CHAPTER 1

INTRODUCTION

1.1 Background
Temporomandibular joint is the only joint that can be handled by
dentists. It is very important for us to learn about this joint because there
are a lot of cases that can be caused by temporomandibular joint disorder.
Temporomandibular joint is formed by bones, muscles,
ligaments, nerves, etc. This joint makes it possible for us to open and
close the mouth. When the joint and surrounding muscles and ligaments
are malfunctioned in some way, it is called temporomandibular joint
disorder. It can be caused by bad habits such as bruxism, clenching, etc,
disc displacement, the degenerative joint, etc.
46 year old female patient came to the dentist with a complaint
that this 1 year, she has been feeling stiffness, dull, clicking sound as
well as pain in the left and right cheek area when she opens her mouth,
especially on mornings when she wakes up, whereas there is no dental
cavities

1.2 Problem Statement

1.3 Purposes
1.4 Objectives
1.5 Methods
Our research is based on journals and textbooks that we get both
from mass and electronic media.
1.6 Hypothesis
The patient feels pain because of there is a temporomandibular
joint disorder. We conclude that there is temporomandibular joint
disorder because of some symptoms that are experienced by the patient
like clicking sound, pain on the right and left cheeks, also muscle pain.
 CHAPTER 2
LITERATURE STUDY

2.1 Anatomical View of Temporomandibular Joint

The temporomandibular joint, or TMJ, is the articulation between
the condyle of the mandible and the squamous portion of the temporal
bone. There are two TMJs, one on either side, working in unison. The
name is derived from the two bones which form the joint : the upper
temporal bone which is part of the cranium ( skull ), and the lower jaw
bone called the mandible . The unique feature of the TMJs is the articular
disc . The disc is composed of fibrocartilagenous tissue (like the firm and
flexible elastic cartilage of the ear) which is positioned between the two
bones that form the joint. The TMJs are one of the only synovial joints in
the human body with an articular disc , another being the sternoclavicular
joint .
The disc divided each joint into two. The lower joint
compartment formed by the mandible and the articular disc is involved in
rotational movement-this is the initial movement of the jaw when the
mouth opens. The upper joint compartment formed by the articular disk
and the temporal bone is involved in translational movements, this is the
secondary gliding motion of the jaw as it is opened widely. The part of
the mandible which mates to the under-surface of the disc is the condyle
and the part of the temporal bone which mates to the upper surface of the
disk is the glenoid (mandibular) fossa. Temporomandibular joint divided
into two components, there are active component and passive component.
Passive component
Passive components are bone, articular capsule, ligament, and
articular disc. Bone component in passive component is fossa
mandibularis, capitulum mandibula (condyle/ processus condyloideus),
tuberculum articulare (articulare eminence). Fossa mandibularis is the
squamous portion of the temporal bone (concave). Anterior boundary of
fossa mandibular is a convex bony eminence (tubercle) or articular
eminence. It is quite thick to arrest the strength, instructing movement of
condyle when the position of mandibular to anterior. Processus
condyloideus is the posterior portion of the ramus mandibula that extends
upward. The condyle is elliptically shaped with its long axis oriented
mediolaterally.Length of mediolateral is 15-20 mm, and length of
anteroposterior is 8-10 mm. the medial pole generally more prominent
than lateral. The articular surface of the temporal bone is composed of
the concave articular fossa and the convex articular eminence.
Capsule articularis or capsular ligament is fibrous structure
surrounds the entire temporomandibular joint. Superior of capsule is
patch with temporal, the borders of the articular surface of the
mandibular fossa and articular eminence. Inferior of articular capsule is
patch to the collum mandibula. The function of capsular ligament is to
resist any medial, lateral or inferior force that tend to separate or
dislocate the articular surface and to retain the synovial fluid.
Ligament of temporomandibular divided into collateral ligament,
temporomandibular ligament, sphenomandibualr ligament,
stylomandibular ligament. Collateral (discal) ligament lies from medial
and lateral borders of the disc to the poles of the condyle. It consist of the
medial discal ligament and the lateral discal ligament. It composed of
collagenous connective tissues. The function is allow the disc move
passively with the condyle as it glides from the anterior to the posterior
and permit the disc to be rotated anterior to posterior on the articular
surface of the condyle. These ligaments are responsible for the hinging
movement between the condyle and the articular disc. They have a
vascular supply and innervated.
Temporomandibular ligament lies at the lateral aspect of capsular
ligament. It composed of two parts, they are outer oblique portion and
inner horizontal portion. Outer oblique portion from the outer surface of
the articular tubercle and zygomatic process posteroinferior to the outer
surface of the condylar neck. It resists excessive dropping of the condyle
so limiting the extent of mouth opening. Inner horizontal portion from
the outer surface of the articular tubercle and zygomatic process
posteriorlyand horizontally to the lateral pole of the condyle and
posterior part of the articular disc. It limits posterior movement of the
condyle and disc.
Sphenomandibularis ligament is an accessory ligament. It lies
from the spine oh the sphenoid bone and extends downward to lingual
mandibula. Stylomandibular ligament is the second accessory ligament.
It lies from the styloid processand extends downward and forward to the
angle and posterior border of the ramus mandibula. It limits excessive
protrusive movement of the mandible.
Articular disc is composed of dense fibrous connective tissue
devoid of any blood vessels or nerve fibers. In sagital plane can be
divided into three regions according to thickness, anterior border,
posterior border(slightly thicker than anterior border), and central area is
the tinnest, in normal condition, the condyle lies in intermediate zone.
The disc is generally thicker medially than laterally, it increased space
between the condyle and the articula fossa toward to the medial of the
joint. The shape of the disc is determined from the morphology of the
condyle and mandibula fossa. During movement the disc is flexible, and
can adapt to the functional demands of the articular surface, but it cannot
be reversible in its function. The disc maintain its morphology unless
destructive forces or structural changes occurs. Its morphology can be
irreversibly altered. It can be happened the biomechanical changes during
its function.
The temporomandibular joint considered as a ginglymoarthrodial
joint in two movement, they are hinging movement (gingly joint) and
gliding movement (arthrodial joint). It is formed by mandibular condyle
fitting into mandibular fossa and the two bones is separated by articular
disc. It is classified as a compound joint ( at least 3 bones ) and
functionally the articular disc served as a non-ossified bone. The
temporomandibular joint is divided into superior cavity (gliding action
between condyle and articular eminence) and inferior cavity (hinge
action between undersurface of the disc and the rotating surface of the
condyle) by the articular disc.
Retrodiscal tissue is a loose connective tissue region that highly
vascularized and innervated. The articular disc is attached posteriorly to
this region. In superior there are superior retrodiscal lamina, it contains of
many elastic fibers. It attaches the disc posteriorly to the tymphanic plate.
Inferior retrodiscal lamina contains of collagenous fibers. It attaches the
inferior border of the posterior edge of the disc to the posterior margin of
the articular surface of the condyle. The remaining body of the tissue is
attached posteriorly to a large venous plexus, it fills with blood as the
condyle moves forward. Anterior region of the disc is attached to the
capsular ligament, in superior there are anterior margin of the articular
surface of the temporal bone and in inferior there are anterior margin of
the articular surface of the condyle. It composed of collagenous fibers.
Anteriorly the disc is also attached by tendonous fibers to the superior
lateral pterygoid muscle.
The articular surface of the mandibular fossa and condyle are
lined with dense fibrous connective tissue. It affords several advantages
over hyaline cartilage , they are less susceptible to the effects of aging,
less likely to break down over time, and a better ability to repair. The
internal surface of the joint cavity are surrounded by specialized
endothelial cells that form a synovial lining, it produces synovial fluid.
The synovial fluid serves two purposes, they are : acts as medium for
providing metabolic requirement, since the articular surfaces of the joint
are nonvascular, and as a lubricant during its function. Two mechanism
of the lubrication is boundary lubrication and weeping lubrication.
Boundary lubrication is prevents friction in the moving joint. Weeping
lubrication is eliminates friction in the compressed but not in moving
joint. So the temporo mandibular joint is a synovial joint.
Active component
Active component consist of masticatory mascle and additional
muscle. Masticatory muscle contains of masseter muscle, temporalis
muscle, pterygoid medial muscle and pterygoid medial muscle. Masseter
muscle is a rectangular muscle. There is two portions or head (caput),
they are :
- Superficial head (caput superficial). It is origo in processus
zygomaticus ossis maxillae and 2/3 ventral of the inferior border of
zygomatic arch. Its insertio extends downward and backward to the
tuberositas masseterica.
- Profundus head (caput profundus). Its origo in 1/3 dorsal of the
inferior border of the zygomatic arch and medial surface of the
zygomatic arch. Its insertio extends downward and forward to
ramus mandibula and lateral surface of processus coronoideus.
Contraction of masseter cause the mandible is elevated and the
teeth are brought into contact. The superficial portion may also aid in
protruding the mandible and biting force, the deep portion is stabilize the
condyle against articular eminence. This muscle give the efficient
mastification strength.
The second masticatory muscle is temporalis muscle. Temporalis
muscle is a fan shaped muscle. Its origo in temporal fossa. Its fibers
extend downward between zygomatic arch and the lateral surface of the
cranial. Its insertio in processus coronoideus and ramus mandibula.
Contraction of the muscle elevates the mandible and the teeth brought
into contact. If only portions contract, the mandible is moved according
to the direction of those fibers that are activated. According to fiber
direction and ultimate function, it can be divided into 3 distinct areas :
- Anterior portion : The fibers are directed almost vertically, the
contraction can cause the mandible is raised vertically
- Middle portion : The fibers run obliquely across the lateral aspect of
the skull (forward as they pass downward ), the contraction can
cause elevate and retrude the mandible
- Posterior portion : Run almost horizontally, coming forward above
the ear to join other temporalis fibers as they pass under the
zygomatic arch. The function is controversial, because it can causes
 elevation and only slight retrusion. This muscle fiber angulation is
various, it can be able to coordinate the movement of closing mouth.
The third muscle of mastification is pterygoid medial muscle.
Pterygoid medial muscle consist of two head (caput), they are :
- Caput superficial : its origo in facies medialis lamina lateralis,
processus pterygoideus (fossa pterygoideus), and processus
pyramidalis ossis palatine.
- Caput profundus : its origo in processus pyramidalis ossis palatine
and tuber maxillae
Extend downward, backward and outward to insert along the
medial surface of the mandibular angle (tuberositas pterygoidea). With
the masseter, it forms a muscular sling to support the mandible. The
contraction can cause mandible is elevated and the teeth are brought into
contact. It is also active in protruding the mandible. The nilateral
contraction can cause mediotrusive movement of the mandible.
Pterygoid lateral muscle is the fourth muscle in mastificatory
muscle. It consists 2 heads or bellies with different function, they are :
- Caput superior : its origo in facies infratemporalis ala magna ossis
sphenoidalis, extending almost horizontally, backward and outward
to insert on the articular capsule, the disc and the neck of the condyle
(fovea pterygoid).
- Caput inferior: its origo in facies lateralis lamina lateralis processus
pterygoideus extends backward, upward and outward to insert on the
neck of the condyle (fovea pterygoid).
The function of pterygoid lateral muscle are :
- The superior lateral pterygoid is active during power stroke can
cause closure mandible against resistance ( chewing and clenching )
- While the inferior active during opening, the superior remains
inactive, becoming active only in conjunction with the elevator
- The right and left inferior contracts simultaneously can cause the
condyles are pulled down the articular eminence and the mandible is
protruded
 - The inferior functions with the mandibular depressorscan cause the
mandible is lowered and the condyles gide forward and downward
on the articular eminences

2.2 Histological View of Temporomandibular Joint

TMJ is one of synovial joints. Becaues it contains 2 bones and
surrounded with a capsule and it’s joint cavity filled by synovial fluid.
Because it’s movement (sliding and rotation), it is classified to sliding-
ginglimoid joint.
TMJ is formed by mandibular fossa, articular disk, and condyle.
It surrounded by an articular capsule.
Mandibular fossa is a part of the temporal bone. It is covered by
thin fibrous layer.
The articular disc separates the upper and lower synovial cavity.
Actually, it is the capsule of the joint but it is placed in the joint itself. It
is formed by collagen and elastic (only a little amount) fibers, cells,
ground substance, and blood vessels. It contains a lot of water inside
because of the water absorption of the glycosaminoglycan. The form of
the cells are flatened (fibrous like), used to distribute foods into the disk;
and rounded (Chondrosite like). Blood vessels are found on the periferal
side. On the superior lamellae, there are a lot of blood vessels, but on the
inferior, there’s no blood vessel (avascular) and inelastic.
The condyle has 4 layers. The first layer is formed by a lot of
collagen fibers and a little elastic fibers. The second layer is the cell rich
layer. The third layer contains fibrous and collagen fibers, and the bone is
proliferating. The fourth layer is the real bone. The condylar head formed
by thick fibrous connective tissue.
Synovial membrane is the capsule’s membrane. It produces the
synovial fluid. There are 2 layers : intima and subintima layer. The
intima layer is formed by 1-4 cells layer. Sub intima layer is formed by
loose connective tissue, vascular elements, and cells.
2.3 Muscles and Nerve inTemporomandibular Joint
2.3.1 Muscle
2.3.2 Nerve
The trigeminal nerve is the principal sensory nerve for the
head and is the motor nerve for the muscles of mastication and
several small muscles, especially for muscles that surround
temporomandibular joint in this case. Functionally as well as
structurally, the trigeminal ganglion is comparable to the dorsal
root ganglion of a spinal nerve. At the lower border of the
trigeminal ganglion, three major nerve bundles arise. These are the
three major divisions of the trigeminal nerve: the ophtalmicus (V

), maxillary (V ) amd mandibular (V ). The ophtalmicus and

maxillary divisions are entirely sensory, the mandibular division is
both sensory and motor. (Barr and Kieman, 1988)
The sensory trigeminal nerve is responsible for sensation
from the skin of the face and forehead, the scalp as far back as the
vertex of the head, the mucosa of the oral and nasal cavities and the
paranasal sinuses and the theeth. The trigeminal nerve also
contributes sensory fibers to most of the duramater. The scalp of
the back of the head and an area of skin at the angle of the jaw are
supplied by the second and third cervical nerves.(Sheppard and
Reed, 1976)
The motor trigeminal nerve supplies the muscles of
mastication (masseter, temporalis, and lateral and medial pterigoid
muscles) and several smaller muscles. Afferents for reflexes come
mainly from the sensory trigeminal nuclei, including the
mesencephalic nucleus. In addition to stretch reflex there is also a
jawopening reflex in which the contractions of the masseter,
temporalis and medial pterygoid muscles are inhibited as a result of
painful pressure applied to the teeth.(Sheppard and Reed, 1976)
The ophtalmicus division of the trigeminal nerve has three
branches, the lacrimalis, the frontalis and the nasociliary nerve. The
lacrimalis nerve supplies the lacrimal gland, conjunctiva and the
skin of the lateral upper eyelied. The frontalis nerve divide into the
supraorbital and supratrochlear nerves. The supraorbital nerve
supplies skin of the forehead and anterior scalp, with small
branches to the upper eyelid and fontal sinus. The supratrochlear
nerve supplies skin of the medial parts of the forehead and upper
eyelid. The nasociliary nerve to skin of the lower half of the nose,
the root of the nose and lowe eyelid. (Burket)

The Ophtalmicus nerve and divisions (www.sciencedaily.com)

The maxillary division, after leaving the trigeminal

ganglion, gives off a meningeal branch to the duramater prior to
passing trough the foramen rotundum. In the pterygopalatina fossa,
the maxillary nerve gives off pterygopalatine, posterior superior
alveolar and zygomatic branches. The zygomatic supplies skin
overlying the lateral surface of the zygoma and skin over the
anterior of the temporal muscles. The posterior superior alveolar
nerve, sends one terminal branch to the gingival of the three
posterior molar teeth and two terminal branches to the molar and
premolar teeth and to the mucous membrane of the maxillary sinus.
The branches pterygopalatine nerve arise some nerve else, they are
pharyngeal, lesser palatine, greater palatine, posterior superior
lateral nasal and nasopalatine. (Ogus and Toller, 1981)
The mandibularis nerve distribution (www.sciencedaily.com)

The mandibular division of the trigeminal nerve exits from

the skull at the foramen ovale. The anterior division of the
mandibular nerve contains a single sensory branch, the general
somatic afferent buccal nerve supplying skin of the check, buccal
mucosa, and gingival of premolar and molar teeth. The posterior
division of the mandibular nerve gives off four sensory branches:
1. The auriculotemporal nerve, which passes through
the parotid gland to skin in front of the ear and scalp, and sends
branches to the temporomandibular joint.
2. The lingual nerve, which conveys general sensation
from the anterior two thirds of the tongue, lingual gingival of the
mandibular teeth and the floor of the mouth
3. The inferior alveolar nerve, which conveys
sensation from molar and premolar teeth
4. The mental nerve, which supplies skin of the chin,
lip and mucosa of the lower lip. The continuation of the inferior
alveolar nerve within bone in the incisive nerve to the remaining
canine ang incisor teeth.
(Barr and Kieman, 1988)
2.4 The contraction and Relaxation of the Muscle
2.4.1 Muscle Contraction
Contraction is the step in which the muscle fiber develops
tension and may shorten (muscles often “contract,” or develop
tension, without shortening, as we see later). How a muscle fiber
shortens remained a mystery until sophisticated techniques in
electron microscopy enabled cytologists to see the molecular
organization of muscle fibers. In 1954, two researchers at the
Massachusetts Institute of Technology, Jean Hanson and Hugh
Huxley, found evidence for a model now called the sliding filament
theory. This theory holds that the thin filaments slide over the thick
ones and pull the Z discs behind them, causing the cell as a whole
to shorten (Saladin, 2003).

A muscle contraction occurs when a muscle fibre generates

tension through the action of actin and myosin cross-bridge
cycling. Though the term contraction implies a shortening or
reduction, when used as a scientific term referring to the muscular
system contraction refers to the generation of tension by muscle
fibers with the help of motor neurons. Locomotion in most higher
animals is possible only through the repeated contraction of many
muscles at the correct times. Contraction is controlled by the
central nervous system (CNS), which comprises the brain and
spinal cord. Voluntary muscle contractions are initiated in the
brain, while the spinal cord initiates involuntary reflexes (Etja,
2008).

Muscle contraction occurs when the actin and myosin

filaments in muscle are driven past each other by a cyclic
interaction of adenosine triphosphate (ATP) and actin with cross-
bridges that extend from myosin. Current biochemical studies
suggest that, during each adenosine triphosphatase cycle, the
myosin cross-bridge alternates between two main conformations,
 which differ markedly in their strength of binding to actin and in
their overall structure. Binding of ATP to the cross-bridge induces
the weak-binding conformation, whereas inorganic phosphate
release returns the cross-bridge to the strong-binding conformation.
This cross-bridge cycle is similar to the kinetic cycle that drives
active transport and illustrates the general principles of free energy
transduction by adenosine triphosphatase systems (Eisenberg and
Hill, 1985).

General mechanism of muscle contraction

The initiation and execution of muscle contraction occur in

the following sequential steps (Guyton and Hall, 2006).

1. An action potential travels along a motor nerve to its endings on

muscle fibers.

2. At each ending, the nerve secretes a small amount of the

neurotransmitter substance acetylcholine.

3. The acetylcholine acts on a local area of the muscle fiber membrane

to open multiple “acetylcholinegated” channels through protein
molecules floating in the membrane.

4. Opening of the acetylcholine-gated channels allows large quantities

of sodium ions to diffuse to the interior of the muscle fiber
membrane. This initiates an action potential at the membrane.

5. The action potential travels along the muscle fiber membrane in the
same way that action potentials travel along nerve fiber
membranes.

6. The action potential depolarizes the muscle membrane, and much of

the action potential electricity flows through the center of the
muscle fiber. Here it causes the sarcoplasmic reticulum to release
 large quantities of calcium ions that have been stored within this
reticulum.

7. The calcium ions initiate attractive forces between the actin and
myosin filaments, causing them to slide alongside each other,
which is the contractile process.

8. After a fraction of a second, the calcium ions are pumped back into
the sarcoplasmic reticulum by a Ca++ membrane pump, and they
remain stored in the reticulum until a new muscle action potential
comes along; this removal of calcium ions from the myofibrils
causes the muscle contraction to cease.

Figure2.: Mechanism of Ca ++ release (Guyton, 1995)

Sliding filament mechanism of muscle contraction

 Sliding filament is a movement of contractile protein
(filament) of skeletal muscle.Skeletal muscle composed by
sarcolemma, sarcoplasma, contractile protein, T tubules ( found
DHP receptor), and cysterna (found ryanodine receptor). Skeletal
muscle filament is a muscle fibers could contraction when skeletal
muscle movement. Skeletal muscle filament consists of actins,
myosin, titin and nebulin (Etja, 2008).
Sliding filament the process of impulse transmitting until
the occurrence of sliding filament are as follows: There is an
enlargement which is usually called as bouton terminale or terminal
bulb. The terminal bulb has a membrane called pre-synaptic
membrane (at the muscular cell) and synaptic fissure (fissure
between two membranes) forming neuromuscular junction. The
synaptic fissure has the thickness of 20 to 30 nanometers. The
fissure is filled with basic substance of gelatin diffused with extra
cell fluid (Etja, 2008).
The pre-synaptic membrane consists of neurotransmitter
acetylcholine (Ach) held in the form of vesicles. The release of the
acetylcholine from the vesicles into the fissure through eksositosys
stage. Synaptic vesicles move down the axon and bind to release
sites on the pre-synaptic membrane via vesicle-membrane proteins
(v-SNARE) and target-membrane proteins (t-SNAREs). This
SNARE complex interacts with both NSF (N-ethylmaleimide
Sensitive Fusion protein) and SNAP (Soluble NSF Attachment
Proteins) to form a fusion complex. If there is a potential action,
thus, Ca+ voltage gated channel will be activated. The opening of
this channel will cause the occurrence calcium influx. The influx
will activate the vesicles to move the side of the membrane. The
vesicle will undergo docking on the side of the membrane. Due to
the docking process, thus, the acetylcholine contained inside the
vesicle will be released into the synaptic fissure called as the
exositocys stage. The Ach released will bind with the
 acetylcholine receptor (AChR) which is in the post-synaptic
membrane. The AChR is located in the hollows of post-synaptic
membrane. AChR consists of 5 subunit protein, namely 2 alpha,
and each of 1 beta, gamma and delta. These sub-units are arranged
to form a circle which is ready to bind the Ach (Etja, 2008).
The bind between Ach and AChR will cause the opening
of the natrium gate at the muscular cell, and soon after that will
influx the Na+. the influx of the Na+ will cause the depolarization
at the post-synaptic membrane, which happens along the sarkolema
or muscle cell membrane and T tubulus. The occurrence of the
depolarization will cause the opening of DHP receptor which form
channel, which stimulates the excretion of Ca2+ from the T tubulus,
which later stimulates the excretion of ryanodine receptor. The
excretion of the receptor will stimulate the excretion of Ca2+ from
the cistern, which later will bind with troponim C, that cause the
part of the active actins to open and bind with myosin, which at the
end causes contraction. Besides, we can say that, if the
depolarization reaches a certain limit value (firing level), thus, the
potential action at muscle cell will potentially occurred. The
potential action will be propagated (spread) to all directions
accordingly to the cell excitable characteristic, and at the end will
cause contraction (Etja, 2008).
The ACh which is still stick to the AChR, will then be
hydrolyzed by acetyl cholinesterase enzyme which is in enough
amount at the synaptic fissure. Ach will be broken into koline and
lactate acid. Colin will re-enter to the pre-synaptic membrane to
form back Ach. The hydrolysis process will be done to prevent the
continuing potential action which will cause the continuous
contraction (Murray, 2003).
2.4.2 Muscle relaxation

Ca2+ is the primary regulator of force generation by cross-

bridges in striated muscle activation and relaxation. Relaxation is
 as necessary as contraction and while the kinetics of Ca2+ induced
force development has been investigated extensively, those of force
relaxation have been both studied and understood less well. A
number of experimental models, from whole muscle organs and
intact muscle fibres down to single myofibrils, have been used to
explore the cascade of kinetic events leading to mechanical
relaxation (Poggesi et al., 2004).

General mechanism of muscle relaxation

When its work is done, a muscle fiber relaxes and returns to

its resting length. This is achieved by these steps (Saladin, 2003).

1. Nerve signals stop arriving at the neuromuscular junction, so the

synaptic knob stops releasing ACh.

2. As ACh dissociates (separates) from its receptor,

acetylcholinesterase breaks it down into fragments that cannot
stimulate the muscle. The synaptic knob reabsorbs these fragments
for recycling. All of this happens continually while the muscle is
being stimulated, too; but when nerve signals stop, no new ACh is
released to replace that which is broken down. Therefore,
stimulation of the muscle fiber by ACh ceases.

3. Active transport pumps in the sarcoplasmic reticulum (SR) begin to

pump Ca2+ from the cytosol back into the cisternae. Here, the
calcium binds to a protein called calsequestrin and is stored until
the fiber is stimulated again.

Since active transport requires ATP, you can see that ATP is needed
for muscle relaxation as well as for muscle contraction.

4. As calcium ions dissociate from troponin, they are pumped into the
SR and are not replaced.
 5. Tropomyosin moves back into the position where it blocks the
active sites of the actin filament. Myosin can no longer bind to
actin, and the muscle fiber ceases to produce or maintain tension.
2.5 Temporomandibular Joint Movement
There are mandible movements that are regulated by
temporomandibular joint.
1. Depression of the Mandible
During simple depression of the mandible (central opening
movement) from it is rest position, both condyles move forward, the
menisci moving with them. It is generally agreed by many authorities
(Prentiss, Lord, Chissin, Brodie, Higley, Stimson, Sicher, and others) that
both condyle heads are pulled forward in this initial opening movement
by the external pterygoid muscles(Wheeler.1984).
While the condyle is being pulled forward in opening the jaw by
the inferior head of the external pterygoid, the meniscus is being pulled
forward by the superior head of the external pterygoid muscle. When the
condyle approaches the articular eminence it rides forward on the thinner
portion of the meniscus-an arrangment which makes allowances for the
downward protuberance of the eminence(Wheeler.1984).
When in “rest position” each condyle rests upon a thick posterior
portion of the meniscus which fills the space between the which fills the
space between the condyle and the deeper portion of the glenoid fossa.
Anterioly, the meniscus is much thinner at the portion which
approximates the dorsal area of the articular eminence and the frontal
area of the condyle(Wheeler.1984).
The relative thickness of the meniscus anteroposteriorly, plus the
compensating activity of the two heads of the external pterygoid muscle,
allows the condyles of the mandible to move forward with a glinding
movement on a “single plane” regardless of the irregularity of the surface
of the glenoid fossa and of that of the articular eminence. The “plane”
has an inclination downward when the head is held erect. It is interesting
to note that the inclined plane of the condylar glide when the mandible is
depressed is seemingly parallel to the occlusal plane of the molars and
the lower border of the body of the mandible when the jaws are
closed(Wheeler.1984).
During the central opening movement of the mandible, the axis of
movement is not in the condyle heads, since these move forward
immediately, even tho ugh the initial movement forward is slight.
Apparently the area of rotation approaches the attachment of the
temporomandibular ligament laterally
and distally to the neck of the condyle. This is a logical conclusion
because of the suspensory character of this strong ligament and the
general directionof its fibers. The central opening movement of the
mandible (depression) in conjuction with the central closing movement
(elevation) provides the action commonly termed “simple hinge
movement”. As far as the relation of the dental arches is concerned in
this opening and closing movement, the action is comparable to the
action of a simple hinge. The occlusal surfaces of the maxillary teeth may
be considered as the upper extension of the hinge, and the occlusal
surfaces of the mandibular teeth as the lower extension in the central
opening movement. Owing to the involved design of the articulation and
the need for jaw support, the rotation point or axis of the hinge cannot be
centered in the condyles as many believes. The uneven shape of the
condyle, added to its forward movement immediately upon jaw opening,
would defeat this argument. The jaw has body and weight and must be
suspended by ligamentous attachment in some area. The design and
location of the temporomandibular ligament makes it the logical choice
among condyle attachment to accomplish ligamentous suspension of the
jaw in the initial opening movement. The attachment superiorly is
forward, wrapped around the zygomatic “bar” of the temporal bone;
inferior, it is down and back, and is strongly attached posteriorly in a
limited area to the neck of the condyle, below the condyle
itself(Wheeler.1984).
 When the jaw is opened no more than necessary for ordinary use
in mastication (10-12mm, maximum), the action of placing the teeth of
one arch in and out of contact with the teeth of the opposing arch in a
sagittal plane may be called a hinge movement, reegardless of our
inability to pinpoint the “hinge axis”.
2. Elevation of the Mandible
The mandible is elevated by the temporal muscles, the masseter
muscles and the internal pterygoid muscles.The temporal muscle has
anterior and posterior fibers. The anterior fibers exert an upward pull; the
posterior fibers pull upward and backward(Wheeler.1984).
The masseter muscle has two sets of fibers: sepurficial and deep
fibers. The deep fibers. The superficial fibers exert a pull upward and
foward on the mandible. The deep fibers exert a pull vertically
upward(Wheeler.1984).
The internal pterygoid muscle has two heads, each of which pulls
in the same general direction. Together they exert a pull on the mandible
which is upward, foward and inward(Wheeler.1984).
When the temporal, masseter and internal pterygoid muscles of the
sides contract simultanecously, the mandible is elevated and returns the
teeth to occlusion(Wheeler.1984).
When the teeth are brought into centric occlusion, both condyles of
the mandible are moved a short distance posteriorly to their rest position
(Wheeler.1984).
3. Protusion of the mandible
The mandible cannot be protruded unless the cuspsof the teeth are
disengaged. Therefore, the mandible must be depressed slightly, the
condyles moving forward before the protrusive movement is
begun(Wheeler.1984).
The muscles which promulgate the protrusive movement which
brings about the protrusive occlusal relation of the teeth are the external
pterygoid muscles, which are assisted by the anterior fibers of the
temporal muscles. The pterygoid pull forward on the condyles and the
temporal pull upward with a counter action on the coronoid processes;
this prevent further depression of the mandible during the protrusive
movement. The tonus and counterbalancing action of other fibers of the
temporal as well as some other muscles may come into play during the
protrusive movement. During this movement the condyles are pulled
forward with their menisci, but their forward movement is quite limited
(Wheeler.1984).
4. Retraction of the Mandible
In retraction, teh mandible returns along the same path it traveled
in the protrusive movement. The retractive movement is, therefore, just
the reverse of the protrusive movement(Wheeler.1984).
The jaw is pulled back by the action of the temporal muscle, the
posterior fibers principally. The codyles with their menisci are returned
to rest position. If it is the purpose of this movement to bring the teeth
back into centric occlusion, the masseter and the internal pterygoid
muscles join the activity of the temporals in the culmination of the
act(Wheeler.1984).
The mandible may be retracted a very small degree posteriorly to
centric occlusal relation of the teeth. This movement is nonfuctional and
consequently very limited. Movement of the condyles distally is resisted
by the posterior wall of the glenoid cavity; the movement is limited to the
compressibility of the soft tissues intervening between the bony
parts(Wheeler.1984).
5. The lateral of the Mandible
The lateral movement (right and left) of the mandible are
asymmetrical movements; the right and left condyles do not follow
similar paths. These movements are made possible by the ability of one
temporomandibular joint to move independently of the
other(Wheeler.1984).
Each internal pterygoid muscle exerts a medial pull on the
mandible, since it does not operate on a line with the forward or
 protrusive movement of the jaw. Its action pulls the condyle inward as
well as forward(Wheeler.1984).
The right lateral movement of the mandible is affected, therefore,
by a slight depressive movement of the mandible, both external pterygoid
operating, which action depresses the mandible and moves both condyles
forward. At this point the left internal pterygoid contracts indepently, the
right internal pterygoid and other muscles relaxing. The activity of the
left internal pterygoid pulls the left condyle forward and inward in a
circular path which rotates about a point in the right condyle, the right
condyle turning on the pivontal point. This action results in the rotation
of the mandible about the pivontal point in the right condyle, moving the
mandible to the right. In the return movement, the condyles retrace their
path. The mandible is returned to rest position, or the teeth into centric
occlusion, through the activity of the left temporal muscle (mainly
posterior fibers), other muscles of mastication of both sides joining forces
as the teeth approach central occlusion with final masticatory
thrust(Wheeler.1984).
The left lateral movement of the mandible is affected in the same
manner. In this instance the right condyle is pulled forward and inward
while the left condyle pivots. The right internal pterygoid muscle contract
an dcauses the movement of the mandible to the left. The right temporal
is the muscle mainly operative which affects the return of the mandible to
centric relation with the assistance of the other mucles in balance with
it(Wheeler.1984)
2.6 Temporomandibular Joint Disorder
Internal derangement is a biomechanical interferences with
smooth gliding movements of temporomandibular joint resulting from
disturbance of the disk, capsule, or articular surfaces of the condyle or
eminentia, including elongation, tearing, adhesion, synovitis, and so
forth.
Disc Displacement
 Disc displacement occurs because of posterior of disc becomes
thinner, and inferior retrodiscal lamina and discal copllateral ligaments
elongate. The disc move to anteriorly to articular surface of the condyle.
This deviation cause joint sound during mouth opening and closing.
Diagnostic criteria for the acute state include pain precipitated by
function, marked limited jaw opening, noise, deviation of mandible to
affected side on opening, limited laterotrusion to contralateral side, and
soft tissue imaging showing nonreducing disk. In the cronic state, there is
generally no pain, there is a past history of joint noise or limitation of the
jaw opening there maybe slightly limited mandibular opening and
laterotrusion to contralateral side and soft tissue imaging reveals
displaced disk without reduction. On the basis of including imaging as
part of the criteria there is the implication that imaging is necessary to
make the diagnosis to acute or chronic (Wright, 2009)
Disc Dislocation
The mandible can dislocate in the anterior, posterior, lateral, or
superior position. Description of the dislocation is based on the location
of the condyle in comparison to the temporal articular groove.(Haddon,
2004)
Anterior dislocations are the most common and result in
displacement of the condyle anterior to the articular eminence of the
temporal bone. These dislocations are classified as acute, chronic
recurrent, or chronic.
• Acute dislocations can be seen after trauma or dystonic reactions,
but they are usually a result of extreme mouth opening such as with
yawning, general anesthesia, dental extraction, vomiting, or
seizures. Anterior dislocations after endoscopic procedures have
been reported.(Mangi, 2004)
• Anterior dislocations are usually secondary to an interruption in the
normal sequence of muscle action when the mouth closes from
extreme opening. The masseter and temporalis muscles elevate the
mandible before the lateral pterygoid muscle relaxes resulting in
 the mandibular condyle being pulled anterior to the bony eminence
and out of the temporal fossa. Spasm of the masseter, temporalis,
and pterygoid muscles causes trismus and keeps the condyle from
returning into the temporal fossa. These dislocations can be both
unilateral and bilateral. (Undt, 1997)
• Acute chronic dislocations result from a similar mechanism in
patients with risk factors such as congenitally shallow mandibular
fossa, loss of joint capsule from previous mandible dislocations, or
hypermobility syndromes.
• Chronic dislocations result from untreated TMJ dislocations and
the condyle remains displaced for an extended time period. Open
reduction is often required. (Undt, 1997; Hoard, 1998; Ozcelik,
2008)
Posterior dislocations typically occur secondary to a direct blow
to the chin. The mandibular condyle is pushed posteriorly toward the
mastoid. Injury to the external auditory canal from the condylar head
may occur from this type of injury.(Haddon, 2004; Stone, 2008)
Superior dislocations, also referred to as central dislocations, can
occur from a direct blow to a partially opened mouth. The angle of the
mandible in this position predisposes upward migration of the condylar
head. This can result in fracture of the glenoid fossa with mandibular
condyle dislocation into the middle skull base. Further injuries from this
type of dislocation can range from facial nerve injury, to intracranial
hematomas, cerebral contusion, leakage of cerebrospinal fluid, and
damage to the eighth cranial nerve resulting in deafness.(Harstall, 2005)
Lateral dislocations are usually associated with mandible
fractures. (Haddon, 2004; Ohura, 2006) The condylar head migrates
laterally and superiorly and can often be palpated in the temporal space.
(Schwab, 1998)
Structural Incompatibility of the articular surfaces
1. Adhesion
 Sticking of the erticular surface, may be found in superior or
inferior joint spaces. The result of prolonged static position is clicking
voice during sleeping. The sign of this deviation is a single click when
patient attempts to move the mandible, click only accurs once and
cannot be repeated without another prolonged period of static loading.
Superior joint space adhesion
Limit the translation of the condyle disc complex it can be cause
to limiting joint movement to only rotation. Clinically limit joint
movement to only 25 – 30 mm
Inferior joint space adhesion
Restrict rotation of the disc on the condyle but allow translation
of the condyle disc complex. The patient can be still opening their mouth
2. Alteration
Alteration in the shape of articular surface of condyle, fossa and
disc resulting in impairment of smooth sliding movement. The clinical
sign of this deviation is clicking or deviation of the mandibular opening
pathway.
Condyle Dislocation
Occurs when the condyle on one ar both sides are displaced
anteriorly over the articular tubercle and locked in place by the spasm of
elevator muscles. Characteristic sign is the patient unable to close their
mouth, Pseudo-prognathism, and complain of pain in TMJ region
Fracture of Condyle
May cause malocclusion (open bite), disturbance of TMJ
functions, ankylosis of the TMJ, and mandibular grown disturbance
There are four kind of fracture of condyle:
1. Effusion or haemathrosis: occurs when there is a bleeding in the joint
because of bump which can be blocked the occlusion.
2. Unilateral Fratcture Duslocation: condyle’s neck has been fracture on
the one side. It can be cause the abridgment dimension on the fracture
region and also cause the other sides doesn’t contact.
3. Bilateral Fracture Dislocation: leher condyle fracture on the both side,
that can be cause the abridgment dimensi ramus on the both side. It
can be cause the posterior region is contact but in the anterior region
doesn’t contact.
4. Bilateral Dislocation: Patient’s mouth cannot be closed because of disc
islocation
Anchylosis
Anchylosis is a stiffness of a joint due to abnormal adhesion and
rigidity of the bones of the joint, which may be the result of injury or
disease. The rigidity may be complete or partial and may be due to
inflammation of the tendinous or muscular structures outside the joint or
of the tissues of the joint itself. Noma—a gangrenous disease still
widespread among malnourished children living on the borders of the
Sahara desert—can cause ankylosis of the maxilla and mandible,
impairing the ability to speak and eat. (Deeb, 1999)
When the structures outside the joint are affected, the term "false"
ankylosis has been used in contradistinction to "true" ankylosis, in which
the disease is within the joint. When inflammation has caused the joint-
ends of the bones to be fused together the ankylosis is termed osseous or
complete. Excision of a completely ankylosed shoulder or elbow may
restore free mobility and usefulness to the limb. "Ankylosis" is also used
as an anatomical term, bones being said to ankylose (or anchylose) when,
from being originally distinct, they coalesce, or become so joined
together that no motion can take place between them.
1. Fibrous ankylosis:
Fibrous ankylosis is a fibrous connective tissue process
which results in decreased range of motion. (Chabner, 2007)
Symptoms present as bony ankylosis, in which osseous tissue
fuses two bones together reducing mobility, which is why fibrous
ankylosis is also known as false ankylosis.
Pathology may be the result of trauma, disease, chronic
inflammation, or surgery.
 Some research suggests fibrous ankylosis may precede the
development of bony ankylosis because someone with bony
ankylosis usually doesn’t use their TMJ. That’s why someone
with bony ankylosis on one side will occur fibrous ankylosis on
the other side. The main cause of fibrous ankylosis in this case is
the TMJ that is not used or no movement in the TMJ (Ikeno,
2006)
2. Bony ankylosis: fusion between head of condyle and glenoid fossa
2.6.1 The Characteristics of Temporomandibular Joint Disorder
There are several characteristics in a person with
temporomandibular joint disorder:
• Restricted Range of Jaw Motion
The mandibular of motion should be sufficient to meet the
normal requirements for talking and masticating foods. Restrictions
of movement are displayed as inability to close the mouth, inability
to open the mouth adequately, or inability to protrusive or
contralateral excursions. This may be accompanied by deflection of
the opening or the protrusive path. Abnormality in this regard is an
individual matter. For a particular individual, restriction of
mandibular movement is symptomatic of masticatory activity.
(Bell, 1990)
The lower limit of normal for individuals of average height
of interincisal opening is about 50 for men mm and 45 mm for
women. Although is may be quite true on average, such
measurements may not apply to the individual. The size of the oral
orifice, the amount of overbite of the teeth, and the resting length of
the elevator muscles are the determinants of a “normal” opening for
an individual. Arbitrary range of motion without proper
consideration of functional compability shold be avoided.
(Bell,1990)
Restricted range of motion can result from a variety of
extra-articular causes, including a shortened elevator muscle, or
from fibrotic contraction of the capsule, intracapsular adhesions, or
discal obstruction. (Bell, 1990)
• Vertigo (dizziness) and Tinnitus (ringing in the ears) can be
associated with severe cases of TMD. There are a number of
competing theories explaining why TMD may cause these
symptoms. Both vertigo and tinnitus are associated with structures
in the inner ear. (Bell,1990)
1. The first theory involves inflammation of the joint capsule
which spreads to adjoining areas in the skull, including the
structures in the inner ear. This would include the vestibular organ
which contains the semicircular canals. Fluid movement in these
canals responds to movements of the head, and provides the sense
of balance. Disease processes in this organ would cause vertigo
(dizziness). The second major organ in the inner ear is the cochlea
which is responsible for converting the vibrations in the air to nerve
impulses that can be perceived by the brain. Disease processes
affecting the cochlea, including inflammation, would cause hearing
loss and tinnitus.
2. A second theory posits that pressure on the
temporomandibular joint not only injures the joint, but allows the
damaged joint itself to place pressure on nerves and blood vessels
that supply the structures in the inner ear. Constrictions in these
nerves and vessels would presumably have negative effects on the
inner ear structures they service.
3. A third theory involves two tiny muscles, the tensor veli
palantini and the tensor tympani, which function in the middle ear.
The tensor veli palatini constricts and dilates the eustachian tube
which in turn is responsible for equalizing the air pressure on either
side of the tympanic membrane (the eardrum). This is the muscle
that functions when you "pop" your ears. The tensor tympani
attaches directly to the eardrum and helps to protect the inner ear
by dampening vibrations within it. The nerves that supply these
muscles are closely associated with the nerves that supply the
medial and lateral pterygoid muscles. These are chewing muscles
and are highly active when the patient is bruxing (grinding) the
teeth. The theory is that spasm in the chewing muscles due to
TMD causes spasm of these two tiny "ear muscles" which in turn
affects the semicircular canals and the cochlea causing dizziness
and tinnitus. This theory seems unlikely since both muscles
function on structures in the middle ear and do not impinge directly
on the inner ear where the organs responsible for balance and
hearing actually reside.
4. A fourth theory, and the one that most experts are leaning
toward right now , involves the reflexive contraction of the
sternocleidomastoid muscles (SCM) when patients clench their
teeth. It has been shown that pressure on certain trigger points in
the SCM can trigger vertigo, although the reasons for this are not
exactly clear. It has also been shown that when subjects clench
their teeth, the SCM will also contract. It is hypothesized that
chronic tension in this muscle triggers periodic episodes of vertigo,
along with headaches and neck aches.
Vertigo associated with TMD is a fairly rare symptom. If
you have a problem with chronic dizziness and think it may be due
to temporomandibular dysfunction, you need to ask yourself if you
have at least some of the symptoms listed above, especially chronic
jaw soreness, headaches, ear aches, neck aches, clicking joints,
chronic jaw dislocation and/or an inability to open the Jaws wide.
Some evidence exists that the vertigo may occur in the absence of
these symptoms, but in a majority of cases, the more obvious
symptoms of TMD precede the vertigo. (Anonymous, 2010)
Tinnitus, on the other hand, is a common disorder and is
frequently associated with severe TMD. People who have learned
to live with all the other symptoms of TMD may finally seek
treatment for the tinnitus, not realizing that the other
craniomandibular symptoms are part of the same syndrome.
(Anonymous, 2010)
• Clicking/Popping or grating sounds in jaw
movement
Clicking jaw, also referred to as popping jaw or TMJ
(temporomandibular joint) syndrome/dysfunction is a symptom
associated with inflammation of the temporomandibular joint or
uncoordinated action of the facial muscles. This situation can occur
in the morning, at midnight, or at night when there was a motion to
open the mouth. clicking can also occur during the motion to close
the mouth as in the motion to open the mouth. (Ogus H.D, Toller
P.A, 1990)
Grating sounds is sliver or swipe sound that occurs during
movement of the mandible, especially the movement from one side
to another. The sound can often be better known under the
palpability than hearing. Sound examination can also be done by
using a stethoscope. (Ogus H.D, Toller P.A, 1990)
• Pain
TMJ dysfunctions result in pain of the joint and related
musculator. The majority of pain is, however, muscular in origin,
and its etiology is the overextertion of the muscles either by
continual contractions in normal physiologic state or, if in a stretch
pathologic length, a combination of contractions and stretch reflex-
relaxation reactions. (Anonymous,2010)
The pain in the jaw is usually at the back of the jaw, near
the ear or around the area of the wisdom teeth. This pain may
radiate to the ear, temples of the head or neck. Refer to the image
above for areas most affected by TMJ dysfunction. Before
diagnosing any jaw pain as TMJ dysfunction, it should be
investigated if other possible causes could be the source of pain in
this region. (Bell,1990)
Although the conditions necessary to initiate pain have
 been explained, the mechanism through which continual
contraction actually produces pain must now be developed.
Generally speaking, overexertion of muscles will produce pain.
Postexertion muscular pain can be divided into the following two
types: pain during and immediately after exercise, which can
persist for hours (immediate pain), and a more localized soreness
that does not appear for 24 to 28 hours (delayed pain). The delayed
type pain is usually referred to as myositis. (Luther,2007)
The immediate pain experienced with muscular
overextertion can be largerly atributted to diffusible end-products
of cellular metabolism acting upon pain receptors within the
muscular tissues. Unexplained headaches is a common symptom of
a TMJ problem. Usually a TMJ-caused headache is located in the
temples or in the back of the head. Pain in the shoulders and back
due to muscle contraction, related to teeth clenching and TMJ.
(Luther,2007)
2.6.2 Pain
Pain is the main characteristic shown in temporomandibular
disorder. Pain sensation is different from others, namely that the
pain gives warning that something is wrong, pain precedes the
other signals, and the pain associated with unpleasant feelings. Pain
is a sensation that was very complicated because if the prolonged
pain and tissue damage, central nosiseptor pathways through
facilitation and reorganization. There is still much to be learned,
but generally feasible if the discussion about the physiological or
acute pain and two pathological conditions: inflammatory pain and
neuropathic pain.(Ganong,2008)
Inflammatory Pain
After experiencing an injury that is not mild, persistent
inflammatory pain arise until the injury healed. Stimulation in areas
of injury that under normal circumstances usually causes only mild
pain cause excessive responses (hiperalgesia), and are usually
harmless stimuli such as touch leading to pain (alodinia). All types
of inflammation causes the release of various cytokines and growth
factors ("dough inflammation") in areas experiencing
inflammation. Many of these substances work to improve the
perception and sensation in the regional distribution of the skin and
in the dorsal cornua. This is what causes hiperalgesia and alodinia.
(Ganong,2008)
Neuropathic Pain
Neuropathic pain can occur if the injured nerve fibers. Pain
is usually severe and difficult to overcome. In humans, neuropathic
pain found in various forms. One of them is a pain (in addition to
other sensation) at the limb that has been amputated. In kausalgia,
burning spontaneously arise after the injury seems minor. Pain is
often accompanied by hiperalgesia and alodinia. Reflex
sympathetic dystrophy are also common. In these circumstances,
the skin in affected areas will be thinned and polished, and an
increase in hair growth. Research on Animals showed that nerve
injury causes excessive growth of nerve fibers into the sympathetic
noradrenergic nerve ganglion sensory dorsal roots of the injured
area. Simpntis discharge then trigger pain. Therefore, it seems to
happen 'short-circuiting' and respective fibers are stimulated by
norepinephrine at the level of the dorsal roots ganglia. In humans,
inhibition of alpha adrenergic-type kausalgia will relieve pain,
although the reasons are not clear-adrenergic inhibitor is more
effective than α1-α2 adrenergic inhibitors. Surgery being
undertaken to overcome severe pain, among others, is the
termination of the nerve from injury or kordotomi anterolateral
spot, ie cutting jaras spinotalamikus done carefully. However, the
effect of this action only for a moment if the network has
undergone peripheral? 'Short-circuiting' by the sympathetic nerves
or other central jaras jaras-experiencing reorganization. Pain can
often be treated with analgesic drugs given in adequate doses,
although not always to be delivered. The most effective drugs for
this is morphine.
Receptors And Pathways
Sensory organs for pain are free nerve endings which at
many places on almost all body tissues. Pain impulses delivered to
the central nervous system by two fibers. One nosiseptor system
formed from fibers small A ∂ bermielin 2-5μm diameter. Another
system that consists of no myelins C fibers with a diameter from
0.4 to 1.2 μm. This latter fibers found in the dorsal lateral roots and
is often called the dorsal roots C fibers. These fibers deliver the
slow speed of 0.5 to 2 m / sec, both groups of fiber ends in the
dorsal cornua; fibers over A ∂ neurons mainly in lamina I and V.
While the fiber ends in C radik dorsalis neurons in lamina I and II.
Sinap transmitter which in secretion by afferents which delivers
mild pain quickly is glutamate, and the transmitter delivers the
latest severe pain is substance P. (Ganong,2008)
Links nosiseptor peripheral synapse between fibers and
cells in the dorsal cornua of the spinal cord is the part that is very
plastic. Because it is also known as the dorsal cornua of the gate /
door, where pain impulses can be modified. (Ganong,2008)
Some axons of neurons ending in the dorsal cornua of the
spinal cord and brain stem. the other half into the ventrolateral
systems, including lateral spinotalamikus tract. Some increase in
the dorsal spinal cord. Some fibers ascending projection to form
the nucleus ventralis posterior, which is a specific sensory relay
nucleus in the thalamus, and from here to kortes cerebral.
(Ganong,2008)
Pain, by Sherrington, referred to as "physical
complementary aspects of protective reflexes absolute." Pain
stimulus triggers a response generally withdraw or avoid strong. in
addition, among the various sensations, pain is unique is that the
pain has "innate" as unpleasant effects. (Ganong,2008)
Muscle Pain
When the muscle to contract rhythmically, but the blood
supply remains adequate, will not usually painful. However, if the
blood supply to the muscle is blocked, the contraction will cause
pain immediately. After the contractions stopped, pain persists until
the blood flow restored. These observations are difficult to interpret
unless the release of chemicals ("P factor" Lewis) during
contraction, which causes pain when its local concentration is high
enough. If the blood supply has been restored, these chemicals can
be cleaned or metabolized. The identity of the P factor is still
unconfirmed, but probably was K+. Sefcara clinical, pain arising
substernum if myocardial ischemia during exercise experience
(angina pectoris) is a classic example of the P factor accumulation in
muscles. Angina disappeared with the rest because it lowered the
needs of 02 myocardial blood flow and allows the cleaning of these
factors. Intermittent claudication, pain arising in the calf muscles
padaorang who suffer from vascular occlusion, is another example.
The pain usually occurs when patients walk and disappeared when
he stopped.(Ganong,2008)
Viscera Pain
Besides not having a good localization, causing an unpleasant
feeling, and associated with nausea and autonomic symptoms, pain,
viscera often spread or transferred to the autonomic nervous
lain.Sistem areas, such as somatic, has afferent components,
integration centers in the central, and effector lines. Receptors for
pain and other sensory modalities contained in the viscera contained
similar to the skin, but there are notable differences Emitter
distribution. There were no proprioseptor in an instrument in, and
only rarely found the temperature and touch receptors. Pain receptors
can be found, although the distribution is much less when compared
with that found in somatic structures. (Ganong,2008)
 Visceral afferents reach the CNS from the structure through the
sympathetic and parasympathetic. Fiber cell bodies are located in the
dorsal roots and cranial nerve ganglia are homologous. Specifically,
there is in the viscera afferent facial nerve, glosofaringeus, and the
vagus; in torakal and lumbar dorsal roots above; and roots in the
sacrum. There is also an eye afferents in the viscera of the trigeminal
nerve. It should be noted that at least there is some substance P-
containing afferent makes relationships through collateral to
pascaganglion sympathetic neurons, as in the inferior ganglion
mesenterikus. This relationship may play a role in reflex control of
viscera that does not depend on the CNS. (Ganong,2008)
In the CNS; Visceral sensation sepanjamg run on the same
line with somatic sensation in the tract spinotalamikus and radiatio
thalami, and cortex area of the recipient for Visceral sensation mixed
with the recipient cortical areas of somatic sensation. (Ganong,2008)
Reffered Pain
Irritation of the internal organs often causes pain that is felt
not in the organs but in some somatic structures that may be located
quite a distance. Pain like this is said to be transferred (Referred) to
the somatic structure. In somatic pain can also be transferred, but the
pain is not superficial. Visceral pain is local if and diverted,
sometimes it looks like the spread of pain (radiation) from local to
distant places. (Ganong,2008)
Clearly, knowledge about pain control and often become the
place where the transfer of pain for each and every organ in the very
important for the doctor. Perhaps the best example is the transfer of
pain to the side of the heart in the left arm. Another dramatic
example is at the top of the shoulder pain caused by irritation at the
center of the diaphragm and the pain in the testes caused by
stretching of the ureter. Another example is found in many areas of
medicine, surgical, and dental. However, where pain control is not
always the same, and there is often a place of pain rather unusual.
 Cardiac pain, for example, can be felt only in the abdomen, or can be
diverted to the right arm or even to the neck. Pain control can be
triggered experimentally by stimulating the cut nerve splanknikus.
(Ganong,2008)
Cause of the Pain
The main cause of pain rather seems to be plasticity in the
CNS are accompanied by the convergence of peripheral pain fibers
and viscera on the second level of the same neurons that berproyeksi
to the brain. Peripheral neurons and viscera together in laminae I-VI
ipsilateral dorsal cornua, but neurons in lamina VII receive afferent
from both sides of the body-terms if convergence will be used to
explain the place of transfer to the side opposite the side of the
source of pain. Peripheral pain fibers normally do not trigger the
second level neurons, but if the viscera prolonged stimulation, there
will be facilitation of peripheral nerve endings. Stimulating the
peripheral fibers are now the second level neurons, and of course the
brain can not distinguish whether the stimulation comes from the
viscera or of pain over the area. (Ganong,2008)

2.6.3 Factors that Can Cause Temporomandibular Joint Disorder

1. Bruxism
Bruxism is the medical term for the grinding, gnashing,
chafing, rubbing of the teeth, clenching of the jaw, especially
during deep sleep. The causes of bruxism are unknown The
word "bruxism" comes from the Greek "brychein" meaning to
grind or gnash the opposing rows of upper and lower molar
teeth. But may be read in any cases that bruxism has two main
causes, stress and malocclusion. This is not true, because the
real cause of malaocclusion, bruxism, TMJ and stress is an
injury to the jaw due to incorrect positions during the day but
especially at night. (Gnatologia it Galiffa's Mandibular
Decubitus Syndrome). Bruxism is the violent and noisy
rubbing of the lower teeth against the upper teeth lasting a few
seconds Bruxism is one of the most common sleep disorder
Bruxism occurs predominantly during sleep, always and only
in those people who sleep lying face downwards on the bed, on
their stomach or on their hips, as they weigh heavily with static
load on their jaws (health and sleeping position). (Slabach,
2007)
Causes of Bruxism
The dental and medical community a like have blamed
stress for the gnawing and gnashing of teeth at night. Our fast-
paced society does indeed pose a considerable level of physical
and emotional stress and we do know that bruxism increases
with additional stressors. From some of the research done on
children, we know there is a link between bruxism and the
body's survival mechanism to keep the airway open. If a child
is grinding his or her teeth at night, the first causative factor to
look for is an obstructed airway. Enlarged tonsils and adenoids
are a common cause for airway obstruction in children and
even contribute to obstructive sleep apnea. Bruxism triggers a
muscle in the back of the throat to spasm and keep the airway
open. It is hard to blame teeth-grinding on stress in a young
child. Most children do not have the level of emotional stress
that adults do. Adults with compromised airways also brux to
keep the airway open. This is particularly apparent in people
suffering from sleep-disordered breathing, the most severe
cases being obstructive sleep apnea. In adults the cause is
usually not enlarged tonsils and adults, but a collapsible
windpipe that contributes to the sleep apnea. (Galiffa, 2010)
When the jaw is in the wrong position, the body
attempts to correct it by bruxism. The muscles of the jaw and
face spasm and attempt to move the jaw to a more comfortable
position. As these muscles spasm, the teeth slide back and
 forth in response to that muscle activity . This can occur
particularly in a person whose facial and jaw muscles are
shortened-a muscle cramp in the jaw. The teeth grind to relieve
the spasms much like stretching the relieves a cramp in the calf
muscles.
Effects of Bruxism
After even a short period of grinding, the lower jaw can
recede backward causing a jaw joint disorder or TMJ disorder.
The lower jaw fits in to a socket of the upper jaw and is
protected by a cartilage disc. If the lower jaw is allowed to
retrude to the back of the socket, a couple of things can occur:
- Compression of the nerves and blood vessels in the back of
the jaw joint, which can cause headaches, face, jaw and neck
pain
- Displacement of the cartilage disc, indicating a dislocation of
the joint and resulting in clicking, popping or grating noises
upon opening and closing of the jaw
- Further compromise of the airway, making obstructive sleep
apnea even more possible
2. Clenching
Sleep clenching, which occurs while dreaming is an
unconscious act. It could be a gift from Nature; a signaling
method, to let us know that Nature is trying to tell us
something, that is, something we fail to acknowledge. In other
words, there is probably a conflict between the conscious and
unconscious mind. Nature sends us messages via dreams,
intuitions, cognitions, etc., but it 'ain't' that easy to figure out.
Most people need help from a qualified Jungian trained
psychiatrist or physchologist. However, a properly trained
dentist in the Tanner methods can make you comfortable.
It is an unconscious act; yet, squeezing teeth together
while sleeping is not always dysfunctional; that is, it is needed
 for the eruption process of teeth. Sleep clenching is only
However, many of us have an episode of clenching that occurs
and will continue until we modify our consciousness to
Nature’s import.
The Clenching Syndrome (also called the TMJ
Syndrome) is a cycle. It has a beginning, which is always the
same, and a final stage, which is always the same, if it
progresses to its end. A slight (subtle) looseness of the teeth is
the first sign of sleep clenching--something you can detect
yourself. The final stage, which is advanced periodontal
disease (teeth that may have to be removed), is not experienced
in every person. Nevertheless, if one continues to clench, the
cycle will continue reaching the final stage.
There are two parts of the clenching syndrome:
occlusomuscular problems and occlusodentition problems. The
first is concerned with irritation of the muscles of the head and
neck with irritation to the TM joints and ear apparatus. The
second deals with damage to teeth and their supporting
structures.
3. Chewing on one side. It forced one side’s muscles to do more
activities so it can cause hyperactivities and hypercontraction.
4. Bad sleeping position that uses one side of the body to prop the
whole body. Usually one side of the face will prop the whole
mass of the body. We all know that TMJ are placed on both
right and left side of the face that’s why if a person do this bad
habit, their TMJ is forced to prop a big mass so it is forced and
can cause pain and will become a disorder.
2.6.4 Types of Temporomandibular Joint Disorder
Temporomandibular joint disorder is disorder of the jaw
joint and chewing muscles. Researchers generally agree that the
conditions fall into three main categories:
1. Myofascial pain
Myofascial pain disorder of the masticatory muscle system is the
most common of all temporomandibular disorders. The vast
majority of patients present with facial pain, limitation of jaw
motion, muscle tenderness and stiffness, along with any number of
associated symptoms in the head, face, and neck region. Imaging
studies of the TMJ usually show no evidence of anatomic
pathology.
2. Internal derangement of the joint involves a displaced disc,
dislocated jaw, or injury to the condyle.
The derangement disorder is defined as a
temporomandibular disorder resulting from displacement of the
TMJ disk from its normal position or from deformation of the disk.
This may lead to synovitis, pain, and limitation of motion. The
diagnosis is confirmed by history, clinical examination, and MRI
scan in the open- and closed-mouth positions. Diagnostic or
therapeutic arthroscopy may also be helpful in confirming the
diagnosis and providing minimally invasive surgical manipulation,
if necessary.
Internal derangements may include anterior displacement of
the disk, with reduction or without reduction. Anterior
displacement with reduction is defined as disk displacement in the
closed-mouth position that reduces (with a click) to the normal
relationship at some time during opening. Reduction implies that to
some extent the disk is gliding normally, with opening and
translational movement. In these circumstances, the patient reports
a click with a variable amount of pain on opening. Often, patients
have no pain with this condition. The mandible deviates to the
affected side on opening until the click occurs and then returns to
the midline. This situation may worsen, and there may be
intermittent locking of the disk.
Intermittent locking may progress over time to anterior disk
 displacement without reduction (closed lock). This implies that the
dislocated disk acts as a mechanical obstruction to the opening and
translation of the condyle. These patients have a marked decrease in
mandibular opening on the affected side and a variable amount of
pain. It feels to them as if there is a mechanical obstruction to
opening in the joint. Maximal opening may be limited to 20 to 25
mm (the normal range of maximal interincisal opening ranges from
35 to 55 mm, with a mean of 40 to 43 mm), with restricted
movement to the contralateral side. There may also be a history of
clicking with intermittent locking. MRI shows a displaced disk
without reduction on opening (closed lock) and may also reveal
degenerative changes in the condyle. In such cases, the signs and
symptoms of degenerative joint disease may also be present.
3. Arthritis refers to a group of degenerative/inflammatory joint
disorders that can affect the temporomandibular joint.
Osteoarthritis
Osteoarthritis of the TMJ may result from trauma (acute or
chronic), infection, metabolic disturbances, and previous joint
surgery. The patient reports pain on moving the mandible, limited
motion, and deviation of the jaw to the affected side. There may be
acute tenderness to palpation of the joint. Joint sounds are described
as grating, grinding, or crunching, but not as clicking or popping.
Imaging studies typically reveal degenerative changes, remodeling,
and a loss of joint space.
Rheumatoid Arthritis
There may be involvement of the TMJ in adults and
children with rheumatoid arthritis. Among children with juvenile
idiopathic arthritis (also known as juvenile rheumatoid arthritis),
50% present with pain, swelling, or limitation of motion in the
TMJ. There may be associated growth restriction of the jaw
resulting in micrognathia and ankylosis. In adults with long-
standing rheumatoid arthritis, symptoms may develop in the TMJ
late in the course of the disease, and these patients may report
discomfort only when they have marked limitation of jaw motion.
Other signs of rheumatoid arthritis will be evident. Imaging of the
TMJ varies depending on the stage of the disease, but ultimately
there is resorption of the condyle, with shortening of the
mandibular ramus–condyle unit and potential reduction of joint
space and hypomobility.
(Steven J. Scrivani et all, 2008)
Here is the classification (subtype) of TMJ disorder from
Japanese Society for the Temporomandibular Joint in 2001:
Type I; Masticatory muscle disorder
There is jaw movement pain in the muscle whose region can be
identified.
Type II; Capsule-ligament disorder
There is movement pain in the TMJ with palpation tenderness.
(This category includes chronic and traumatic diseases of either the
retrodiscal tissue, joint capsule or ligament)
Type III; Disc disorder
Type IIIa; Disc displacement with reduction
There is a clicking sound or temporal sticking motion when
opening and closing the mouth
Type IIIb; Disc displacement without reduction
There is trismus and jaw opening pain or clenching pain after the
disappearance of clicking. A protrusive slide of the mandibular
condyle is usually disturbed on the problem side.
Type IV; Degenerative joint diseases, osteoarthritis, osteoarthrosis
There is at least one of joint pain, a trismus or a joint sound. A
picture image reveals marginal proliferation (osteophyte), erosion
or a deformity of the mandibular condyle.
Type V; Cases not included type I-IV
(Yasuyuki Shibuya et all, 2007)
 The first type of TMJ disorder is caused by pain on
mastication muscles around the TMJ which region can not be
identified. It happens because TMJ pain can not be centralized and
can even affect other parts that are all around TMJ area such as
ears, the whole head, and other muscles in the face.
The second type of TMJ disorder is caused by the damaged
capsule and ligaments, also the trauma in retrodiscal tissue. With
the existence of such defects, the patient will feel pain when he
opens his jaws.
The third type of TMJ disorder is caused by the abnormality
of disc’s position. Given this disparity, the condylus head placed
not on the central zone of the disc because of depletion and
elevation of the disc. That situation resulted in a click when the
head moves translational condylus through the disc. In type IIIA,
head condylus can back into place after the movement, whereas in
type IIIB condylus head can not go back into place.
Is there at least one of joint pain, a trismus or a joint sound with imaging
findings of marginal
The fourth
proliferation
type of (osteophyte),
TMJ disordererosion
is caused
or by
deformity
inflammation
of
mandibular condyle?
of the joints or degenerative joint disease. Pain is felt in at least one
YES joint. There can be clicking sounds
NO because it is possible that the
condylus head changed place (not on the central zone pf the disc).
Is there a clicking sound or a temporal sticking motion
TYPE IV The fifth type of TMJ disorder is uncharacterized well.
when opening and closing the mouth? Are there a
trismus
Patients only feel andwithout
the pain a jaw opening pain or clenching　pain
any indication as found in typeafter
the disappearance of clicking which are usually
I-IV. complicated with a protrusive sliding disorder of the
TMJ disorder typemandibular condyle isonperformed
determination the problemwith
side?analysis
Is a discof
displacement revealed by magnetic resonance imaging
YES, ATsome
LEASTof the following
(MRI)?questions: (Yasuyuki Shibuya et all, 2007)
ONE OF THE
QUESTIONS
NO

TYPE III
Is there jaw movement pain in the muscle
whose region can be identified?
YES
NO

TYPE I
Is there movement pain in the TMJ with palpation
tenderness?

YES NO

TYPE II TYPE V
Isi
Ibu 46 tahun terkena TMJ disorder karena 2 kemungkinan. Pertama
karena impaksi yang bisa menyebabkan kaku otot dan maloklusi.
Impaksi atau gigi yang tertanam lama dapat menyebabkan kaku otot yang
mengakibatkan TMD. Maloklusi menyebabkan ketidaknyamanan pada
pasien sehingga menimbulkan kebiasaan buruk bruxism dan clenching
yang akan dijelaskan pada tahap berikutnya. Kemungkinan kedua karena
ia telah memasuki masa menopause atau pra menopause. Pada masa ini,
hormon estrogen dan progesteron akan menurun. Pada masa ini pula
terjadi penurunan jumlah cairan synovial serta elastisitas ligamen. Kedua
hal tersebut dapat menyebabkan gangguan saat pergerakan sendi hingga
menyebabkan TMD. Hormon progesteron yang merupakan antidepresan
alami juga menurun sehingga pasien tersebut menjadi stress hingga
sering mengkonsumsi obat antidepresan. Dengan stress ini, pasien
menjadi sering gelisah hingga dapat menimbulkan kebiasaan buruk
burxism dan clenching. Kebiasaan ini dapat menyebabkan hiperaktivitas
dan hiperkontraksi otot. Hal ini menyebabkan spasme otot yang
menyebabkan kaku dan dull pada otot serta menyebabkan TMD.
Kebiasaan buruk tersebut juga dapat mengakibatkan disc displacement
 bila telah menjadi amat parah. Disc displacement dapat menimbulkan
clicking sound saat membuka dan menutup mulut. Hal ini menjadi salah
satu tanda seseorang menderita TMD.

CHAPTER 3
CASE REPORT

46 year old female patient came to the dentist with a complaint that this 1
year, she has been feeling stiffness, dull, clicking sound as well as pain in the left
and right cheek area when she opens her mouth, especially on mornings when she
wakes up, whereas there is no dental cavities

CHAPTER 4
DISCUSSION
In general, women who are at the age of 40 years experienced a period of
transition to menopause. At this stage there is a change in a woman, for example,
changes in mood. At this stage, women tend to become unstable emotions and
thoughts expenses increased. At this time a woman's emotions become
overwhelming, a woman tends to be a serious thinker and a highly-sensitive
person to other people so that women are particularly vulnerable to stress at the
time. Stress can cause the jaw to tense, as a result during sleep the muscles around
the jaw depressed to do work, so that during sleep there is movement of the jaw or
grinding. That movement is called bruxism, bruxism is caused by a condition
known as sleep apnea and stress. sleep disorder in which sufferers of bruxism
sliver teeth during sleep. If left untreated it can cause headaches, jaw pain and can
decrease tooth enamel of teeth and if it is done consequently, it can produce a
sudden sensitivity when consuming hot or cold foods. It also can cause loss of
teeth or broken fillings from teeth. So the anatomical form of the teeth of someone
who experienced bruxism will be changed because of abrasion, resulting in errors
in occlussion. Someone who experienced bruxism is caused by anxiety that
clearly, was awakened from sleep, the sensitivity of brain chemicals
(neurotransmitters such as dopamine and serotonin). Anxiety is seen as a trigger
or exacerbating factors. Serotonin Reuptake Antidepressants such as selective
inhibitors or SSRIs (eg Prozac, Paxil, Zoloft) known to worsen the grinding. In
the past, malocclusion is viewed as a major factor in bruxism.
We can say that the patient is in depression because she is in menopause
age. She consumes antidepresan because she feels stress that is one of
menopause’s symptoms. Depression is a feeling of sadness can be normal,
appropriate and even necessary during life's setbacks or losses. Or you may feel
blue or unhappy for short periods of time without reason or warning, which also is
normal and ordinary. But if such feelings persist or impair your daily life, you
may have a depressive disorder. Severity, duration and the presence of other
symptoms are the factors that distinguish ordinary sadness from a depressive
disorder. This is called: Depression, or irritability, which is a significant change in
mood for an extended period of time associated with loss of interest in usual
activities, sleep and eating disorders, and withdrawal from family and friends
(Nanette, 2002).
Depression can happen to anyone of any age. It afflicts almost 19 million
Americans each year, and up to one in five American women will suffer from
clinical depression at some point in her life. Women are two to three times more
likely than men to suffer from depression. Many women first experience
symptoms of depression during their 20s and 30s (Nanette, 2002).
Menopause can cause TMJ disorder because in it’s symptom, there’s
reducing of estrogen and progesteron hormone. It can cause joint and muscles
problems. Aching Joints and muscle problems is one of the most common
symptoms of menopause. It is thought that more than half of all postmenopausal
women experience varying degrees of joint pain. Joint pain is basically an
unexplained soreness in muscles and joints, which are unrelated to trauma or
exercise, but may be related to immune system effects mostly caused by
fluctuating hormone levels. It is not wise to ignore these aches and pains (Nanette,
2002).
Menopause can also cause stiffness of the muscles because of the reducing
endorphine. An increase of aches and pains throughout the body muscles
associated with soreness and stiffness in muscles. Women whose general health
and resistance are good are apt to have less premenstrual tension than those
women suffering from poor nutrition and lack of physical exercise. There are
some things you can do to try to keep symptoms to a minimum: Exercise helps
boost endorphins, the body's natural painkillers, so it may help improve moods
and has been found to significantly reduce many physical and psychological PMS
symptoms. Next time you have a build-up of tension or anxiety, try to run it off
(Nanette, 2002).
Stress can cause a bad habit called bruxism and clenching. It results from a
physiological and highly functional activity: Spontaneous Deglutition or
Spontaneous Swallowing. Normally, in the rest position and in the absence of
disease, the jaw is centred, balanced and suspended under the skull while muscles
are relaxed, balanced and tonic, condyles are symmetrical in their position in
articular cavities, teeth are not in contact, and enjoy the Benefits of inactivity .
This precious gift of nature and health can only occur whether the jaw is free to
move and make contact with the teeth in the right position, (maximum
Intercuspidation occlusion), in anatomical and functional harmony with the other
chewing elements. In wrong sleeping position ( sleep stomach, face down) the
weight of the head pushes the mandibula to lateral occlusion and exerts non-stop
compression ( for many hours) on the teeth, gum, periodontium and TMJ ,
therefore obstructing blood circulation and moving the teeth to a lateral bad
occlusion position(TMJD). In order to swallowing, masticatory muscles must
activate themselves to centre the jaw and then they must bring the teeth from
forced lateral malocclusion to centred occlusion (maximum Intercuspidation
occlusion), rubbing , grinding teeth between them, this is the cause of nocturnal
bruxism and negative trophic action on the gum , periodontium and TMJ
disfunction. Throughout the night the Neuromuscular component, instead of being
relaxed, has pledged to oppose the thrust of the weight that lies heavily on the jaw
This is the real reason for the bruxism is especially active during sleep. The teeth
are pushed sideways for hours, months, years move sideways, their movement
generates a bad occlusion. Malocclusion, in which the upper and lower teeth
occlude in a disharmonic way, through premature contact of back tooth the
relationship disharmony between the teeth and the imbalance of the jaw, can also
cause bruxism during the day in an attempt to reposition the teeth. The rubbing
causes tooth facet wear but also mobility and parodontal disease pyorrhoea .
Compression lasting all night on the teeth, face and mandibular joints, prevents
the circulation of blood in all components, in particular in support of the teeth
(periodontium). The ischemia and dystrophy, which might ensue cause suffering
to all the anatomical components of chewing. The joints , which are under
pressure all night , are subject to structural and functional damage , hence they
deform. This explains why bruxism is often associated to limitations, pain,
buzzing and crackling, clicks, teeth chafing, gnashing of teeth, teeth grinding and
dysfunction of the jaw joint, TMJ, persistent face pimples, headache, migraine,
hum, tinnitus, cervical and lumbar pain from postural problems, gingivitis,
periodontitis, pyorrhoea. Stress and psychological problems are not the cause but
pro-factors. (Galiffa, 2010)
It is explained before that bruxism and clenching activity causes pain,
clicking sound, etc. It happens because that activities force the muscles and joints
to work hard while it is time for the muscles to be relaxed. So that habits cause
hyperactivity, hypercontraction, and even can change the position of the disc in
TMJ.
Articular disc displacement can occur which increases the activity so that
the discus experienced over use causes decreased flexibility in the discus, if it
continues, it can cause disc rupture or inflammation that causes pain. In the
muscle occurs as a reaction from hiperfungsi hipertonus musculoskeletal system,
which can cause hipertonus / muscle spasm or hipotonus which can cause muscle
weakness and inflammation that can cause pain. (Kopp,2003)
Ligaments associated with the TMJ will also experience stiffness as a
result emphases of muscle contractions that cause the flexibility of these
ligaments will decrease or decreases can cause stiffness hipomobile contractures
that resulted occurred and caused laxity resulting hipermobile occur and can lead
to rupture pain. In the nerve sensation of pain caused due to local iskhemia as a
result of strong muscle contractions and continuous or inadequate
microcirculation as a result of the sympathetic system in which disregulation with
the excessive activation of the sympathetic nervous system will lead to nutritional
microcirculation resulting in reduced network resulting in ischemic tissue, it will
be painful.
TMJ disorder will be followed by pain. The mechanism of pain is
modulated are extremely complex and only partially understood. Many
neurochemicals that take part have been identified, including the enkephalins,
betaendorphin, serotonin, dynorphin, γ-aminobutyric acid (GABA), glycine, and
substance P. The discovery of endrigenous opioids that act as inhibitory
neuromodulator in nociceptive pathways opened a door to pain behavior at a
molecular level. Endorphin (endogenous morphine) exerts a definite analgesic
effect that is reversible by naloxone, a known morphine antagonist. Endorphin are
proyein molecules composed of chains of amino acids (peptide). They are
secreted by brain tissues into cerebrospinal fluid (CSF) and by the pituitary gland
into the bloodstream. This endogenous antinociceptive system is activated by
intermittent painful stimuli as well as by acupuncture, electroacupunture, and
electroanalgesia. Its effects decreases with the duration of the pain, an important
element pain chronicity. (Bell, 1990)
The brain stem descending inhibitory mechanism obtunds pain by way of
serotonin released into the CSF when the serotoninergic neurons in the
periaqueductal gray (PAG) and the nucleus raphe magnus (NRM) are activated by
nonpainful stimulation of thick cutaneous neurons. Thus, mild stimulation of
cutaneous sensory nerves exerts an inhibitory influence of pain. This forms the
basis of various treatment modalities such as massage, analgesic balms, vibration,
thermal applications, vapoocolants, hydrotherapy, and counterirritation. The
development of transcutaneous electrical nerve simulation (so-called TENS units)
for the symptomatic relief of pain is based on inhibitory effects of cutaneous
stimulation. (Bell, 1990)
Cerebral cortex can inhibit the activity of afferent sensory pathways which
bring painful stimuli. If central nociceptive neuron’s stimulability is increased, the
activity of afferent sensory paths is greater. Anxious and depressive patients have
lowered levels of painful stimuli. Brain stem with monoamine cores has the most
significant role in pain modulation; lowered monoamine activity (serotonin,
noradrenalin, opioid peptide β-endorphin – “endogen morphine”) decreases the
possibility of modulating the activities of afferent sensory pathways and control of
pain stimuli entrance from the peripheral part to the central nervous system (Gate
control theory). (Buljan, 2010)
Serotonin is probably the most important transmitter in descendent
inhibitory pathways and a lowered activity of serotonergic system is considered
responsible for painful symptoms in depressive or anxious patients. Theoretically
speaking, the lowered activity of noradrenaline system, which plays a role in the
development of depression, has also a role in the development of painful
symptoms. (Buljan, 2010)
Endorphin, endogen opioid, has a major role in the modulation of pain in
the central nervous system as well. Lack of endorphin is considered to be
correlating with the increased entrance of painful sensory stimuli. Hypothetically,
emotionally, biochemically and physically sensitive individuals react to stress by
releasing ACTH that antagonizes the analgesic effects of β-endorphin .
Biochemical basis of chronic pain is confirmed by its connection with depression
and efficacy of tryciclic antidepressants in the treatment. However, alleviating
pain with tryciclic antidepressants is as successful as in non-depressed,
psychiatrically healthy persons. A precise way of antidepressants’ activity is
unknown but can be the result of an increased concentration of monoamines in
midbrain whose role is to modulate the pain. (Buljan, 2010)
There is extensive convergence of sensory nerves that serves the orofacial
region. The areas of the higher center receiving input from the TMJ also receive
input from facial skin and intraoral sites. It has been observed that 80 percent of
the neurons from the TMJ and masseter muscle converge in the trigeminal sub-
nucleus caudalis. (Wright, 2000)
It also has been demonstrated that the trigeminal sensory complex receives
pain input from the trigeminal nerve, as well as converging input from the facial,
glossopharyngeal, vagus and hypoglossal cranial nerves and the upper cervical
nerves. It has been shown that at least one-half of the pain-carrying neurons that
normally are activated by the trigeminal nerve can be activated by electrical
stimulation outside their normal receptive field. (Wright, 2000)
 Convergence is believed to occur to a greater degree among neurons
carrying information from deeper structures such as muscles, joints or tooth pulp
than from cutaneous structures. This has been hypothesized as the reason people
with pain from deep structures have difficulty localizing it and often sense it as
referred to regions distant from their source, while people with cutaneous pain can
localize it with great accuracy. (Wright, 2000)
Psychological modulating effects on pain are particular importance. The
cerebral evaluation of nociception, which is peculiar to humans, markedly
influences the level of suffering as consequences of the pain experience are
recognized. Other powerful excitatory factors are fear, anxiety, emotional
instability, expectancy, and the level of attention directed toward to experienced.
Inhibitory influence is exerted by relaxation, confidence, distraction, pleasant
sensations, an physical activities of different kinds. (Bell, 1990)

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