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CHAPTER 1

INTRODUCTION

1.1. Background

Pain is a common complaint of patients complained of by both as the

primary reason patients seek treatment or as an additional complaint. The main

therapy is to eliminate the causes of pain should ideally pain. However, it is often

the cause of the loss is not necessarily lost causes pain and sometimes in certain

cases, the pain so great that relief of pain-relieving therapy to important.

Statement, in terms of time goes by, the pain can be classified into two acute pain

and pain chronic. Both have different characteristics that also make a range of

therapeutic modalities for pain distinguished. Especially for this discussion will

focus primarily on chronic pain. Management of the chronic pain is often difficult

for both the physician and for patient cause pain are often difficult to find and

time consuming for physicians and emotionally feel very burdensome. Typically,

the medical approach is unusual to find the primary pathological process is not

successful and often required a multidisciplinary treatment, including the

management of aspects physicosocial. The inclusion of these psychosocial

modalities for chronic pain cases have a basic psychological disorders and or

psychological problems that arise secondary to frustration patients deal with

illness and contributed to the exacerbation the disease. One cause of chronic pain

that is often pretty di the TMJ ( TemporoMandibular junction ). Approximately

60-70% of the general population has at least one complaint TMJ disorders, but

only a quarter are aware of the complaint itu. Furthermore, the only 5% of at least

one group of people with the disorder who seek treatment to doctor. One

complaint of TMJ disorders is pain that are chronic (Child and Todd, 2000).

TMJ disorder is a complex disorder with many interrelated factors that are

modulated by psychological factors, especially stress, anxiety, and depression. As

mentioned above, chronic pain management is often difficult for both physicians

and patients. Therapy is not exactly going to cause a long and consuming vast

amounts of time and attention. For patients with TMJ, it is certainly very

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disturbing and will aggravate the disease condition. Therefore, for a doctor in the

treatment of chronic pain, TMJ disorders should be included in a possible

diagnosis of these patients. Thus, the expected treatment in these patients can

more quickly and can reduce the burden on both patient time, material, and

emotionally (Rantala, 2010).

1.2. Problems

The following is the problem to be discussed in this paper are:

- what is the anatomical and histological structure of the temporo mandibular?

- what is the physiological basis of muscle and nerve?

- how is the process of relaxation of muscle contraction?

- How is the physiological movements that occur in the temporo mandibular joint?

- How is the possibility of triggering factors that cause TMJ disorders occur with

signs of pain?

1.3. Purpose

The following is the purpose of making this paper are:

- to explain the anatomical and histological structure of the temporo mandibular

- to explain the physiological basis of muscle and nerve

- to explain the process of relaxation of muscle contraction

- to explain the physiological movements that occur in the temporo mandibular

joint

- to explain the possibility of triggering factors that cause TMJ disorders occur

with signs of pain

1.4. Benefits

This paper could be useful for giving the information of the anatomical

and histological structure of the temporo mandibular, physiological basis of

muscle and nerve, process of relaxation of muscle contraction, physiological

movements that occur in the temporo mandibular joint and the possibility of

triggering factors that can cause TMJ disorders.

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1.5. Hipotesis

Unfinished removable orthodontic (retainer) treatment can lead to

temporomandibular disorder type mylofacial pain.

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CHAPTER 2

THEORITICAL REVIEW

2.1 Anatomy and Histology of Temporomandibular Joint

The articulatory system comprises of a hinge (the TMJ), motors (the

masticatory and accessory muscles) and the contacts between the teeth

(occlusion).

Temporomandibular joint is located between the mandible and cranium is

one of the joints in the body’s most complexes. Temporomandibular joints can

perform rotational motion as a ginglymoid joint, but at the same time can make

such a sliding movement arthrodial joints. Thus technically temporomandibular

joint is a ginglymoarthrodial.

Figure 2.1 Structure of Temporomandibular Joint at Lateral Side (Soboleva et al, 2005).

The TMJ is the articulation between the condyle of the mandible and the

squamous portion of the temporal bone. The condyle is elliptically shaped with its

long axis oriented mediolaterally, whilst the articular surface of the temporal bone

is composed of the concave articular fossa and the convex articular eminence

(Johnson and Moore, 1997).

The TMJ is a bilateral synovial joint that functions in speech, mastication,

and deglutition and allows movement of the mandible in three planes of space. It

is atypical in that the articular surfaces are covered by white fibrocartilage (mostly

collagen with only a few cartilage cells), rather than the more usual hyaline

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cartilage. Beneath the articular covering of the head of the condyle is a layer of

hyaline cartilage (Johnson and Moore, 1997).

The TMJ consists of:

1. Mandibular condyle

2. Temporomandibular fossa

3. Articular disc

4. Joint capsule (lined by synovial membrane)

5. Ligaments

6. Muscles of mastication

7. Blood and nerve supply

2.1.1 Mandibular Condyle

The mandible consists of a curved body and two vertical rami which

project upwards. At the superior border of the ramus are the coronoid and

condylar processes, separated by the mandibular incisure. The coronoid process is

a triangular plate of bone which projects upwards (Johnson and Moore, 1997).

Mandibular condyle (capitulum mandible) is located above the mandibular

ramus. In adults, such as the condyles form an elliptical tube with a width of 20

mm in anterior-posterior dimension. The average distance between the left and

right condyles are calculated from the midpoint between 100 mm. Condyle shape

when viewed from the anterior (frontal aspect) can be classified into 4 categories:

convex, flat, angular, and rounded (Bernard, 2001).

Condyle has a joint capsule, medial tubercle, and lateral tubercle. Tubercle

supported by attachment to the lateral and medial collateral ligament of. Condyle

that articulates part covered by a thick fibroelastic tissue, containing fibroblasts

and chondrocytes. At the age condyle cartilage and found a little place

classification. In this situation, the trauma of the burden of excessive chewing can

lead to degenerative joint disease (Bernard, 2001).

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Figure 2.2 the Mandible (Encyclopaedia Britannica, 2007)

The condyle is approximately cylindrical in shape, being expanded from

side to side but narrowing from front to back (Johnson and Moore, 1997) and it

measures between 13 and 25 mm mediolaterally (Bernard, 2001). The long axis is

not quite in the transverse plane but is directed posteriorly and superiorly as well

as medially. The constricted part of the condylar process below the head is termed

the neck of the mandible. Part of the lateral pterygoid muscle is inserted into the

anterior aspect of the condyle.

2.1.2 Temporomandibular fossa (glenoid fossa)

The temporomandibular fossa forms the superior articular surface of the

TMJ and is located on the squamous part of the temporal bone. It is bounded

anteriorly by the articular tubercle and posteriorly by the tympanic part of the

bone; which separates it from the external acoustic meatus. The

temporomandibular fossa is divided into two parts by a narrow fissure, which is

termed the petrotympanic fissure (Johnson and Moore, 1997).

Condyle articulates with the squamous part of temporal bone that forms

the base of skull. Component of the temporal bone is composed of concave-

shaped mandibular fossa and articular eminence of the convex-shaped and located

in the anterior mandibular fossa. Mandibular fossa has articulation surface

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(functional parts) and non-articulation or non-functional parts. The posterior

surface of the non-articulation is limited by the tympanic bone that makes up the

anterior wall of the external acoustic meatus.

Figure 2.3 The Temporomandibular fossa (Soboleva et al, 2005).

Between the mandibular fossa (lateral part) and there is a fissure

squamotympanic tympanic bone that runs from the medial and branched into two,

namely anterior (petrosquamosa fissure) and posterior (petrotympanic fissure).

Part of the lateral fissure petrotympanic traversed by chorda tympani nerve

ganglion and tympanic arteries.

Articular eminence (articulation surface) is in the anterior and inferior part

of the mandibular fossa and consists of a down slope, or called by the transverse

ridge (medial extension of the tubercle zygomatikum), and a rising slope. This

section is covered by fibrous connective tissue indicating a functional part of the

joint while chewing.

2.1.3 Articular Disc (meniscus)

Is part of the articular disc of the temporomandibular joint that separates

the mandibular condyle with the fossa and eminence. Articular disc is composed

of fibrous connective tissue (collagen type 1) which can and most of the structure

is traversed by blood vessels and nerves. Based on the thickness of the cross-

section when viewed from the sagittal section, the articular disc is divided into 3

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parts. The middle is the most thin and intermediate zone known. While in both its

edges, the anterior and posterior, have a thicker cross section than the middle, and

traversed by fine nerve fibers. Edge of the area is often called the anterior band

and posterior band. The anterior band of the articular disc is attached to the

ligaments of the capsule, either on the superior and inferiornya. The ligament is a

capsule of collagen fibers. In addition to the ligament attachment of the capsule,

between the second attachments, the anterior band is also attached to the tendon of

the muscle fibers of the lateral superior pterigoideus. Meanwhile, the posterior

band will extend to the posterior and bilaminar zone. Bilaminar zone will then be

divided into 2, which is composed of the superior layer and attached to the

processus fibroelastin postglenoid of squamotymponic fissure, and posterior part

composed of the fibrous layer and attached to the posterior condyle of the neck

below the surface of the articulation. Both parts are separated by loose connective

tissue attached to the posterior wall of the joint capsule called retrodiscal tissue.

Lateral and medial parts of the articular disc is attached to the joint capsule

(capsule ligaments), but attached to the poles and the lateral condyle of

mandibulaoleh medial collateral ligament. Attachment causes the articular disc

moved with the mandibular condyle.

The meniscus is a fibrous, saddle shaped structure that separates the

condyle and the temporal bone and it is separated into bands which vary in

thickness (Bernard, 2001):

1. The thinner, central intermediate zone,

2. Thicker portions, called the anterior band, lying below the posterior

edge of the articular eminence and

3. A thick posterior band that lays on top of the condyle.

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Figure 2.4 The articular disc of the TMJ (Joannes,1995)

Anteriorly, the disc is attached to the articular eminence above and to the

articular margin of the condyle below. It also has an anterior attachment to the

superior head of the lateral pterygoid muscle. Posteriorly, it is attached to the

posterior wall of the glenoid fossa above and to the distal aspect of neck of the

condyle below. This area is called the posterior bilaminar zone and was first

described by Rees in 1954. The bilaminar zone is formed of a vascular, innervated

tissue that plays an important role in allowing the condyle to move forward.

The meniscus and its attachments divide the joint into superior and inferior

joint spaces. The superior joint space is bounded above by the articular fossa and the

articular eminence and this allows translatory movement. The inferior joint space is

bounded below by the condylar head, which allows a hinge or rotatory movement

(Bernard, 2001). Both joint spaces have small capacities, generally in the region of

1cc or less. The TMJ is thus not considered a stationary hinge, as it allows both

gliding and hinge actions, but is described as a synovial sliding joint (Bell, 1982).

2.1.4 Joint capsule

The articular capsule is a thin, loose envelope which is attached above to

the circumference of the mandibular fossa, to the articular tubercle immediately in

front and, below, to the neck of the condyle of the mandible. The capsule encloses

the joint and acts as a stabiliser which allows complex function.

The synovial membranes line the inner aspect of the joint capsule (Bell,

1982) and are located above and below the articular disc. The upper, which is the

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larger and looser of the two, is continued from the margin of the cartilage

covering the mandibular fossa and articular tubercle onto the upper surface of the

disc. The lower one passes from the under surface of the disc to the neck of the

condyle. The synovial membrane consists of two layers, a cellular layer and a

vascular layer. The cellular layer contains type A cells, which are phagocytic, and

type B cells, which synthesise hyalorunate found in synovial fluid. The vascular

layer consists of blood vessels and lymphatics within a loose connective tissue

matrix. The synovial membrane secretes synovial fluid for lubrication and

nourishment of the articular surfaces and the lining of both compartments.

2.1.5 Ligaments

There are three ligaments associated with the TMJ, one major and two

minor. The temporomandibular ligament is a lateral thickening of the joint capsule

which consists of two short, narrow fasciculi, one in front of the other. It is

attached, above, to the lateral surface of the zygomatic arch and to the tubercle on

its lower border and, below, to the lateral surface and posterior border of the neck

of the mandible. It is broader above than below and its fibres are directed

obliquely downward and backward. It is covered by the parotid gland and by the

integument (Standring, 2004).

Two minor ligaments are classed among the ligaments of the TMJ, but can

only be considered as accessory to it:

1. The sphenomandibular ligament is a flat, thin band which is attached above to

the spina angularis of the sphenoid bone and becomes broader as it descends to

the lingula of the mandibular foramen. Its lateral surface is in relation, above, with

the lateral pterygoid whilst, below, it is separated from the neck of the condyle by

the internal maxillary vessels. Below this, the inferior alveolar vessels and nerve

and a lobule of the parotid gland lie between it and the ramus of the mandible. Its

medial surface is in close relation with the medial pterygoid.

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Figure 2.5 The sphenomandibular ligament (indicated by the arrows)(Bumann and Lotzmann, 2002).

2. The stylomandibular ligament is a specialised band of the cervical fascia, which

extends from near the apex of the styloid process of the temporal bone to the

angle and posterior border of the ramus of the mandible, between the masseter and

medial pterygoid. This ligament separates the parotid from the submaxillary gland

and some fibres of the styloglossus take origin from its deep surfaces (Standring,

2004).

Figure 2.6 The Stylomandibular ligament (indicated by the arrows)(Bumann and Lotzmann,2002).

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2.1.6 Muscles of Mastication

The chief muscles of mastication are:

Masseter. Pterygoideus externus.

Temporalis. Pterygoideus internus.

Parotideomasseteric Fascia (masseteric fascia).—Covering the

Masseter, and firmly connected with it, is a strong layer of fascia derived from the

deep cervical fascia. Above, this fascia is attached to the lower border of the

zygomatic arch, and behind, it invests the parotid gland.

The Masseter is a thick, somewhat quadrilateral muscle, consisting of two

portions, superficial and deep. The superficial portion, the larger, arises by a

thick, tendinous aponeurosis from the zygomatic process of the maxilla, and from

the anterior two-thirds of the lower border of the zygomatic arch; its fibers pass

downward and backward, to be inserted into the angle and lower half of the lateral

surface of the ramus of the mandible. The deep portion is much smaller, and more

muscular in texture; it arises from the posterior third of the lower border and from

the whole of the medial surface of the zygomatic arch; its fibers pass downward

and forward, to be inserted into the upper half of the ramus and the lateral surface

of the coronoid process of the mandible. The deep portion of the muscle is partly

concealed, in front, by the superficial portion; behind, it is covered by the parotid

gland. The fibers of the two portions are continuous at their insertion.

Temporal Fascia.—The temporal fascia covers the Temporalis muscle. It

is a strong, fibrous investment, covered, laterally, by the Auricularis anterior and

superior, by the galea aponeurotica, and by part of the Orbicularis oculi. The

superficial temporal vessels and the auriculotemporal nerve cross it from below

upward. Above, it is a single layer, attached to the entire extent of the superior

temporal line; but below, where it is fixed to the zygomatic arch, it consists of two

layers, one of which is inserted into the lateral, and the other into the medial

border of the arch. A small quantity of fat, the orbital branch of the superficial

temporal artery, and a filament from the zygomatic branch of the maxillary nerve,

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are contained between these two layers. It affords attachment by its deep surface

to the superficial fibers of the Temporalis.

Figure 2.7 The Temporalis; the zygomatic arch and Masseter have been removed

(Soboleva et al, 2005).

The Temporalis (Temporal muscle) is a broad, radiating muscle, situated

at the side of the head. It arises from the whole of the temporal fossa (except that

portion of it which is formed by the zygomatic bone) and from the deep surface of

the temporal fascia. Its fibers converge as they descend, and end in a tendon,

which passes deep to the zygomatic arch and is inserted into the medial surface,

apex, and anterior border of the coronoid process, and the anterior border of the

ramus of the mandible nearly as far forward as the last molar tooth. The

Pterygoideus externus (External pterygoid muscle) is a short, thick muscle,

somewhat conical in form, which extends almost horizontally between the

infratemporal fossa and the condyle of the mandible. It arises by two heads; an

upper from the lower part of the lateral surface of the great wing of the sphenoid

and from the infratemporal crest; a lower from the lateral surface of the lateral

pterygoid plate. Its fibers pass horizontally backward and lateralward, to be

inserted into a depression in front of the neck of the condyle of the mandible, and

into the front margin of the articular disk of the temporomandibular

articulation. The Pterygoideus internus (Internal pterygoid muscle) is a thick,

quadrilateral muscle. It arises from the medial surface of the lateral pterygoid

plate and the grooved surface of the pyramidal process of the palatine bone; it has

a second slip of origin from the lateral surfaces of the pyramidal process of the

palatine and tuberosity of the maxilla. Its fibers pass downward, lateralward, and

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backward, and are inserted, by a strong tendinous lamina, into the lower and back

part of the medial surface of the ramus and angle of the mandible, as high as the

mandibular foramen.

Figure 2.8 The Pterygoidei; the zygomatic arch and a portion of the ramus of the

mandible have been removed (Soboleva et al, 2005).

Nerves.—The muscles of mastication are supplied by the mandibular

nerve. Actions.—The Temporalis, Masseter, and Pterygoideus internus raise the

mandible against the maxillæ with great force. The Pterygoideus externus assists

in opening the mouth, but its main action is to draw forward the condyle and

articular disk so that the mandible is protruded and the inferior incisors projected

in front of the upper; in this action it is assisted by the Pterygoideus internus. The

mandible is retracted by the posterior fibers of the Temporalis. If the Pterygoidei

internus and externus of one side act, the corresponding side of the mandible is

drawn forward while the opposite condyle remains comparatively fixed, and side-

to-side movements. Such as occur during the trituration of food, take place.

The masticatory system is a functional unit composed of the teeth; their

supporting structures, the jaws; the temporomandibular joints; the muscles

involved directly or indirectly in mastication (including the muscles of the lips

and tongue); and the vascular and nervous systems supplying these tissues.

Functional and structural disturbances in any one of the components of the

masticatory system may be reflected by functional or structural disorders in one or

more of its other components. However, there is a lot of evidence that the

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masticatory system has ability to the wide range of adaptive modalities. These

adaptations can be functional and/or structural and may respond to transient

and/or permanent demands. Therefore, this system, like any biological system,

cannot be viewed as a rigid and immutable. Masticatory muscle physiology has

been evaluated mostly from electromyographic recordings. However,

electromyography coupled with jaw -tracking devices has provided much more

information of the cor relation between jaw movements and muscle activity. (Ash

et al, 1995. Soboleva et al, 2005)

Knowledge of how the mandible moves during mastication has greatly

influenced procedures in clinical dentistry. Historically, an understanding of

mandibular movement was considered important in removable prosthodontics.

Later, this information was used in the design and setting of articulators, and in

the design of the dentures and denture teeth themselves. Today the importance of

jaw movements has become apparent in fixed prosthodontics, periodontics,

orthodontics, and in the diagnosis and treatment of pain disorders of the

masticatory system (3). The most important reason why dentists maintain and

replace missing teeth should be to provide patients with good masticatory

abilities. Therefore, it is important that dentists know how mastication normally

occurs. This knowledge should ensure that dental procedures improve, rather than

reduce, patient's functional abilities. The aim of this overview is to give basic

description of the classical studies of the physiology, function and neural control

principles of the mastication.

2.2 Physiology of temporomandibular joint movement

Based on the results of electromyographic studies, the motion of the

mandible

in conjunction with the upper jaw can be classified as the following are:

1. Motion to open

2. Motion to close

3. protusi

4. Retention

5. Lateral motion

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2.2.1 Motion to open

As expected, the motion to open up to general smaller than the maximum

bite force (closing). Muscular functions of the lateral pterygoid pull ahead

prosessus condyloideus to the articular eminence. At the same time, the posterior

temporalis muscular condition must be relaxed and this will be followed by

masseter muscular relaxation, muscular fibers of the anterior temporal and

muscular medial pterygoid that goes fast and smoothly. This situation will allow

the mandible rotates around the axis horizontal, so prosessus condyle will move

forward while angle of the mandible moves backward. Chin be depressed, this

situation takes place with the help of a strong opening movement of the muscular

digastricus, muscular and muscular mylohyoideus geniohyoideus the contractions

of the relatively stable os hyoideum, was arrested on place by muscular

infrahyoidei. Berotasinya mandibular axis point cannot remain stable during the

opening movement, but will move down and forward along the line (in a resting

state) of prosessus kondiloideus to orifisum mandibular canal.

2.2.2 Motion to close

Prime mover is muscular masseter, temporalis muscular, and muscular

medial pterygoid. The jaws can be closed at various positions, from fully closed

position to close the protrusion on the state of the processus kondiloideus is at

most posterior position in the glenoid fossa. Motion to close the position requires

protrusion of the lateral pterygoid muscular contraction, aided by the muscular

medial pterygoid. Mandibular caput will remain in position next to the articular

eminence. On the motion to close retrusi, muscular posterior temporalis fibers will

work together with the muscular process of the masseter to restore glenoid fossa

kondiloideus into, so that the teeth may come into contact with each other in

normal occlusion.

On the motion to close the cavum oris, masticatory muscle strength

incurred will be passed on mainly through the teeth to the upper frame the face.

Pterygoid muscular fibers of the lateral and posterior temporalis muscular tend to

eliminate the pressure of mandibular caput when these muscles contract, with a

little depression during moving the teeth. This situation is related to the fact that

17

the axis of rotation will pass around the mandibular ramus, in any area near

orifisum mandibular canal. Although this is still debated about whether articulatio

temporomandibular joint that is resistant to stress or not. The results of recent

research using photoelastic models and with the light polarization in various load

conditions showed that the joints are directly involved in the mechanism of stress.

2.2.3 Protusi

In the case of bilateral protrusion, both processes are kondiloideus moves

forward and down the articular eminence and the teeth will remain in sliding

contact is closed. Prime mover in this state is assisted by the lateral pterygoid

muscular muscular medial pterygoid. Muscular fibers of the posterior temporalis

are an antagonist of the muscular contraction of the lateral pterygoid. Muscular

masseter, medial pterygoid and the muscular fibers of the anterior temporalis

muscular contraction will attempt to maintain muscle tone to prevent rotational

movement of the mandible that would separate the teeth. Muscular contraction of

the lateral pterygoid will also pull down the articular disc and articular eminence

to the next. Fibroelastic posterior attachment area of the discs and ligaments to the

fissure tympanosquamosa capsularis will serve to limit the range of motion of this

protrusion.

2.2.4 Retention

During movement, the head of the mandible together with artikularisnya

disc will slide toward the mandibular fossa through muscular contraction of the

posterior temporalis. The lateral pterygoid is muscular and the antagonist muscles

will relax the situation. Other masticatory muscles tonus contraction would serve

to maintain and keep your teeth remain in sliding contact. The elasticity of the

posterior disc and capsula articularis articulatio temporomandibularis will be able

to hold the discs remain on the proper relationship of the mandible when the

processus kondiloideus caput moving backwards.

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2.2.5 Lateral Motion

At the time of the jaw is moved from one side to the other side to get a

chewing motion between the occlusal surface of premolars and molars, the

processus kondiloideus on the side of the mandible is moving toward goal will

remain at rest position held by the posterior temporalis muscular contractions

while the tone will be retained by the muscle other masticatory muscles are found

on the side. On the opposite side of the processus kondiloideus and articular disc

will be pushed forward to the articular eminence through muscular contraction of

the lateral and medial pterygoid, in conjunction with muscular relaxation of the

posterior temporalis. Thus, the motion of the mandible from side to side is formed

through contraction and relaxation of the muscles of mastication takes place

alternately, which also plays a role in protrusion and retrusi motion.

On lateral movement, the mandible on the side ipsilateral caput, the

direction of the movement, will remain on hold in the mandibular fossa. At the

same time, the mandibular caput of the contralateral side will move forward

translational. Mandible will rotate on a horizontal plane around a vertical axis

passing through the caput is not a 'fixed', but came a little behind. As a result,

ipsilateral caput will move slightly to the lateral, the movement known as the

Bennett movement.

In addition to causing active movement, the muscles of mastication also

have an important action in maintaining postural mandibular position against the

force of gravity. When the mandible is at rest position, the teeth are had not

occlusion and will look the freeway gap or space between the arch of the superior

and inferior dentalis.

2.2.6 Masticatory Function

Mastication is the action of breaking down of food,preparatory to

deglutition. This breaking-down action ishighly organized complex of

neuromuscular and digestive activities that, in normal individuals, integrate the

various components of the masticatory system, such as the teeth and their

investing structures, the muscles, the temporomandibular joints, the lips, the

cheeks, the palate, the tongue, and the salivary secretions. The object of chewing

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is to crush, triturate and mix food with saliva, so that food can be transported by

deglutition down the digestive canal. (Soboleva et al, 2005)

The most important muscles for this purpose are temporal (anterior and

posterior), the masseter (superficial and deep), the medial pterygoid, the lateral

pterygoid (superior and inferior), and the digastric muscles. The trigeminal motor

nucleus of motoneurons innervating the jaw muscles lies across the midline of the

brainstem. However, mastication involves far more muscles than these "muscles

of mastication" innervated by the trigeminal nerve. Synergestic movements of

muscles innervated by facial and hypoglossal nerves are equally important

(Soboleva et al, 2005)

The masticatory sequence is the whole set of movements from ingestion to

swallowing. It is made up of masticatory cycles that change in form as the food is

gathered, moved backward to the molar teeth, then broken down and prepared for

swallowing (6). It is possible to distinguish between cycles which occur at the

beginning of the masticatory sequence and form the preparatory series of

movements, cycles of particle reduction and cycles related to preswallowing . The

cycles of reduction are intermediate in duration, longer than the preparatory

cycles, but shorter than the preswallowing ones. Differences in type, number, and

size of food particles appear to influence almost all the parameters of mastication.

The length of the masticatory sequence is short for soft foods and long for those

those are hard or tough. (Soboleva et al, 2005)

2.2.7 Jaw Muscles and Movements

More than 20 muscles are involved in the process of mastication. The

temporalis muscle, as shown in Fig. 1(a), is a large, flat muscle. Its fibres can be

divided into two parts: the anterior fibres that elevate the mandible (lower jaw)

and close the mouth and the posterior fibres which contribute to the complex

grinding movement by retracting the mandible. The pterygoid (Fig. 1(b)) are a

family of muscles: lateral and medial pterygoids. The lateral pterygoids work to

protract the mandible and open the mouth, and medial pterygoids mostly protracts

the mandible.

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The masseter, as shown in Fig. 1(c), is a flat quadrilateral muscle with

deep and superficial parts. It contributes mostly to the mandible elevation (mouth

closing), and also plays a role in protracting the mandible. Underneath the

mandible, the hyoid bone supports a set of muscles called suprahyoid muscles

(Fig. 1(d)). Among them, digastric, stylohyoid, mylohyoid, geniohyoid and

platysma muscles are involved in the mouth opening and then the depression of

the mandible. (Palastanga, N 1998. Daumas et al, 2005)

Figure 2.9 Muscles for mastication (reconstructed after [19,20]): (a) left temporalismuscles, (b) left pterygoids muscles,(c) right masseter and (d) suprahyoid muscles

The mandible, or the lower jaw, is attached to the rest of the skull by

muscles through a socalled temporo-mandibular joint, as shown in Fig. 2.9 (b).

Thus, it cannot move as a free body in space as it is constrained by biological

joints and muscles. Human chewing behaviour can be described by two basic

movements of the mandible: the clenching and the grinding movements (Fig. 2).

Clenching consists of the successive elevation and depression of the mandible and

uses a lot of muscles but especially the masseter and temporalis anterior.

21

.

Fig. 2.10 Two basic chewing movements: (a) basic clenching and (b) basic grinding (Daumas et

al, 2005).

Grinding involves almost all the jawmuscles and the incisal point (the

point between the two lower incisives) traces a circle in the horizontalplane. Thus,

a complex human mastication can be regarded as aggregate clenching andgrinding

movements. (Daumas et al, 2005)

2.3 Pathology of Temporomandibular Joint

2.3.1 Neurogical Control

Jaw movements are among the most complex andunique movements

performed by the human body. The mandible, unlike any other bones in the

human body, is lung between two nearly symmetrical joints, which are close to

being the mirror image of one another. Each muscle involved in the control of

mastication has its counterpart on the opposite side of the jaw. (Soboleva et al,

2005)

To create precise mandibular movements, inputs from various sensory

receptors must be received by the central nervous system through afferent nerve

fibers. The brain assimilates and organizes these inputs and elicits appropriate

motor activities through the efferent nerve fibers. These motor activities involve

the contraction of some muscle groups and the inhibition of others. Chewing is a

subconscious activity, yet can be brought to conscious control at any time.

(Okeson, 1993)

22

The coordination and rhythmicity of mastication has been attributed to the

alternate activation of two simple brain stem reflexes. These are the jaw opening

reflex, activated by tooth pressure or tactile stimulation of wide areas of the mouth

and lips, and the jaw-closing reflex, which follows stretching of the elevator

muscles during opening. The introduction of a food bolus into the mouth was

thought to initiate a self-perpetuating cycle by producing jaw opening, and the

consequent stretching of the elevator muscles would produce jaw closure on the

bolus, SCIENTIFIC ARTICLES (Soboļeva et al, 2005). again producing jaw

opening by stimulation of periodontal and soft tissue receptors. The same authors

found that in rabbits the timing of rhythmic chewing occurs within the brainstem.

They suggested that mastication is controlled by a pattern generator brought about

by reverberatingcircuits within the brainstem and that this patterning can be

activated by adequate inputs from higher centers or from feedback through

sensors in the oral cavity. (Soboleva et al, 2005)

The control of mastication is dependent in large part on sensory feedback,

which consists of epithelial mechanoreceptor afferents, periodontal afferents,

temporomandibular joint afferents and muscle afferents. Sensory feedback may

explain the coordination of the tongue, lips, and jaws to move the food around, the

reason why different foodstuffs influence the pattern of masticatory movement, or

the abrupt changes from cycle to cycle. While the cortex is the main determiner of

action, centers in the brain-stem maintain homeostasis and control normally

subconscious body functions. (Soboleva et al, 2005)

Within the brain-stem is a pool of neurons - a central pattern generator

(CPG) - that controls rhythmic muscle activities. The neurons can be activated by

adequate inputs from higher centers or from the oral cavity, and it is responsible

for the precise timing of activity between synergetic and antagonistic muscles, so

that specific functions can be carried out. Sensory feedback interact with the

control system at several levels to adapt the rhythmic program to characteristics of

the food. This feedback is also a source of the variability in masticatory

movements. Once an efficient chewing pattern is found, it is learned and repeated.

This learned pattern is called a muscle engram. Chewing therefore can be thought

of as an extremely complex reflex activity. The brain-stem also contains other

23

areas, such as the reticular system, the limbic system and the hypothalamus, that

have influence on masticatory function. These structures can modify the response

of the cortex to any given stimulus, modify motor neuron activity, and even

initiate irrelevant muscle activity. Thus, features of mastication can be

programmed by the brain stem in the absence of sensory inputs, but such

movements would be highly inefficient and even dangerous to the masticatory

system. (Soboleva et al, 2005)

2.3.2 Normal Masticatory Movements

The earliest human jaw reflex is the jaw-opening reflex, which may be

produced by mechanical stimulation of the lip. The explanation is that the

digastric neurons differentiate before those of the jaw closing muscle neurons in

the fetus. Jaw closing occurs passively at first. After birth it is possible to observe

functions such as crying, sucking, swallowing, and scowling, but not chewing.

Chewing must be learned, and occurs only after tooth eruption. It is possible that

periodontal ligament receptors and their stimulation are essential for this learning

process

Chewing becomes well coordinated around 4-5 years of age, by which

time the primary teeth have erupted (16). Different investigations have shown that

the pattern of masticatory movements varies considerably from one individual to

another. It is believed that each individual has a characteristic basic pattern of

masticatory movement. However, consecutive cycles are never exactly alike.

Significant differences in chewing are presented between men and women, as well

as between young and elderly people. (Soboleva et al, 2005)

The wide variation within and between individuals of the masticatory

movements is explained by the infinite variation of afferent inflow during natural

chewing. The masticatory envelope is usually described as a "tear-drop shape"

with a slight displacement at the beginning of the opening phase. This means that

the opening movement rarely goes straight down. In most cases it deviates to the

chewing side. The maximum extent of vertical and lateral movement in normal

masticaton is about half of the maximum vertical and lateral movement possible.

When a subject deliberately chews on the right side, the jaw follows a cyclic

24

pathway is a clockwise direction, and chewing on the left side is associated with

movement in a counterclockwise direction. Neill & Howell reported that 75% of

chewing strokes describe a regular cyclic pattern. Less than 6% of the strokes

began with a vertical opening. The most lateral point of the chewing cycle is

situated about midway through the closing cycle for grinding movements, but is

lower for chopping movements. (Soboleva et al, 2005)

Usually the closing phase is lateral to the opening phase although often

this relationship is reversed, and the closing phase passes medial to the opening

movement, i. e., a reversed masticatory stroke takes place. (Soboleva et al, 2005)

Neill & Howell showed that in the sagittal plane approximately half of the

subjects had the opening stroke anterior to the closing stroke. The angulation of

the sagittal pathway was normally directed upward and backward, reflecting the

rotational element in mandibular opening. (Neill et al, 1986)

The character of the food influences the chewing pattern. The opening

length depends on the size and the hardness of the food bolus. As the food is

softened, the lateral and the vertical extend of the jaw movements decrease.

(Soboleva et al, 2005)

The hardness of the food also has an effect on the number of chewing

strokes necessary before a swallow is initiated. The harder the food, the more

chewing strokes are needed. Each chewing cycle has duration of about 700 ms

and tooth contact of about 200 ms. (Ash et al, 1995)

2.3.3 Electromyography (EMG) Activity During Mastication

During mastication the relationship between muscle actions is generally

similar between subjects. During the chewing cycle, muscle activity begins from

the static position of maximum intercuspation, and initially occurs in the

ipsilateral inferior head of the lateral pterygoid muscle approximately halfway

through the tooth contact period. This activity is shortly followed by activity in

the inferior head of the contralateral pterygoid muscle. These two muscles are

active through the entire duration of the opening phase. The digastric muscles are

also active during the opening phase and contribute mainly to a rotational

component of mandibular opening. The opening phase ends when the activity in

25

the two inferior heads of the lateral pterygoid muscles and digastric muscles

ceases. Correspondingly an activity in the medial pterygoid muscle is initiated .

This muscle controls the upward and lateral position of the jaw. The medial

pterygoid is much more active in wide strokes than in narrow chopping strokes,

and during early closing. The electromyographic activity ceases during the

intercuspal phase. However, during narrow strokes both the ipsilateral and the

contralateral medial pterygoid muscles are active at the onset of intercuspation. At

the beginning of the closing phase the ipsilateral temporal muscle contracts first,

and thereafter the contralateral temporal muscle and both masseter muscles

become active simultaneously. The electromyographic activity in these muscles is

very low, but it gradually increases and reaches a peak at the end of the closing

movement during the occlusal level phase. (Soboleva et al, 2005)

During the ingestion and mastication of a piece of hard food, the cyclical

EMG activity in the jaw closing muscles generally decreases with the progressive

comminution and softening of a single small piece of food. The force generated

by the jaw muscles depends on the food consistency. (Thexton, 1992)

Perioral facial muscles, such as the buccinator, the superior and inferior

orbicularis oris, the triangularis and the inferior quadratus labii muscles are active

during normal mastication. Their activity is predominant during the period in

which the mandible is lowered, is out of phase with that of the master muscle, and

overlaps in part with that of the digastric muscle. The activity starts in the first

part of the opening phase of the chewing cycle, and terminates in the closing

phase, before the masseter activity leading to the clenching phase reaches its peak.

(Soboleva et al, 2005)

Electromyographic records taken before the loss of posterior teeth, after

the loss of posterior teeth with only anterior teeth present, and after insertion of

dentures following the loss of posterior teeth, show that the facial and circumoral

muscles become very active in mastication, whereas there is minimal masseter

activity. Normal muscle activity resumes following insertion of well-fitting

dentures. (Soboleva et al, 2005)

26

Besides the masticatory muscles, a number of head and neck muscles

actively and passively participate in the act of mastication, and a muscle activity is

always guided toward the optimum functional result. (Ash et al, 1995)

2.3.4 Masticatory Function In Individuals With Temporomandibular

Disorders

It has been suggested that the observation of masticatory movements may

be of diagnostic value for assessing disorders of the stomatognathic system.

Many authors reported that certain aspects of the chewing patterns of

temporomandibular disorders (TMD) patients were different from controls. On the

contrary, were not able to show significant differences in chewing movements

between small groups of healthy subjects and TMD-patients. Specific chewing

patterns appeared to be associated with specific TMJ disorders. Yet, the chewing

movements of patients with myofascial pain had the same pattern as healthy

subjects. Thus, people with pain in the masticatory muscles or with joint sounds

may have normal mandibular range of movement. There is no strong evidence

that any particular chewing feature is charactiristic of TMD-patients. (Soboleva et

al, 2005)

2.4 Reatainer (Removable Orthodonthic)

Orthodontic is that specific area of the dental profession that has as its

responbility the study and supervision of the growth and development of the

dentition and is related anatomical structures from birth to dental

maturity,including all preventive and corrective procedure of dental irregularities

requiring the repositioning of teeth by functional and mechanical means to

establish normal occlusion and pleasing facial contours. There are two types of

orthodontic removable and fixed orthodontic (Gurkeerat Singh,2007).

Removable orthodontics are used for patients who have mild cases or the

lower jaw abnormalities are minimal, so the disorder is experienced not only the

teeth involves abnormalities of the jaw. Principles of tooth movement by means of

a removable orthodontics are pushing the teeth into an empty place bit by bit

using a flexible stainless steel wire (Gurkeerat Singh,2007).

27

Wire that is placed on the teeth can not move because they sit on a wire

edge pedestal or base transparent pink or attached to the surface of the

gums.[1]Pedestal or base is mounted on the surface of the tongue on the teeth

facing down and the base of the maxilla covering the surface of the palate.

Orthodontics removable appliance can be used within a certain timeframe. If it is

found good results, the patient is not obliged to wear it again. In fact, it is

recommended to stop using it (Hamamci et al, 2008)

Removable orthodontic appliance wearers are generally used for class 1

malocclusion with limited types, which has been discussed in previous chapters.

Because the movement of the tool tends to be skewed a removable ortho (tipping)

that have removable ortho appliance pull lightly but optimal. The desired

movement is the movement of the entire tooth, including akarya.

Ortho removable appliance is also an alternative for patients who have not been

able to properly care for their teeth. Ortho tool easily removed and installed again,

making it easier for patients to brush their teeth thoroughly.

Although practical, removable orthodontics tool also has some

disadvantages, namely, the tool can only move ortho removable tilting / tipping

and only focus on the crown of teeth, tooth loss is not on the whole the teeth and

their roots. The second drawback for such a device could be removed by the

patient whenever he wanted, and patients who do not obey the rules then ortho

treatment be stopped, and would create additional problems for further treatment.

If patients are reluctant to use this removable appliance orthodontics, that

sometimes is used sometimes not. Could result in the slow movement of teeth to

be so regular. For example, if the tooth is already running, but the removable

orthodontics dental appliance will return to its original place. If the patient wear it

again so there is pressure, bone resorption occurs in the direction of pressure, not

yet formed bone in the back, re-used tool.

Force required to produce a simple tipping movements in single-rooted teeth in

one region of between 30-50 grams, with the lowest limit of 20 grams. If it is

lower than that, the tooth movement is not going to happen. If the tensile strength

is too large, there will be a contraction in the body that will lead to bleeding gums.

28

While the destruction of the bone below it occurs slowly, resulting in the

formation of new tooth will also cause teeth to slow the excessive rocking. For the

use of a removable orthodontics should be diligent in control, so that optimum

strength and constant pull. You can not ask the doctor to give a big attraction for

some time could not control. It is too risky.

2.4.1 Problems Faced In Removable Orthodontic Care.

The dentist has a tremendous responsibility to the success of the treatment

because she is choosing cases, treatment plan, and manage care mendsain devices.

In managed care, likelihood of success is influenced treatment three interrelated

things:

1. Patient

2. Device

3. Movement of teeth

2.4.1.1 Patient

Change in patients, such as milk teeth or permanent teeth on the eruption that

could cause the device does not fit anymore. Some patients do not want to wear

the device as required. If the patient does not want to wear the device state can be

observed are: The device still looks like new, still shiny acrylic plate,Unskilled-

patient look like install devices

-The device does not match

-There is no elevation of bite marks on anterior occlusion

Some patients pay less attention to oral hygiene so that his teeth are less

clear and may present chronic gingivitis marginalis. Sometimes it goes gingival

inflammation and gingival thickening occurs. plaque can also occur on the acrylic

plate attached to the mucosa. When this situation happens then you need to do is

to improve oral hygiene and the cleaning device is used. If things like this still

happens the patient is advised not to wear the device a few days in a row.

Thickening of the palatal gingival retraction is often found at the upper anterior

teeth, if there is a narrow space between the teeth and plate akriik, saa lower teeth

29

will be in contact with the elevation of the anterior bite. Lower anterior teeth

beroklusi with anterior bite that causes the elevation of the acrylic plate rocking

and happening hyperplastic gingivitis. Tend to accumulate into the palatal mucosa

due to the palatal teeth pulled ( Choi et al, 2008).

To reduce this need to be examined whether the elevation gigitann been

honed enough and good enough if the retention device that can hold the device in

order not to move at the time the patient beroklusi. Reduction should be

performed prior to retract overlapping teeth to bite on.

The use of removable devices will add to the stagnation that will lead to

the possibility of caries. This situation can be overcome by keeping the mouth

kebersihal as possible. Areas prone to dental caries is a closed surface elevation of

both anterior and posterior bite. Routine dental examination should be done to

prevent caries (Hamamci et al, 2008).

2.4.1.2. Device

Before the device to be adjusted or turned, keep in mind the state of

various components of a removable perranti namely: retention, the active

component and the acrylic plate. Be aware when the device is worn continuously

distortion can occur.

Retention components need to be examined as possible after use for some

time because the device can be somewhat mendendor removed and installed.

When the device is less retentive, retentive components need to be adjusted. Do

not make adjustments retentive component as a routine action because this action

will cause the device to lose power when adjustments excessive retentifnya

Active components need to be examined, for example, the contact springs

or other active components of the tooth. Necessary adjustments if the suspected

tooth is not moving in the direction desired. For accurate measurements can be

used tension gauge. Widely used way is to directly estimate the deflection of the

spring (Bhalaji, 2004).

Check the acrylic plate is used to move teeth; when dental acrylic plates

can be blocked digrinda. When the bold elevation to a good bite to relieve

obstruction and to reduce overlap of occlusal bite, the addition of cold-cured

30

acrylic needs to be done. Acrylic palatal plate next to the upper anterior teeth is

not enough to cause terjepitnyadigrinda mucosa between teeth and the acrylic

plate at the upper anterior teeth retraction Planned intraoral anchorage when

designing devices. If anchoring is less likely needs to be supplemented with

extraoral anchorage. If it appears there was loss of anchorage and extraoral

anchorage necessary adjustments when necessary, use (Choi et al, 2008)

2.4.1.3. Movement Teeth

General assumption is acceptable tooth movement of 1 mm per month

when the device is used continuously. When the device is not used continuously

tooth movement will also be slower.

although the device has been used continuously but sometimes the tooth

movement is not as expected due to several things, namely: Wrong-way

movement. Usually caused by incorrect placement of the spring, especially the

contact between the teeth gelgi and spring arm. It should be noted at the time of

activation to make adjustments to the location where the spring is still possible. If

not possible then the spring should be replaced.

Excessive tipping movements. Removable devices produced by a tipping

movement as fulcrum is located approximately one third of the root. Use of

excessive force and away from the edge of the gingiva causes the fulcrum shifted

toward the crown. The most important state for diperhatikanadalah original tooth

inclination. When the location of the original tooth was not beneficial, excessive

tipping movement and a less favorable occlusion will easily occur.

-Loss of anchorage. Is one cause of failure of orthodontic treatment. Examination

required anchorage at each visit. Anchoring the teeth in order not to move to the

mesial necessary measures such as teeth move as little as possible at one time or a

quadrant. Excessive force will cause the teeth to move into the mesial anchoring.

Buccal spring of 0.7 mm wire will give great strength and causes loss of

anchorage(Hamamci et al , 2008)

31

2.5 Premature Contact

Premature contact is a symptom felt by Temporo Mandibular Joint or TMJ

disorder sufferer. The imbalance of occlusion occurs when teeth are in contact

prior to a certain region of the amount is less than 50% of the number of teeth in

the region or one or two teeth in contact in advance. When resistance occurs at

centric occlusion is called premature contact. Based on kamus kedokteran gigi

book, premature contact is an early contact that caused the deviation on the

closure of the jaw (Laksitowati and Rina Hestu, 2009).

If there is premature contact between one of the teeth, then shift the contact

would be not smoothly. These conditions caused several effects, are:

2.5.1 Direct effect

Premature contact would cause trauma that called secondary occlusal

trauma.Trauma is caused by premature occlusal force called jiggling forces.

Jiggling forces are intermittent power in two different directions which causes

dilation of the alveoli and increased mobility. Jiggling forces could increase.

When occlusal pressure increases, the effect of pressure will be received directly

by the involved teeth. In general, if there is attrition periodontium remains healthy

tissue, but a number of cases shows that although the attrition occurred, there

remains the periodontium tissue damage, especially if there are local irritants,

such as plaque which, according to some experts this is related to the formation of

infraboni pocket (Wiriadidjaja, 2007).

2.5.2 Indirect effect

Direction of the shift which depends on the end closure centric cusp

inclination involved. Premature contacts on mesial inclination that leads to the

upper cusp would result in a shift to the front. In many cases the shift may occur

either forward, backward or sideways. If the next shift occlusal, dental insisif on

the subject of increasing horizontal load. But if the shift to the back, TMJ would

receive pressure (Wiriadidjaja, 2007)

32

Figure 2.11 Premature contact on anterior teeth (Wiriadidjaja, 2007)

Figure 2.12 Premature contact on posterior teeth (Wiriadidjaja, 2007)

Effect on premature contact are,

1. Tooth that lost contact causes impaction of food.

The food will be stuck because can not affordable by the teeth.

2. Decrease periodontal tissue health.

Tissue surrounding the teeth and serves as buffer gear, consisting of

the gingiva, cementum, periodontal ligaments and alveolar bone.

3. Occurance interstitial caries.

Caries which start from mesial or distal side, usually near at the

contact point.

In many cases, the patient unconsciously adjust the closure of the abnormal

pathway to avoid premature contact, in this case not only the teeth but the

pressure of the nerves and muscles to change the muscle tension may occur

(Aryanti, 2007).

33

If there is premature contact between one of the teeth, then shift the contact

would be not smoothly and will probably make the mandible must deviate from

the normal pattern of movement, so that the final position reached will also

diverge from normal. If the deviation were long then the position of the end of the

condyles right and left would be an asymmetry that is followed by its articular

disc. This can lead to dysfunction of the mandible and articulations temporo-

muscles that cause pain spasms. And the premature contact puts extra stress on

chewing muscles, causing them to go into spasms, which cause pain and more

spasms (Laksitowati and Rina Hestu, 2009).

Based on TMJ Association journal, people with bad occlusions are no more

prone to TMJ than people with the good occlusions. The fact is, some people with

good occlusions get TMJ and some people who have a severe malocclusion never

develop TMJ. In addition, there is a wide variation of normal occlusion.

2.6 Definition of Myospasm ( Muscle Spasm )

Muscle tissue at the trigger point area, tendon adhesions, often perceived

as a link that will produce pain. But, presumably due to the nerve endings in

muscles sensitized by a substance that produces hypersensitive zone (Dhanrajani

and Jonaidel, 2002).

Perhaps an increase in local temperature in the area trigger point,

suggesting an increase in metabolic demand, reduction of blood flow, or both.

Trigger point is a region where there are few parts of the contract. If all the motor

units to contract, will occur muscle shortening. This condition is called a muscle

spasm (Dhanrajani and Jonaidel, 2002).

2.6.1 Factors That Causing Myospasm

Muscles of mastication hypersensitivity

Psychological factors ( emotional stress )

Hyperactivity of the muscles of mastication

Other factors such as, grind teeth, often too wide yawn, chew on one side

34

2.6.2 Effect Of Myospasme

Pain and pain in the face

Limited opening of the oral cavity

Abnormalities of the TMJ

Changes in muscle function of mastication

2.6.3 Muscle Pain

The sensation of muscle pain is usually the result of activation of

polymodal muscle nociceptors; groups III and IV, functionally and anatomically

equivalent to Ad and C fibres, respectively. These fibres have a high stimulation

threshold and, under normal conditions, are therefore not activated to physiologic

movement or normal muscle stretch. However, muscle nociceptors may be

sensitized by peripherally released neuropeptides that increase their response to

suprathreshold stimuli and may induce long-term changes in the central nervous

system, such as central sensitization (Mense 2003). Damage to individual muscle

cells releases sufficient intracellular adenosine triphosphate to activate purinergic

receptors and induce pain (Dommerholt, 2006)

However, there are subgroups of patients with muscle pain such as in

fibromyalgia where pain may not be dependent on any peripheral input. Indeed as

discussed below pain can occur secondary to a dysfunctional descending

antinociceptive system or overactive descending facilitatory system, or due to a

loss of central inhibitory neurons (Dommerholt, 2006).

Figure 2.13 The integrated trigger point hypothesis. Ach- acetylcholine; AchE-acetylcholinesterase; AchRacetylcholine receptor (Dommerholt, 2006).

35

Figure 2.15 The expanded MTrP hypothesis. Ach- acetylcholine; AchE- acetylcholinesterase;AchRacetylcholine receptor; ATP-adenosine triphosphate; SP- substance P; CGRP- calcitonin

gene-related peptide; MEPP- miniature endplate potential (Fields and Martin, 2005)

2.6.3.1 Psychological Factor

Figure 2.16 Psychological factor because of emotional stress (Rantala, 2010).

2.6.4 Role of occlusion in facial pain

Although the significance of occlusal interferences in the etiology of TMD

has been questioned ( De Boever et al. 2000 ), the findings of the present study

suggest an association between posterior tooth interferences and facial pain. In the

clinical examination included in the case-control study, an association between

36

PTR interferences and facial pain, and in the patient sample, a correlation between

severe MTR interferences and masticatory muscle pain on palpation, was found.

These findings support the finding of Kerstein and Farrell ( 1990 ), who found a

link between the length of time that posterior teeth disclude and masticatory

muscle contraction levels. PTR interferences have also been reported by

Williamson and Lundquist ( 1983 ) to sustain a high level of muscle activity by

diminishing the rest period for muscular recovery between contractions. In

addition, complete anterior guidance in order to reduce the disclusion time has

been described by Kerstein and Farrell ( 1990 ) as a successful method of

lessening muscle activity in the masseter and temporalis muscles, and of reducing

chronic pain symptoms. Additionally, experimental occlusal interferences have

been reported to cause changes in the myoelectric contraction pattern of the

muscles of the mandible and, at least in short term, to increase signs and

symptoms of TMD ( Christensen & Rassouli, 1995 ).

An interesting point of view was the relation of reported ”lower jaw

clearly backward” to facial pain, according to the computer-aided questionnaire.

Although understanding and interpreting these kinds of questions may cause a

large spectrum of variations and make the diagnostic significance questionable,

the result may suggest a correlation of type Angle II-malocclusion with facial

pain. This connection has been suggested by clinical studies of Raustia et al.

(1995b) and Henrikson et al. (2000), although in a population-based study of Kitai

et al. (1997) no correlation between malocclusions and TMD symptoms was

found. In any case, no conclusions of the association can be drawn based on the

questionnaire, and additional examinations are needed to clarify the connection in

the cohort sample.

Muscle tissue at the trigger point area, tendon adhesions, often perceived

as a link that will produce pain. But, presumably due to the nerve endings in

muscles sensitized by a substance that produces hypersensitive zone. Perhaps an

increase in local temperature in the area trigger point, suggesting an increase in

metabolic demand, reduction of blood flow, or both. Trigger point is a region

where there are few parts of the contract. If all the motor units to contract, will

37

occur muscle shortening. This condition is called a muscle spasm (Henrikson et

al. (2000).

2.6.5 Nervous System Alterations in TMD

There have been numerous studies documenting neurophysiological

characteristics of TMD patients. Unfortunately many of these did not differentiate

between muscular and joint-based aetiologies so that their usefulness is extremely

limited. Moreover, most of these studies have been inconclusive and have largely

been replaced by quantitative sensory testing and functional studies of the sensory

system (Guy, 2009).

QST studies frequently reveal abnormal somatosensory processing in

TMD patients. Large myelinated fibre hypersensitivity was shown in the skin

overlying TMJs in patients with clinical pain and TMJ pathology (Eliav et al

2003). However, patients with MMP demonstrated superficial (skin) large

myelinated nerve fibre hyposensitivity (Eliav et al 2003). Similarly, MMP patients

show higher detection, discomfort and pain thresholds (decreased sensitivity) to

stimuli applied to the skin over the masseter muscle (Hagberg et al 1990). Within

the patient group, those with the greatest spontaneous pain had the lowest

threshold values. Tonic muscular pain has been shown to induce an elevation of

detection threshold to graded monofilaments both in the affected and in the

contralateral side, suggesting involvement of central mechanisms (Stohler et al

2001). Impaired vibrotactile function and discrimination from the skin overlying

muscles in MMP patients has been shown (Hollins and Sigurdsson 1998).

In contrast, lowered pressure-pain thresholds in deep tissues have been

consistently reported in MMP patients, suggesting peripheral sensitization of

muscle nociceptors (Hedenberg-Magnusson et al 1997; Maixner et al 1998;

Svensson et al 2001). What exactly activates the peripheral muscle nociceptor and

induces muscle hyperalgesia is unclear. Stimuli may include peripheral chemical

or mechanical agents and trigger point activity (see below) in addition to reactive

or even primary central mechanisms that may lead, for example, to neurogenic

inflammation (Svensson and Graven-Nielsen 2001). Experimental inflammatory

conditions of the TMJ and pericranial muscles lead to changes classically

38

associated with central sensitization which can be reversed with central delivery

of N-methyl-D-aspartate (NMDA) antagonists (Sessle 1999). These findings

implicate central neuroplasticity in initiating and maintaining chronic muscle pain.

Altered pain regulation is suggested by findings of significantly more prevalent

generalized body pain (e.g. fibromyalgia and back pain) and headache in TMD

patients (John et al 2003). In support of this theory, TMD patients exhibit lower

pain thresholds, greater temporal summation of mechanically and thermally

evoked pain, stronger aftersensations and multisite hyperalgesia (Maixner et al

1998; Sarlani et al 2004). These indicate generalized hyperexcitability of the

central nervous system and generalized upregulation of nociceptive processing

(decreased inhibition or increased facilitation) and have been suggested as

important pathophysiologic mechanisms (Sarlani et al 2004). In support of this

hypothesis, pain from TMDs was not attenuated after peripheral noxious stimuli

(ischaemic tourniquet test), which would normally activate noxious inhibitory

modulation, suggesting differential or faulty recruitment of inhibitory controls

(Maixner et al 1995). The response of MMP patients to experimental ischaemic

pain was subsequently shown to also depend on depression and somatization

scores (Sherman et al 2004). This suggests a complex interaction between

psychosocial and biological variables in TMD patients.

Patients with TMD show enhanced C-fibre-mediated temporal summation

to thermal stimuli applied to either the face or the forearm compared to control

subjects and have impaired ability to discriminate stimulus frequency (Maixner et

al 1998). These findings further suggest a component of central hyperexcitability

which contributes to the enhanced pain sensitivity observed in TMD patients. In

clinical studies about two-thirds of facial pain patients report widespread pain

outside the craniocervical region (Turp et al 1998). However, no generalized

hypersensitivity in MMP patients has been shown in other experiments (Carlson

et al 1998). Thus although some cases of MMP have multisite hyperalgesia, others

do not a situation reflected in clinical experience. This may suggest two clinical

and possibly therapeutic subtypes of MMP: with or without extracranial muscle

involvement. Alternatively multisite hyperalgesia may be a graded, time-

dependent phenomenon (Svensson and Graven-Nielsen 2001), and indeed

39

experimental studies show that somatosensory sensitivity develops in the presence

of experimental jaw muscle pain (Svensson et al 1998a).

2.6.6 Trigger Points, Muscle Hypoperfusion and Muscle Pain

Myofascial pain syndrome whether in the facial area, head or other body

parts is often characterized by the presence of trigger points (Gerwin et al 2004;

Simons 2004). It is thought that muscular pain arises from trigger points and

indeed in many MMP patients pressure on a trigger point will activate intense

pain and induce referral to characteristic sites. The muscle around a trigger point

(TrP) is usually hard and may be nodular or appear as a taut band. Data suggest

that TrPs are found in the area of the neuromuscular junction at the motor

endplate and that these are tonically active, resulting in localized contraction that

together with adjacent active endplates contributes to the formation of the taut

band or nodule (Gerwin et al 2004).

The continuous electrophysiological activity of motor endplates is

secondary to unchecked release of acetylcholine. Endplate activity or noise is

significantly more common in myofascial pain patients than in controls.

Continued contraction in the area of TrPs leads to localized hypoxia

(hypoperfusion), lowered pH and the accumulation of proinflammatory mediators

(Simons 2004; Shah et al 2005). Lowered pH increases the activity of peripheral

receptors including the vanilloid receptor, further sensitizing muscle nociceptors

(Mense 2003). This localized contraction in TrPs is not, however, associated with

generalized muscle hyperactivity so this should not be confused with the

hyperactivity theory discussed below. The appearance of active TrPs is thought to

be related to muscle trauma particularly eccentric muscle lengthening during

contraction (Gerwin et al 2004). However, experiments directed at inducing such

damage have largely been inconclusive.

It has been suggested that muscle hypoperfusion maybe the primary factor

in initiating muscle pain, possibly due to changes in sympathetic control

(Maekawa et al 2002). Moreover the unchecked motor endplate activity described

above develops sensitivity to sympathetic nervous system activity (Gerwin et al

2004).

40

2.6.7 Treatment or Management Of Myospasm

Treatment of myospasm varies depending on the aetiological factor. Some

difficulty in opening the jaw on the day following dental treatment in which a

superior alveolar or inferior alveolar nerve block was administered is frequently

encountered. The degree of discomfort and dysfunction varies, but is usually mild.

When a patient reports mild pain and dysfunction, an appointment for

examination should be arranged (Holdcroft, 2003). In the interim, the practitioner

should prescribe the following:

heat therapy;

analgesics;

a soft diet; and (if necessary)

muscle relaxants

To manage the initial phase of muscle myospasm. Heat therapy consists of

placing moist hot towels on the affected area for 15–20 minutes every hour.

Aspirin is usually adequate in managing the pain associated with myospasm; its

anti inflammatory properties are also beneficial. A narcotic analgesic may be

required if the discomfort is more intense. If necessary, diazepam (2.5–5mg three

times daily) or other benzodiazepine may be prescribed for muscle relaxation.

When the acute phase is over the patient should be advised to initiate

physiotherapy for opening and closing the jaws and to perform lateral excursions

of the mandible for 5 minutes every 3–4 hours. Sugarless chewing gum is another

means of providing lateral movement of the TMJ. Any trauma or event that may

be suspected of having triggered the TMD should be recorded in the patient’s

dental record, as should the findings and the treatment. Further dental treatment in

the involved region should be avoided until symptoms resolve and the patientis

more comfortable (Holdcroft, 2003).

2.7 Estrogen

2.7.1 Definition

Estrogens (AmE), oestrogens (BE), or œstrogens, are a group of steroid

compounds, named for their importance in the estrous cycle, and functioning as

41

the primary female sex hormone, their name comes from estrus/oistros (period of

fertility for female mammals) + gen/gonos = to generate (Nussey S 2001).

Estrogens are found in all vertebrates. Studies have shown that insects

make use of the steroids estradiol and estriol, which are androgen and estrogen-

like substances. These steroids suggest that vertebrate sex hormones have an

ancient evolutionary history(Nussey S 2001).

Estrogens are used as part of some oral contraceptives, in estrogen

replacement therapy for postmenopausal women, and in hormone replacement

therapy for trans women (Nussey S, 2001).

Like all steroid hormones, estrogens readily diffuse across the cell

membrane. Once inside the cell, they bind to and activate estrogen receptors

which in turn up-regulate the expression of many genes (Nussey S, 2001).

Additionally, estrogens have been shown to activate a G protein-coupled receptor,

GPR30 (Sklar, et al 2007).

Estrogens are produced primarily by developing follicles in the ovaries,

the corpus luteum, and the placenta. Luteinizing hormone (LH) stimulates the

production of estrogen in the ovaries. Some estrogens are also produced in smaller

amounts by other tissues such as the liver, adrenal glands, and the breasts. These

secondary sources of estrogens are especially important in postmenopausal

women. Fat cells also produce estrogen, potentially being the reason why

underweight or overweight are risk factors for infertility (Sklar, et al 2007).

In females, synthesis of estrogens starts in theca interna cells in the ovary,

by the synthesis of androstenedione from cholesterol. Androstenedione is a

substance of moderate androgenic activity. This compound crosses the basal

membrane into the surrounding granulosa cells, where it is converted to estrone or

estradiol, either immediately or through testosterone. The conversion of

testosterone to estradiol, and of androstenedione to estrone, is catalyzed by the

enzyme aromatase. Estradiol levels vary through the menstrual cycle, with levels

highest just before ovulation (Tata, 2005).

42

2.7.2 Types of estrogen

2.7.2.1 Steroidal

The three major naturally occurring estrogens in women are estrone (E1),

estradiol (E2), and estriol (E3). Estradiol (E2) is the predominant form in

nonpregnant females, estrone is produced during menopause, and estriol is the

primary estrogen of pregnancy. In the body these are all produced from androgens

through actions of enzymes ( Nelson 2001).

a) From menarche to menopause the primary estrogen is 17β-

estradiol. In postmenopausal women more estrone is present than

estradiol.

b) Estradiol is produced from testosterone and estrone from

androstenedione by aromatase.

c) Estrone is weaker than estradiol (Sheehan et,all 2001).

2.7.2.2 Nonsteroidal

A range of synthetic and natural substances have been identified that also

possess estrogenic activity ( Nelson 2001).

a) Synthetic substances of this kind are known as xenoestrogens.

b) Plant products with estrogenic activity are called phytoestrogens.

c) Those produced by fungi are known as mycoestrogens (Sheehan

et,all 2001).

Unlike estrogens produced by mammals, these substances are not

necessarily steroids

2.7.3.Estrogen functions

While estrogens are present in both men and women, they are usually

present at significantly higher levels in women of reproductive age. They promote

the development of female secondary sex characteristics, such as breasts, and are

also involved in the thickening of the endometrium and other aspects of regulating

the menstrual cycle. In males estrogen regulates certain functions of the

reproductive system important to the maturation of sperm (Sklar, et al 2007) and

may be necessary for a healthy libido (Nussey S 2001). Estradiol levels vary

43

through the menstrual cycle, with levels highest just before ovulation. More

specific function are :

a) promote formation of female secondary sex characteristics

b) stimulate endometrial growth

c) increase uterine growth

d) maintenance of vessel and skin

e) reduce bone resorption, increase bone formation

f) increase hepatic production of binding proteins

g) increase circulating level of factors 2,7,9,10, antithrombin III,

plasminogen

h) increase platelet adhesiveness

i) increase HDL, triglyceride, fat depositition

j) decrease LDL (Nussey S 2001).

In studies involving mice and rats, it was found that lung function may be

improved by estrogen. In one study involving 16 animals, female mice that had

their ovaries removed to deprive them of estrogen lost 45 percent of their working

alveoli from their lungs. Upon receiving estrogen, the mice recovered full lung

function (ASRM, 2009).

2.7.4 Estrogen effect on bone metabolism

It is well known that estrogen is essential for healthy bone, and that when

the production of estrogen is reduced, as occurs normally in postmenopausal

women and pathogenically after exposure to radiation or chemotherapeutic drugs,

bones become brittle and break easily. However, the mechanisms involved aren't

clearly understood. The new study found that one way estradiol helps to maintain

bone density is by stopping the activation of an enzyme known as caspase-3. Also

called the executioner caspase, caspase-3 is the central player in initiating the

process of apoptosis, or programmed cell death of osteoblasts, the bone cells that

aid in the growth and development of new bone and teeth. Results of the study

will be presented at the International Association of Dental Research meeting in

New Orleans. Peter G. Bradford, Ph.D., said of the results: "Basic and clinical

studies have shown that estrogens can prevent both bone loss and reduce the

44

incidence of bone fractures. this protective effect of estrogens involves the

prevention of apoptosis in osteoblasts and that the key event in this prevention is

the inhibition of caspase-3 activity." .To determine the effect of estradiol on

caspase-3 activity, one group of human osteoblasts was treated with estradiol for

24 hours and another group was not. Both groups then were exposed for 24 hours

to a drug called etoposide, a cancer chemotherapeutic drug that promotes

apoptosis.Results showed that caspace-3 activity decreased in cells treated with

estrogen, but increased in cells not treated with estrogen. Anti-osteoporotic effects

of estradiol may result in part from its anti-apoptotic effects on osteoblasts

(Bradford 2005).

2.7.5 Estrogen Effect on Temporo mandibular joint

Temporomandibular muscle and joint disorders (TMJD) are the most

common cause of chronic pain in the orofacial region (Dworkin et al, 2002) The

prime manifestations of these disorders are disc displacement with clicking or

crepitus sounds produced during mandibular function and persistent, recurring, or

chronic pain in the temporomandibular joint (TMJ). Epidemiologic data

consistently have shown that women are at greater risk for TMD compared with

men (Dworkin et al, 2002), though the reasons for this female predominance have

not been determined. Interestingly, women experience more inflammation, facial

pain, and tenderness in jaw muscle and temporomandibular joint then

men.(Warren & Fried, 2001) Some evidence suggests that increased inflammatory

response can lead to loss of the articular cartilage. Therefore, sex differences in

inflammation may also explain the higher prevalence of TMD among women

(Warren & Fried, 2001). Moreover, other inflammatory diseases such as

osteoarthritis and rheumatoid arthritis are also more prevalent among women than

men (Akkus, et al 2004). However, sex differences in pain processing may also

play a role, since abundant evidence demonstrates that women display greater

sensitivity to experimental pain than men (fillingin,2000). These sex differences

in both inflammation and pain sensitivity could be driven by common underlying

mechanisms, such as the influence of gonadal hormones. That TMD is equally

prevalent before puberty and that the higher prevalence of TMD in females

45

emerges in young adulthood (Warren & Fried, 2001) may implicate sex hormones

in the pathophysiology of this condition.

In particular, ERα was found in the articular cartilage and subchondral

bone of TMJ which implies that estrogen directly acted on the cells in the TMJ

tissue to alter the gene expression and cellular physiology (Kang, et al, 2007) In

addition ER knockout studies have shown a major role for ERα in immune

modulation (kubota, et al , 1998). Because ERα is present in the immune cells in

the human TMJ ,a likely target of 17 β-estradiol in the human TMJ is ERα-

positive immune cell (Kang, et al, 2007). Furthermore ER-α gene polymorphisms

is associated with a predisposition to TMJ disorders (LeResche,1997). Such data

from both animal and clinical studies support a significant role of ERα in the

increased incidence of TMJ inflammation

Steroid hormones, particularly estrogen, act through their receptors

(estrogen receptor-α [Erα] and estrogen receptor-β [ERβ]) in the periphery as well

as the central nervous system (CNS), producing effects on the inflammatory

process as well as on central pain transmission (Laflamme,1997). For example,

estrogen can directly act on monocytes and macrophages to regulate the

production of cytokines (eg, interleukin-1 [IL-1], IL-6, and tumor necrosis factor-

α [TNF-α]).(Massart,2001) The cytokines IL-1β and IL-6 are present in the TMJ

synovium during inflammation, and IL-1 and TNF-α promote cartilage

reabsorption, inhibit synthesis of proteoglycans, and promote inflammation in the

majority of TMD structures (Kubota, et al , 1998). Additionally,

monocytes/macrophages are the immune cells present within the synovial tissues

and are also frequently recruited in synovial inflammation, suggesting that a

majority of IL-1 and TNF-α released within the joint may originate from those

immune cells (Henderson,1985). Finally, TMJD, especially when associated with

acute trauma, internal derangements, or osteoarthritis, often includes an

inflammatory component (Kopp, 1998). Therefore, estrogen as well other sex

hormones can play an important role in pain severity and TMJD predisposition.

As a result, a genetic variation at the ERα could lead to significant modifications

in the physiological role of estrogen and consequently in TMJ derangements.

46

2.7.6. Estrogen as an Antidepressant for Women

Estrogen has antidepressant actions in perimenopausal women. Estrogen

may also have antidepressant actions in postpartum women and across the life

cycle for women who are resistant to treatment with various antidepressants

(Schmidt, 2000). The question, however, of which depressed women to treat with

antidepressants, which with estrogen, and which with both remains unanswered.

Estrogen has long been suspected to be linked to depression in women

(Sthal, 2007). A critical observation is that the incidence of depression somewhat

mirrors shifts in estrogen across a woman's life cycle . Thus, the risk for

depression is higher in women when shifts in estrogen levels are large, beginning

especially after estrogen levels rise during puberty, after estrogen levels fall

immediately postpartum, and while estrogen levels fluctuate in a declining

manner during perimenopause (Schmidt, 2000).

By contrast, depression is not closely linked to testosterone levels in men,

since the incidence of depression is essentially constant after puberty, but

testosterone levels decline steadily after age 25 (Sthal, 2007).

Despite observations that estrogen can cause depression in some women,

especially at high doses and when administered as oral contraceptives

concomitantly with estrogen antagonist progestins, it has long been recognized

that estrogen replacement therapy generally reduces mood fluctuations in

perimenopausal women who have vasomotor instability (Jensvold, 1996).On the

other hand, such women do not generally suffer from a major depressive disorder

(MDD). Until recently, it has been unclear from clinical trials whether physiologic

doses of natural estrogens such as 17beta-estradiol showed any antidepressant

properties in women with MDD (Cohen, 2001).

Clinicians, on the other hand, have observed, anecdotally and in open

studies of small numbers of patients, that estrogen apparently exerts

antidepressant actions as a monotherapy when administered to some women who

have MDD both in the postpartum period and during perimenopause (Schmidt,

2000). It is somewhat astounding that controlled clinical trials of estrogen for

depressed women across their life cycle are only now being published, since not

47

only do women of child-bearing potential have the highest rates of depression, but

also women on the whole consume over 70% of antidepressants (Jensvold, 1996).

17beta-estradiol may indeed be an antidepressant for women with

depression during perimenopause, including women with MDD. In fact, estradiol

treatment was associated with a robust treatment effect, including complete

remission in the majority of patients studied (Cohen, 2001).

2.7.6.1 Types of estrogen as Antidepressant for Women With Depression

Just as there are a wide variety of antidepressants, there are a wide variety

of estrogens. Even though the 2 recent studies mentioned above (Jensvold, 1996).

were of 17beta-estradiol, the major circulating estrogen in women, many other

estrogens administered to women today have agonist actions upon CNS estrogen

receptors. This includes a mixture of estrogens extracted from the urine of

pregnant mare that contains estrone, equilin, and 17alpha-dihydroequilin, as well

as a new class of estrogen agonists known as SERMs (selective estrogen receptor

modulators), such as raloxiphene and others (Schmidt, 2000). Much further

research needs to be done to determine the potential antidepressant actions of

these estrogens, how they should be combined with antidepressants, and which

women are most likely to benefit. Hopefully, the new data emerging will rapidly

lead to the development of treatment guidelines so that new insights into the CNS

actions of estrogen can be applied in clinical practice (Cohen, 2001).

2.7.7 Estrogen as Pain reliever

Estrogen plays an important role in determining how sensitive a person is

to pain, and the estrogen receptor known as ER-beta is particularly significant in

this context (Sthal, 2007).

estrogen affects how we experience pain, but the mechanisms behind this

have been unclear. Estrogen can bind to two different receptors, known as ER-

alpha and ER-beta, and the new study describes results obtained concerning the

expression of these two receptors in the spinal cord (Cohen, 2001).

ER-beta plays an important role in the development of the part of the

spinal cord that contains nerve fibres that carry information to the brain. These

48

nerves are important in several functions, including determining how sensitive a

person is to pain, and response to sensation in general. ER-beta is the dominant

estrogen receptor during the development of the embryo. Estrogen as substances

that stimulate ER-beta can give pain relief", says Jan-Åke Gustafsson (Schmidt,

2000).

2.7.7.1. How to ease the joint pain

There are some way to relieve joint pain, starting with solving the

underlying cause. A few simple dietary changes, like reducing refined

carbohydrates and sugar, can make a dramatic difference to joints.Eating more

fruits and vegetables, which contain natural anti-inflammatories, and adding a

high-quality multivitamin to fill any nutritional gaps is recomended. An

elimination diet can help identify any food allergies or sensitivitie (almeida,et, al ,

2001).

High-quality omega-3 fatty acid supplement is recomended to ease the

inflamation. Essential fatty acids are very effective at fighting inflammation, but

it’s almost impossible to include sufficient omega-3’s in the average diet.

Omega-3 intake can be increased by eating fish, but be careful to choose smaller

species, like tilapia, that are low in mercury (Cohen, 2001).

Lifestyle changes like stress relief and moderate exercise can help regulate

cortisol levels and reduce your inflammatory burden. A gentle but regular exercise

program will also help you maintain a healthy weight and prevent excess wear on

your hips and knees (Schmidt, 2000).

For women whose joint pain is related to hormonal fluctuations,

phytotherapy can gently and effectively support hormonal balance and, for some,

help lessen joint pain (almeida,et.al , 2001).

49

CHAPTER 3

CONCEPTUAL MAPPING

result of

because oftrigger

TMJ Dissorder

Type Mylofacial pain

TMJGeneral

TMJ

Anatomy

Histology

Physiology

Pathology

Prevalency

>Women Men

Hormonalsystem

Over contraction andoverload pressure at

digestive muscle

Decrease ofEsterogen

Unfinished removeableorthodontic treatment

premature contact atprosterior tooth

Occlusion disharmony

Fatique on 3 digestive muscle

massetertemporalis Pterygoideus

medialis

Miospasme Inflamation At Trigger point(digestive muscle)

Symtoms : hard toopen the mouth

30 years oldWomen

50

CHAPTER 4

DISCUSSION

Removable orthodontics are used only in patients who have dental

problems mild abnormalities and are used for disorders of malocclusion class 1

but with limited types. Removable orthodontics are not associated with

abnormalities of the lower jaw is minimal. Produce a shift in the use of removable

dental orthodontics 1mm per month, and even then if the patient regularly in use.

The movement of the tool is really slow because only fill in the empty tooth and

just moving sideways or tipping.

In many cases, the patient unconsciously adjust the closure of the abnormal

pathway to avoid premature contact, in this case not only the teeth but the

pressure of the nerves and muscles to change the muscle tension may occur.

Also if there is premature contact between one of the teeth, then shift the

contact would be not smoothly and will probably make the mandible must deviate

from the normal pattern of movement, so that the final position reached will also

diverge from normal. If the deviation were long then the position of the end of the

condyles right and left would be an asymmetry that is followed by its articular

disc. This can lead to dysfunction of the mandible and articulations temporo-

muscles that cause pain spasms. And the premature contact puts extra stress on

chewing muscles, causing them to go into spasms, which cause pain and more

spasms.

Figure 2.17 Premature contact on prosterior teeth (Wiriadidjaja, 2007)

51

There are six main components of the TMJ , Mandibular condyles,

Articular surface of the temporal bone, Capsule,Articular disc, Ligaments , Lateral

pterygoid . The temporomandibular joint is the joint of the jaw and is frequently

referred to as TMJ. 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 few synovial joints in the human body with an articular

disc, another being the sternoclavicular joint .

The disc divides 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.

Figure 2.18 : The Mechanism of blocking mandibular (Dorland, 2012)

Miospasm or muscle spasms, which is involuntary contraction of a muscle

or group that occur suddenly, usually painful and can often lead to impaired

function. Devisiasi mandible when opening the mouth and various kinds of

interference or limitation of movement is an objective sign of miospasme. When

the musculus masseter and temporalis experienced spasms on one hand, the

52

opening movement of the mandible will be captured, and there will be deviation

of the mandible to the side of the seizure.

At the time of open and closed mouth chewing movements will arise Extra

pain. When the inferior lateral pterygoid musculus suffered acute spasms will

occur malocclusion, as indicated with malocclusion posterior teeth on the same

side as the musculus, and premature contacts occur anterior teeth on the opposite

side. Pain due to spasm of the lateral pterygoid is sometimes felt in the joint itself.

If there is spasm in the musculus masseter, temporalis, lateral pterygoid and

inferior musculus occur sequentially, either unilateral or bilateral, it may present

an acute malocclusion.

Temporo mandibular joint functional disorders are problems that arise

from a distorted because they function abnormalities in the position and function

of the teeth, or chewing muscles. A state of physiological or so-called

orthofunction the tolerance limits of each individual during a shift of the mandible

during mandibular shift without complaint give rise to muscle characterized by

the harmony between morphology and function of neuromuscular occlusion. The

term state is known as physiological tolerance zone. If there is any stimulus that

deviates from the usual due to occlusion of teeth that causes premature contact,

the response arising from a biological vary which is generally an adaptive

response or adaptation period.

Here, adaptive changes occur in tissues that are involved in an effort to

receive a stimulus such deviating example of adaptive change is occlusal surfaces

disorders of teeth, the onset of changes in the periodontal membrane, alveolar

local resorbtion. This occlusion period will run continuously until the limit of

physiological tolerance muscles or surrounding tissue has been exceeded. The

duration of this adaptation will take place between individuals who differ from

one another, and are affected by pathology. Once the limit is exceeded the

psychological suffered tissue response that is more pathological changes. Pain is

felt in the muscles of the mandibular movement, or they can be in the temporo

mandibular joint.

The fourth disorder is muscle contracture. Muscle contractur is a chronic

condition characterized by persistent shortening of the muscle. It can begin after

53

trauma, infection, or prolonged hypomobility. If the muscle is maintained in a

shortened state, muscular fibrosis and contracture may develop over several

months.

The fifth disorder is fibromyalgia. Fibromyalgia is a chronic condition that

causes pain, stiffness, and tenderness of the muscles, tendons, and joints.

Fibromyalgia is also characterized by restless sleep, awakening feeling tired,

chronic fatigue, anxiety, depression, and disturbances in bowel function.

Trismus is a motor disturbance of the trigeminal nerve, especially spasm of

the masticatory muscles, with difficulty in opening the mouth, a characteristic

early symptom of tetanus.

Cause of trismus seen in general practice is trauma of the zygomatic arch

and zygomaticomaxillary complex (ZMC), which interferes with the movement of

the coronoid process.

Fibromyalgia affects predominantly women (over 80% of those affected

are women) between the ages of 35 and 55. Less commonly, fibromyalgia can

also affect men, children, and the elderly. It can occur independently or can be

associated with another disease, such as systemic lupus or rheumatoid arthritis.

Epidemiologic data consistently have shown that women are at greater risk for

TMD compared with men, though the reasons for this female predominance have

not been determined. Interestingly, women experience more inflammation, facial

pain, and tenderness in jaw muscle and temporomandibular joint then men. Some

evidence suggests that increased inflammatory response can lead to loss of the

articular cartilage. Therefore, sex differences in inflammation may also explain

the higher prevalence of TMD among women. sex differences in pain processing

may also play a role, since abundant evidence demonstrates that women display

greater sensitivity to experimental pain than men.

Estrogen has antidepressant actions in perimenopausal women. Estrogen

may also have antidepressant actions in postpartum women and across the life

cycle for women who are resistant to treatment with various antidepressants.

Estrogen plays an important role in determining how sensitive a person is

to pain, and the estrogen receptor known as ER-beta is particularly significant in

this context. trogen affects how we experience pain, but the mechanisms behind

54

this have been unclear. Estrogen can bind to two different receptors, known as

ER-alpha and ER-beta, and the new study describes results obtained concerning

the expression of these two receptors in the spinal cord.

55

CHAPTER 5

CLOSING

5.1 Conclusion

Same as the hypothesis, that the unfinished removable orthodontic therapy

that cause premature contact due myospame can lead to temporomandibular

disorder type mylofacial pain.

5.2 Solution

In the case of temporomandibular disorder pain mylofacial type should

take precedence in the conventional and conservative treatment prior to return to

normal functioning, if it is severe can be taken any further action that leads to

surgery.

Prevention

To prevent temporomandibular (TM) disorders, try to reduce muscle

tension in your jaw. You can reduce muscle tension with these steps:

Relax.

Learn to recognize when you are clenching your teeth.

Practice keeping your teeth apart, bringing them together only when

swallowing or eating. When driving, avoid clenching the wheel with both

hands, because often your teeth will be clenched as well.

Do not overuse and stress your jaw muscles.

Avoid constantly chewing gum, biting your nails, resting your chin on

your hand, or cradling the telephone receiver between your shoulder and

jaw.

Change your diet.

Eat softer foods, and use both sides of your mouth to chew your food.

Avoid hard or chewy foods, such as popcorn, apples, carrots, taffy, hard

breads, and bagels.

56

Maintain good posture.

Poor posture may disturb the natural alignment of your facial bones and

muscles, causing pain.

Treatment

Treatments for TMD range from simple self-care practices and

conservative treatments to injections and surgery. Most experts agree that

treatment should begin with conservative, nonsurgical therapies first, with surgery

left as the last resort. Many of the treatments listed below often work best when

used in combination.

Basic Treatments for TMD

Some basic, conservative treatments for TMD include:

Apply moist heat or cold packs.

Eat soft foods.

Low-level laser therapy.

This is used to reduce the pain and inflammation, as well as increase range

of motion to the neck and in opening the mouth.

Wear a splint or night guard.

Splints and night guards are plastic mouthpieces that fit over the upper and

lower teeth. They prevent the upper and lower teeth from coming together,

lessening the effects of clenching or grinding the teeth.

Undergo corrective dental treatments.

Corrective treatments including replacing missing teeth and using crowns,

bridges, or braces to balance the biting surfaces of your teeth or to correct

a bite problem.

Take Pharmacologic Management

Nonsteroidal anti-inflammatory drug (NSAIDs)

Several studies have found a small benefit of NSAIDs for

management of pain in fibromyalgia if used in combination with

alprazolam, amitriptyline, or cyclobenzaprine. NSAIDs were

57

considered more effective than acetaminophen for pain

management by patients with fibromyalgia.

Tramadol

Tramadol is a combination of a weak opioid agonist and an

inhibitor of the reuptake of serotonin and norepinephrine in the

dorsal horn.

Antidepressants

Such as amitriptyline are effective for chronic tension-type

headache, fibromyalgia, and intractable pain syndromes associated

with muscle spasm.

Alpha-2 adrenergic agonists

The two major alpha-2 adrenergic agonists available for clinical

use are clonidine and tizanidine.

Botulinum toxin

Botulinum toxin type A is emerging as a promising but expensive

agent with efficacy in chronic MPS and chronic daily headache

Controversial Treatments for TMD

Transcutaneous electrical nerve stimulation (TENS).

This therapy uses low-level electrical currents to provide pain relief by

relaxing the jaw joint and facial muscles. This treatment can be done at the

dentist's office or at home.

Ultrasound.

Ultrasound treatment is deep heat that is applied to the TMJ to relieve

soreness or improve mobility.

Trigger-point injections.

Pain medication or anesthesia is injected into tender facial muscles called

"trigger points" to relieve pain.

Radio wave therapy.

Radio waves create a low level electrical stimulation to the joint, which

increases blood flow. The patient experiences relief of pain in the joint.

58

Surgery for TMD

Surgery for TMD should only be considered after all other treatment

options have been unsuccessful. There are three types of surgery for TMD:

arthrocentesis, arthroscopy, and open-joint surgery. The type of surgery needed

depends on the TMD problem.

Arthrocentesis.

The surgery involves inserting needles inside the affected joint and

washing out the joint with sterile fluids. Occasionally, the procedure may

involve inserting a blunt instrument inside of the joint. The instrument is

used in a sweeping motion to remove tissue adhesion bands and to

dislodge a disc that is stuck in front of the condyle.

Arthroscopy.

The surgeon makes a small incision in front of the ear and inserts a small,

thin instrument that contains a lens and light. This instrument is hooked up

to a video screen, allowing the surgeon to examine the TMJ and

surrounding area. Depending on the cause of the TMD, the surgeon may

remove inflamed tissue or realign the disc or condyle.

Open-joint surgery.

Patients undergoing open-joint surgery also are first given general

anesthesia. Unlike arthroscopy, the entire area around the TMJ is opened

so that the surgeon can get a full view and better access. There are many

types of open-joint surgeries. This treatment may be necessary if:

1. The bony structures that comprise the jaw joint are deteriorating

2. There are tumors in or around your TMJ

3. There is severe scarring or chips of bone in the joint

Compared with arthroscopy, open-joint surgery for TMD results in a

longer healing time and there is a greater chance of scarring and nerve injury.

59

REFERENCES

1. Akkus S, Senol A, Ayvacioglu NB, Tunc E, Eren I, Isler M. Is female

predominance in irritable bowel syndrome related to fibromyalgia?

Rheumatol Int. 2004;24:106–109.

2. Altshuler LL, Cohen LS, Moline ML, et al. Treatment of Depression in

Women 2001: Expert Consensus Guideline Series. Postgraduate

Medicine, March 2001. New York, NY: McGraw Hill; 2001

3. Anonymous. 2006. TMJ And Jaw Pain. Accesed from :

www.wholisticphysicaltherapy.com accessed june 9th, 2012

4. Arthritis Foundation. 2003. Myositis. www.arthritis.org. Accessed

June 9th,2012.

5. Aryanti, Sartika, 2007, Penanggulangan Gangguan Sendi

Temporomandibular Akibat Kelainan Oklusi Secara Konservatif,

Universitas Sumatra Utara, Medan.

6. Ash MM,, 1995. Ramfjord S. Occlusion. 4th ed.W.B. Saunders

Company.

7. Bhalaji, S. I., 2004, Orthodontics : The Art anfd Sciense, Arya (meddi)

Publ. House, New Delhi.

8. Brenman, Ephraim K. 2007. Myositis. http://www.medicinenet.com .

Accessed June 9th,2012.

9. Cheynet, F; Guyot, L; Richard, O; Layoun, W; Gola, R. Discomallear

and malleomandibular ligaments: anatomical study and clinical

applications. Surg. Radiol. Anat., 25:152-7, 2003.

10. Child, Todd A. 2000. Myofascial Pain-Dysfunction Syndrome,

Crainiomandibular Syndrome, Temporomandibular Joint Dysfunction.

www. Intermountainhealthcare.org. Accessed June 9th,2012.

11. Choi, J. Y., Lim, W. H., Chun, Y. S., 2008, Class III

Nonsurgical Treatment Using IndirectSkeletal Anchorage: A

Case Report, Korean J. Orthod , vol.38, no.1, p.60-7.

60

12. Daumas, B et al. 2005. Jaw Mechanism Modeling and Simulation,

Mechanism and Machine Theory: Elsevier, vol 40, p 821-233

13. deNovaes Soares C, Almeida OP, Joffe H, et al. Efficacy of estradiol

for the treatment of depressive disorders in perimenopausal women: a

double blind, randomized, placebo-controlled trial. Arch Gen

Psychiatry. In press. 2001

14. Dhanrajani, P.J. and Jonaidel, O. 2002. Trismus: Aetiology,

Differential Diagnosis And Treatment. Dental Update : Oral Surgery,

29: 88–94

15. Dimitroulis, G. 1998. Temporomandibular Disorders : A Clinical

Update. Bmj;317:190-4

16. Dommerholt, Jan. 2006. Myofascial Trigger Points: An Evidence-

Informed Review. Netherland : The Journal Of Manual & Manipulative

Therapy Vol. 14 No. 4, 203 – 221. Accesed from : www.dgs.edu.com.

17. Dorland, W. A Newman. 2012. Dorland's Illustrated Medical

Dictionary 32 th edition. Philadelphia : Saunders/ Elsiever.

18. Dworkin SF, Tuner JA, Mancl L, Wilson L, Massoth D, Huggins KH,

Le Reshe L, Truelove E. A randomized clinical trial of a tailored

comprehensive care treatment program for temporomandibular

disorders. J Orafac Pain. 2002;16:259–276.

19. Eckerdal, O. The petrotympanic fissure: a link connecting the

tympanic cavity and the temporomandibular joint. Cranio, 9:15-22,

1991.

20. Fields Hl, Martin Jb. 2005. Pain: Pathophysiology And Management.

In: Kasper Dl, Braunwald E, Fauci As, Hauser Sl, Longo Dl, Jameson

Jl, Editors. Harrison’s Principle Of Internal Medicine; 16th Edition.

Mcgraw-Hill:Philladelphia; 71-6

21. Falzon, Gail. 2000. Science of Medical Massage.

http://www.scienceofmassage.com. Accessed June 9th, 2012.

22. Fang H, Tong W, Shi LM, Blair R, Perkins R, Branham W, Hass BS,

Xie Q, Dial SL, Moland CL, Sheehan DM (2001). "Structure-activity

61

23. Female Risks By the American Society for Reproductive Medicine

(ASRM). Retrieved on Jan 4, 2009

24. Fillingim RB. Sex, gender, and pain: Women and men really are

different. Curr Rev Pain. 2000;4:24–30.

25. Fricton, James R. 2004. Temporomandibular Muscle and Joint

Disorders . International Association For The Study Of Pain. Volume

XII, No. 2.

26. Gelgor I.E., Karaman A.I., 2005, Non-Surgical Treatment of

Class III Malocclusion in Adult :Two Case Reports, Journal of

Orthodontic.32:89-97 12

27. Guan G, Kerins CC, Bellinger LL, Kramer PR. Estrogenic effect on

swelling and monocytic receptor expression in an arthritic

temporomandibular joint model. J Steroid Biochem Mol Biol.

2005;97:241–250.

28. Guy, Dr. Michael J. 2009. TMD (Temporomandibular Disorder.)

Accesed from : www.drmikeguy.com

29. Hamamci, N., Tumen, E. C., Basaran, G., Agackiran, E., 2008,

Nonsurgical Treatment of a CaseW i t h S k e l e t a l C l a s I I I

M a l o c c l u s i o n a n d T o t a l O p e n - B i t e : A C a s e

R e s p o r t , International Dental and Medicine Disorders, vol.1,

no.1,p.15-23

30. Harty, F.J, 1995, Kamus Kedokteran Gigi (alih bahasa drg. Narlan

Sumawinata), Buku Kedokteran EGC, Jakarta.

31. Henderson B, Pettipher ER. The synovial lining cell: Biology and

pathobiology. Semin Arthritis Rheum. 1985;15:1–32.

32. Herb, DMD, MD, Kathleen et All. 2006. Temporomandibular Joint

Pain And Dysfunction. USA : Department Of Oral And Maxillofacial

Surgery, Thomas Jefferson. Accesed from : www.tju.edu

33. Holdcroft A, Power I. 2003. Management Of Pain. Bmj : 326:635-9

62

34. Jena, A.K., Duggal, R., Mathur, V.P., Parkash, H., 2005,

Class-III Malocclusion:Genetics or Environment?A Twin

Study. Journal of Indian Society of Pedodontics and

Preventive Dentistry, vol 23:27-30

35. J, Dersh et All. 2002. Chronic Pain And Psychopathology: Research

Findings And Theoretical Consideration. USA : Psychosomatic

Medicine 64:773-86

36. Jensvold MF, Halbreich U, Hamilton JA, eds. Psychopharmacology

and Women: Sex, Gender and Hormones. Washington, DC: American

Psychiatric Press; 1996

37. Joanne Borg-Stein, MD David G. Sion. 2001. Myofascial Pain.

http://www.archives-pmr.org. Accessed June 9th,2012.

38. Joanne Borg-Stein, MD.2006. Treatment of Fibromyalgia,

Myofascial Pain, and Related Disorders. Physical Medicine and

Rehabilitation Clinics of North America 491-510. Accessed may 30

th, 2012.

39. Kang SC, Lee DG, Choi JH, Kim ST, Kim YK, Ahn HJ. Association

between estrogen receptor polymorphism and pain susceptibility in

female temporomandibular joint osteoarthritis patients. Int J Oral

Maxillofac Surg. 2007;36:391–394.

40. Keith L.Moore and Arthur F.Dalley Clininal Oriented Anatomy, 4th

Edition, Canada, Lippincott Williams & Wilkins; 1992 p. 926

41. Kim, HJ; Jung, HS; Kwak, HH; Shim, KS; Hu, KS; Park, HD; Park,

HW; Chung, IH. The discomallear ligament and the anterior ligament

of malleus: an anatomic study in human adults and fetuses. Surg.

Radiol. Anat., 26:39-45, 2004.

42. Kopp SP. The influence of neuropeptides, serotonin, and interleukin

1beta on temporomandibular joint pain and inflammation. J Oral

Maxillofac Surg. 1998;56:189–56.

43. Kubota E, Kubota T, Matsumoto J, Shibata T, Murakami KI. Synovial

fluid cytokines and proteinases as markers of temporomandibular joint

disease. J Oral Maxillofac Surg. 1998;56:192–198.

63

44. Kuttila, S; Kuttila, M; Le Bell, BY; Alanen, P; Suonpaa, J. Recurrent

tinnitus and associated ear symptoms in adults. Int. J. Audiol., 44:164-

70, 2005

45. Laflamme N, Nappi RE, Drolet G, Labrie C, Rivest S. Expression and

neuropeptidergic characterization of estrogen receptor (ER alpha and

ER beta) throughout the rat brain: Anatomical evidence of distinct

roles of each subtype. J Neurobiol. 1998;36:357

46. Laksitowati, Rina Hestu, 2009, Frequency of Temporomandibular

Joint Dysfunction with Clicking Symptom Due To Primary Molar

Premature Loss, Universitas Padjajaran, Bandung, available from

http://pustaka.unpad.ac.id/wpcontent/uploads/2010/06/frequency_of_te

mporomandibular_joint_dysfunction.pdf accessed on 9th June 2012

47. LeReshe L. Epidemiology of temporomandibular disorders:

Implications for the investigation of etiologic factors. Crit Ver Oral

Biol Med. 1997;8:291–305.

48. Langendoen, J; Müller, J; Jull, GA, Retrodiscal Tissue of the

Temporomandibular Joint: Clinical Anatomy and its Role in Diagnosis

and Treatment of Arthropathies, Manual Therapy, 2(4), 191-198, 1997.

49. Loughner BA, Larkin LH, Mahan PE. Discomalleolar and anterior

malleolar ligaments: possible causes of middle ear damage during

temporomandibular joint surgery. Oral Surg Oral Med Oral Pathol. Jul;

68(1):14-22, 1989.

50. Mayo Clinic Staff . 2009. "Myofascial pain syndrome: Symptoms".

Retrieved 8 May 2011.

51. M i l l e t , D . , a n d W e l b u r y , R . , 2 0 0 0 , O r th od on t i c s

a n d Pa e d i a t r i c De n t i s t r y , ChurchillLivingstone, Toronto, p.47-

48

52. Miloro, M; Ghali, GE; Larsen, P; Waite, P; Peterson's principles of

oral and maxillofacial surgery, Volume 2, Chapter 47, 2004.

53. Neill, DJ. Howell, PGT. 1986. Computerized kinesiography in the

studyof mastication in dentate subjects. J Prosthet Dent, vol 55, p 629-

38

64

54. Nelson LR, Bulun SE (September 2001). "Estrogen production and

action". J. Am. Acad. Dermatol. 45 (3 Suppl): S116–24.

55. New England Dental Care. 2004. TMD.

http://www.newenglanddental.com . Accessed June 9th,2012.

56. Okeson, JP. 1993. Management of temporomandibular disorders and

occlusion. Mosby Year Book

57. Palastanga, N. 1998, Anatomy and Human Movement: Structure and

Function, Butterworth-Heinemann, Oxford, Boston.

58. Peter G. Bradford "Estrogen deficiency leads to apoptosis in

dopaminergic neurons in the medial preoptic area and arcuate nucleus

of male mice". Mol. Cell. Neurosci. 27 (4): 466–76.

59. P.J. Dhanrajani And O. Jonaidel. 2002. Trismus: Aetiology,

Differential Diagnosis and Treatment. Dent Update 2002; 29: 88–94.

60. Prossnitz ER, Arterburn JB, Sklar LA (2007). "GPR30: A G protein-

coupled receptor for estrogen". Mol. Cell. Endocrinol. 265-266: 138–

42.

61. Rabie, A.M., Wong,R . W . K. , a nd Mi n , G .U . ,

2 0 08 , m T re a t me n t i n B o rde r l i ne C la s s I I I

Ma loc c l us i on : Orthodontic Camouflage (Extraction) Versus

Orthognathic Surgery,Open Dent J,vol 2:38–48

62. Rahardjo, pambudi. 2009. Peranti Ortodonti Lepasan. Surabaya:

Airlangga University Press

63. Ramírez, LM; Ballesteros, ALE; Sandoval, OGP. A direct anatomical

study of the morphology and functionality of disco-malleolar and

anterior malleolar ligaments. Int. J. Morphol., 27(2):367-379, 2009.

64. Rantala, Mikko. 2010. Academic Dissertation - Temporomandibular

Disorders and Related Psychosocial Factors In Non-Patients : A

Survey and A Clinical Follow-Up Study Based On The RDC/TMD.

Finland : Faculty Of Medicine, University Of Helsinki. Accesed from :

www.doria.fi

65

65. Rauhala K, Oikarinen KS, Raustia AM. Role of temporomandibular

disorders (TMD) in facial pain: Occlusion, muscle and TMJ pain.

Cranio. 1999;17:254–261.

66. Relationships for a large diverse set of natural, synthetic, and

environmental estrogens". Chem. Res. Toxicol. 14 (3): 280–94

67. Ren, YF; Isberg, A. Tinnitus in patients with temporomandibular joint

internal derangement. Cranio, 13:75-80, 1995.

68. Rugh JD, Smith BR. Mastication. In: Mohl ND, Zarb GA, Carlsson

GE, Rugh JD. 1988, A Textbook of Occlusion. Quintessence books.

p.143-52

69. Rowicki, T; Zakrzewska, J. "A study of the discomalleolar ligament in

the adult human." Folia Morphol. (Warsz). 65 (2): 121–125, 2006.

70. Saladin, KS; Human Anatomy. New York, NY: McGraw-Hill, 2005.

71. Schmidt PJ, Nierman L, Danaceau MA, et al. Estrogen replacement in

perimenopausal-related depression: a preliminary report. Am J Obstet

Gynecol 2000;183:414420

72. Singh, G., ----,Textbook of Orthodontics,Jaypee Brothers Publisher,

New Delhi

73. Stahl SM. Effects of estrogen on the central nervous system

[Brainstorms]. J Clin Psychiatry 2001;62:317¬318

74. Stahl SM. Essential Psychopharmacology. 2nd ed. New York, NY:

Cambridge University Press; 2000

75. Standring, S, Editor, Gray’s Anatomy, 40th edition, Elsevier, Churchill

Livingstone, 2008.

76. Starlanyl, Devin J, Copeland, Mary Ellen. 2001. "Fibromyalgia &

Chronic Myofascial Pain: A Survival Manual." (2nd ed.). Oakland,

CA: New Harbinger Publications. ISBN 978-1-57224-238-8.

77. Soboleva, U. Laurina, L. Staidina, A. 2005. The Masticatory System -

an Overview, Stomatologija, Baltic Dental an Maxillofacial Journal,

vol 7(3), p77-80

66

78. Tata JR (2005). "One hundred years of hormones". EMBO Rep. 6 (6):

490–6.

79. Thexton ,AJ. 1992. Mastication and swallowing: an overview. Br Dent

J, vol 173, p197-206

80. TMJ Association, Temporo Mandibular Joint Diseases and Disorder,

Taylor MicroTechnology, Inc, available from http://www.tmj.org

81. Yap, Eng-Ching. 2007. Myofascial Pain – An Overview. Vol. 36 No. 1.

Singapore : Department Of Rehabilitation Medicine, Tan Tock Seng

Hospital.

82. Warren MP, Fried JL. Temporomandibular disorders and hormones in

women. Cells Tissues Organs. 2001;169:187–192.

83. WebMD Medical Reference from Healthwise.2010.

Temporomandibular (TM) Disorder Prevention and Treatment.

http://www.webmd.com . Accessed June 7th, 2012.

84. Whitehead SA, Nussey S (2001). Endocrinology: an integrated

approach. Oxford: BIOS: Taylor & Francis. ISBN 1-85996-252-1

85. William C. Shiel Jr , et all. 2012. Fibromyalgia (Fibrositis).

http://www.medicinenet.com. Accesses June 9th ,2012.

86. Wiriadidjaja, Kartika, 2007, Kerusakan Jaringan Periodonsium Pada

Gigi Premolar yang Disebabkan Oleh Oklusi Traumatik, Universitas

Indonesia, Jakarta.

87. Wright, EF; Bifano, SL. Tinnitus improvement through TMD therapy.

J. Am. Dent. Assoc., 128:1424-32, 1997.