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.

The fourth type of TMJ disorder is caused by inflammation

of the joints or degenerative joint disease. Pain is felt in at least one

joint. There can be clicking sounds because it is possible that the

condylus head changed place (not on the central zone pf the disc).

The fifth type of TMJ disorder is uncharacterized well.

Patients only feel the pain without any indication as found in type

I-IV.

TMJ disorder type determination is performed with analysis of

some of the following questions: (Yasuyuki Shibuya et all, 2007)

Isi

Is there at least one of joint pain, a trismus or a joint sound with imaging findings of marginal proliferation (osteophyte), erosion or deformity of mandibular condyle?

YES NO

TYPE IVIs there a clicking sound or a temporal sticking motion when opening and closing the mouth? Are there a trismus and a jaw opening pain or clenching　pain after the disappearance of clicking which are usually complicated with a protrusive sliding disorder of the mandibular condyle on the problem side? Is a disc displacement revealed by magnetic resonance imaging (MRI)?YES, AT LEAST ONE OF

THE QUESTIONS

TYPE III

NO

Is there jaw movement pain in the musclewhose region can be identified?

YES

TYPE I

NO

Is there movement pain in the TMJ with palpation tenderness?

YES NO

TYPE II TYPE V

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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