscles are striated.
NON-STRIATED MUSCLE
The muscle with out cross striations are called non striated muscle
or plain muscle.
Eg. Smooth muscles.

DEPENDING UPON THE CONTROL
These are classified into two types namely
• VOLUNTARY MUSCLE AND
• INVOLUNTARY MUSCLE
VOLUNTARY MUSCLE:
• These muscles can be controlled voluntarily.
• They are innervated by neurons that are part of the somatic division of the
nervous system.
• E.g. Skeletal muscles.
INVOLUNTARY MUSCLE
• These muscles cannot be controlled voluntarily.
• Their action is involuntary either by anatomic nervous system or by
hormones selected by the endocrine system.
• E.g. Cardiac and smooth muscles, and some skeletal muscles
like muscles, which cause contraction and relaxation of the diaphragm.

DEPENDING UPON THE FUNCTION
They are classified into three types namely
SKELETAL MUSCLE
CARDIAC MUSCLE AND
SMOOTH MUSCLE
• SKELETAL MUSCLE:
These muscles are in association with bones forming the skeletal
system.
They constitute 40% of body mass.
These are about 600 skeletal muscles identified.

• CARDIAC MUSCLE
This muscles form the musculature of the heart.
• SMOOTH MUSCLE
These are the muscle, which are in association with viscera.
So they are also called visceral muscles.
They form the contractile units of wall of the various visceral organs and are
present in the following structures like:
Wall of organs of GIT like oesophagus, stomach and intestine.
Ducts of digestive glands.
Trachea, bronchial tube and alveolar ducts of respiratory tract.
Ureter, urinary bladder, urethra and genital ducts.
Wall of the blood vessels.
Arrector pilorum of skin
Mammary glands.
Iris and ciliary body of the eye.
Prostate gland.

Function of muscles
•Feeding
•Deglutition
•Mastication
•speech and
•Postural maintenance.

The primary etiologic sites of malocclusion are
•Muscular system
•Bone
•Teeth and
•Soft tissues (excluding muscles).
Among these factors Muscular system plays its primary role in the
etiology of dentofacial deformity. The teeth and supporting structures are
constantly under the influence of muscles of face and neck. The active
functional and resting forces of muscles are responsible for the integrity
of the dental arches and relations of the teeth to each other . Any
aberration of these muscles will affect the integrity of the dental and
skeletal structures and cause maloccluion.

• As clinicians we need to have a clear and in-depth
understanding of the mechanisms of both normal and
abnormal facial growth.
• Advances in surgical techniques and methods of fixation
enable us to correct a variety of established
malocclusions, primarily of skeletal origin, through the
use of a combination of orthodontics and orthognathic
surgery.
• Of all the problems that confronts us it is abnormalities in
the vertical dimension, whether they be in the growing
child or the adult, which still present the greatest
difficulties both in treatment itself, as well as maintenance
of the treatment outcome.

• For normal, vertical facial growth and development, growth in
the anterior part of the face must equal that occurring in the
posterior part of the face. If this doesnot occur, then a relative
growth rotation of the mandible develops.
• For example, if growth in the posterior part of the face exceeds
that occurring anteriorly, then the net effect is an anterior,
forward closing rotation of the mandible producing the typical
short face deformity and deep overbite associated with the
short face syndrome.
• At the opposite extreme where growth in the posterior part of
the face may be severely reduced in comparison to that
occurring anteriorly, an opening or clockwise rotation of the
mandible is evident with the net effect being an excessive
anterior facial height and frequently an anterior open bite,
associated with a long face deformity.

COMPARISON OF
SHORT FACE SYNDROME
AND
LONG FACE SYNDROME

1) Short face syndrome
They are characterized by short
anterior lower face height with
excessive forward rotation of the
mandible during growth resulting
from both an increases in the
normal internal rotation and
decrease in external compensation.
This results in:
Nearly horizontal palatal plane
Mandibular morphology of the “
square jaw” type
Low mandiular plane angle
Square gonial angle
Deep bite
Crowded incisors

CLASSIFICATION OF SHORT FACE SYNDROME
• Based on the parameters like ramus length, the SN to MP
angle, and posterior vertical maxillary dentoalveolar height the
short face syndrome group is divided into two sub types.
SUBTYPE I:
It is characterised by a long ramus and extremely low SN-
MP angle and slightly redused posterior maxillary
dentoalveolar height.
SUBTYPE II:
A short ramus and a vertical maxillary deficiency were the
dominant findings, while the SN-MP angle was only slightly
redused. These persons manifest extreme reduction of lower
anterior face height.

2)Long face syndrome
• This is characterized by
increased anterior and total face
height and results primarily from
a lack of the normal forward
internal rotation or even a
backward internal rotation. The
internal rotation in turn is
primarily matrix rotation not
intramatrix rotatio.
• This results in:
Palatal plane rotates down
posteriorly.
Mandible shows an opposite
backward rotation.
Increase in mandibular plane
angle.
Associated with open bites

Classification of Long face syndrome
SUBTYPE I: Is characterised by a long ramus, increased
occlusal plane to palatal plane angle, an increased SN to MP
angle, and excessive lower anterior facial height. These
persons manifest the most typical clinical characteristics of the
the long face syndrome and have excessively long face.
SUBTYPE II: However, extreme backward and downward
rotation of the mandible combined with a short or extremely
short ramus, is associated with an increase in LAFH. The
increase in posterior maxillary height was not striking in this
subtype.

The role of muscles in the aetiology
of vertical facial deformity
• Patients with a short vertical dimension are capable of producing
occlusal forces far in excess of those recorded from patients with
normal vertical facial form.
• Conversely, individuals with long face deformities produce very
weak occlusal forces as measured either during swallowing,
chewing or maximum clenching.
• With regard to muscle volume, 3-D ultrasound studies have
shown that patients with large posterior face heights and low
maxillary mandibular plane angles are associated with large
masticatory muscles.
• The article tries to find an answer to if these functional differences
are a reflection of a primary inherent abnormality of muscle
structure or merely a reflection of an adaptive response to the
relative efficiency of the muscle system? To address the
conundrum as to whether or not muscles are a prime aetiological
factor in the development of aberrant vertical facial form.

• Histochemical staining techniques have shown that
the muscles of mastication, in accordance with
other skeletal muscles of the body consist of a
mixture of muscle fibre types, and which are
broadly categorized as type I or type II fibres.
• These fibres differ in both their speed of contraction
and in their metabolic activity.
• Type I fibres are slow acting, but fatigue resistant
and it is believed that they are responsible for such
activity as generation of posture.
• While ,type II fibres are fast acting, but fatigue
easily and it is understood that these fibres produce
maximum force of short duration such as that
occurring during clenching of teeth.

• The typical picture, therefore, seen in a
patient with a short face deformity is
such that the type II fibres are present
in greater numbers than those seen in
patients with normal facial dimensions.
• In contrast, patients with long face
deformity show not only a reduced
number of type II fibres, but these
fibres also appear smaller in size in
comparison to the normal size type I
fibres.
• The type II fibres are the major
contributor to maximum force, these
observations concur with the clinical
observations of measurements of
occlusal force.

MUSCLE PROTEINS
• Myofibrils are made up of three kinds of proteins.
1. Contractile proteins
• Generates force during contraction.
1. Regulatory proteins
• Regulates the process of contraction.
1. Structural proteins
• Keeps the filaments in alignment, gives the myofibril
elasticity and extensibility, link the myofibrils to the
sarcolemma and extracellular matrix.

CONTRACTILE PROTEINS
MYOSIN
• Functions as a motor protein in all the three types of
muscles.
• 300 molecular of myosin forms – single thick filament.
• The myosin molecules is composed of six polypeptide
chains, two heavy chains each with a molecular weight of
about 200,000 and four light chains with M.W of about
20,000 each.
• Two heavy chains wrap spirally around each other to form a
double helix, which is called the fail of the myosin molecule.
• It helps in contraction process.

ACTIN FILAMENT
• Actin is the main component of the thin filament.
• Actin filament is a double – stranded F-actin each protein
molecule. Which is 1 micrometer long.
• There are 13 molecules in each revolution of each strand of
helix.
• One molecule of ADP is attached to one G-actin molecule
which is the active site on actin myosin filament where the
cross bridges of the myosin filament interact to cause muscle
contraction.

REGULATORY PROTEINS
Tropomyosin molecules
• Tropomyosin Is regulatory protein present on the actin filament.
• Its mol.wt is 70,000 length is 40nm.
• Tropomyosin molecules are wrapped around the side of the F-actin
helix.
• When the muscle is resting, the tropomyosin molecules lie on top
of the active sites of the actin filament, and does not allow the
myosin filament to bind with the actin filament and thus not allowing
the contraction to occur.

TROPONIN
• Troponin molecules are attached along the sides of the
tropomyosin molecules.
• Troponin is made up of three subunits
• Troponin I – strong affinity for actin
• Troponin T – strong affinity for tropomyosin
• Troponin c – strong affinity for calcium ions.
• This complex helps in attachment of tropomyosin to actin.
• The affinity for ca2+ ions initiates the contraction process.

STRUCTURAL PROTEINS
TITIN
• These structural proteins helps in alignment, stability, elasticity and
extensibility of myofibrils.
• It is the third most plentiful protein after action and myosin in skeletal
muscle
• Titin anchors a thick filament to both, Z disc and the M line, and helps in
stabilizing the position of the thick filament.
• It extends from Z disc to the beginning of thick filaments.
• It can stretch atleast 4 times its resting length and then spring back un
harmed.
• Thus it helps in elasticity and extensibility of myofibrils.

• This forms the M line in the middle of the sarcomeres.
• This binds to titin and also connect adjacent thick filaments to
one another.
MYOMESIN
• It is a large but in elastic protein and lies along side the thin
filament.
• It is also attached to the Z disc.
• It helps maintain alignment of thin filaments in the sarcomeres.
NEBULIN
DYSTROPHIN
• It is a cyto-skeletal protein that links thin filaments of the
sarcomeres to integral membrane proteins of the sarcolemma.
• Dystrophin reinforce the sarcolemma and help transmit the
tension generated by sarcomeres to the tendon.

• Although many proteins, including Troponin and Tropomyosin B, are involved in
muscle contraction, it is the interaction of the rod-like myosin molecules with the
globular-like actin molecules which is fundamental to the process.
• The myosin molecules involved in this contractile arrangement are the heavy
molecular weight proteins referred to as the myosin heavy chain proteins
(MHCs).
• The adult masseter muscle is shown to contain at least five myosin heavy chain
isoforms ranging from the type I myosin heavy chain gene (MYH 7), which is
primarily responsible for the slow phenotype, and the fast phenotype components
represented as type IIX and IIA heavy chain proteins (MYH 1 and MYH 2 genes,
respectively).
• In addition, there are at least two more isoforms not normally found in adult limb
skeletal muscles, but which can be considered as normal components of the
masticatory muscles. These include the alpha cardiac myosin heavy chains
(MYH 6 gene), normally found in heart muscle, and developmental myosin heavy
chains which normally disappear from other skeletal muscles shortly after birth
(MYH 3 and 8 genes).
• Comparing the myosin heavy chain isoform expression of patients with long face
deformity as opposed to those with normal vertical dimensions, it is apparent that
there are at least two variations from this typical picture. First, the fast isoform is
markedly reduced in its presence and, secondly, the proportion of developmental
isoforms is frequently increased albeit with large individual variation

• The changes in myosin heavy chain expression are an inherent
genetic abnormality or whether they are merely a response to
altered function is tested by the experimental manipulation of
skeletal muscles.
• With regard to masticatory muscle, the differences in fibre size
evident in patients with increased vertical facial deformities is a
reduction in the size of the fast fibres only. Although there may not
be an increased expression of slow isoforms per se, for a given
volume of muscle, because the fast isoforms are smaller in size
and number, there may be a relative increase in expression of the
slow isoforms.
• At the opposite extreme, if a muscle is unloaded, for example by
applying plaster cast fixation to a limb, then the adaptive changes
seen are typically those of fibre atrophy. Again, both slow and fast
fibres are affected but with an overall increased expression of fast
isoforms.

• The second change noted in patients with long
face deformity with regard to myosin heavy
chain expression is the increased presence of
developmental heavy chain myosin isoforms.
• It has been postulated that such developmental
isoforms may form part of the adaptive process
whereby these rudimentary isoforms can adapt
into either slow or fast isoforms depending
upon the functional requirements.
• With regard to masticatory muscles, it has been
postulated that this could reflect the quality of
the occlusion and the efficiency of the occlusal
forces.

• As indicated by a study which
compared the presence of
developmental myosin heavy
chains in relation to the number of
occlusal contacts seen in a group
of patients with a variety of both
normal and abnormal facial form.
• There is an inverse relationship
present such that the greater the
number of occlusal contacts, the
lower the presence of
developmental myosin heavy
chains .One explanation for this
could be that in patients with a
poor occlusion and few occlusal
contacts, the muscles are
repeatedly undergoing micro-
trauma, and are regenerating and
adapting in order to try to produce
a more efficient functioning
muscle-occlusal system.

• Following the publication of the human genome it has now
become possible to examine the total gene expression in
a particular body tissue using micro-array technology.
• Both clinicians and scientists have argued for
generations, as to the respective contribution of genetics
and environmental factors in influencing ultimate facial
form and associated malocclusion.
• Gene expression from a long face patient is compared
with that from a patient with normal facial form.It was seen
that the genes responsible for the IIX myosin heavy chain
protein, as well as the myosin binding proteins and alpha
6 integrin expression in addition to other components of
the extra-cellular matrix such as fibronectin, showed
between a two and four-fold reduction in gene expression
compared with a patient with normal facial form.

• Conversely, there is between a four- and six-fold
increase in other myosin heavy chain components; for
example, the alpha-cardiac and developmental
isoforms. Again, it is emphasized that there is large
individual variation between patients with a specific
facial form.
• Although gene expression differences exist in both the
contractile and extra-cellular matrix components of
masseter muscle in some patients with increased
vertical facial deformity, there is large individual
variation.
• The majority of changes in muscle fibers and protein
content are probably of an adaptive nature in response
to changing functional demands.

The role of muscles in response to
treatment
• A knowledge of how muscles respond to clinical
interventions is pivotal to treatment success and can
influence the way in which a particular treatment modality
is applied.
• Many forms of interceptive treatment, whether they be
purely orthodontic in nature or in combination with surgery,
bring about changes in the muscles of mastication with
regard to one or more of the following changes:
• in muscle fibre orientation;
• in the functioning length of fibres;
• in muscle structure;
• in muscle phenotype.

• Successful treatment requires both
reorganization in the connective tissue and
regeneration of muscle fibres.
• Reorganization of connective tissue is an
extremely complex process involving muscle
derived stem cells (satellite cells), extra-cellular
matrix molecules and receptors for the extra-
cellular matrix (for example integrins).
• Remodelling of the extra-cellular matrix is
mediated by a family of enzymes known as
matrix metalloproteinases (MMPs).MMP2 is
expressed during the regeneration of new
myofibres and is a known mechano-responsive
gene

• Muscle cell were grown in a 3 dimensional
muscle cell culture,to study the fate of
developing muscle cells and assess how they
respond to stretch.
• Using MMP2 production as a marker of muscle
adaptation in response to stretch, it was found
that the muscle response is greater with a
continuous stretch regime in contrast to an
intermittent or cyclical stretch process.
• Furthermore, the muscle response is directly
proportional to the amplitude of the stretch.

• Clinically, this suggests that posturing the
mandible both horizontally and vertically, to
an extent that it exceeds the freeway
space,will help in greater likelihood of an
adaptive muscle response, rather than one
that is in limited vertical opening.
• Furthermore, a fixed form of functional
appliance, is expected to bring about a more
responsive change than a removable
appliance due to the likely intermittent wear
of the latter.

• The exact mechanism of muscle fibre adaptation remains
somewhat controversial.
• It has been postulated that a group of muscle fibres with a
particular phenotype, which contains the developmental myosin
heavy chains, may provide a source of ‘immature’ muscle fibres,
which could adapt in response to differing functional needs into
predominantly slow or fast fibre types.
• Bearing in mind the relationship between quality of the occlusion
and prevalence of developmental myosin heavy chain isoforms it
merely reflects the change to a more efficient musculo-occlusal
relationship.
• However, based upon the very limited results of gene expression
analysis it is noteworthy that those patients who have
experienced considerable relapse have evidence of a pre-
treatment deficiency of the developmental MHC isoforms in
comparison to those patients in whom a stable result was
achieved.

Conclussion
• The question as to whether muscles play a part in the
control of facial form remains unanswered, although
increasing evidence would indicate that the muscle
response is likely to be more adaptive to underlying
skeletal development rather than a primary driving force.
• A change in muscle function can initiate morphologic
variation in the normal configuration of the teeth and
supporting bone, or it can enhance an already existing
inherent malocclusionc due to compensatory or adaptive
muscle activity and functions.
• Orthodonticaly finished result should reflect a balance
between the structural changes obtained and the functional
forces acting on the teeth and investing tissues at that time
for proper functional activity and to prevent relapse.

References
• Hunt N,Shah R,Sinanan A,Lewis M. Muscling in on
malocclusions: Current concepts on the role of muscles in
the aetiology and treatment of malocclusion.Jr of
Orthodontics,Vol 33;pg 187-97;2006
• Benington PC, Gardener JE, Hunt NP. Masseter
muscle volume measured using ultrasonography and its
relationship with facial morphology.EJO 1999; 21:659–70.
• Nelson-Moon Z, Morgan MJ, Hunt NP, Madgwick
AJA.Does occlusion determine perinatal myosin heavy
chain expression in masseter muscles? EJO 1998; 20:
Abs.63, 635.
• Graber TM. The "three M's": Muscles, malformation, and
malocclusion.AJO Vol (418 - 450) 1963 Jun
• Orthodontics-principles and practice T.M.Graber

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Role of Muscles in Malocclusion Etiology and Treatment

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