Modul IV

TEMPORO MANDIBULAR JOINT DISORDER

Written By :
Monica Cynthia H 021611133150 Azizah Aqilah 021611133158
Anissa Zahra N 021611133151 Karthiyayinee 021611133159
Amalia Nurul Fitri 021611133152 Alisa Sufia 021611133160
M. Alwino Bayu 021611133154 Eshleen Nisha 021611133161
Candrika Thiyagu 021611133155 Ellyonord Diana 021611133162
Koh Wan Huei 021611133156 Indira Arella 021611133163
Chong Sin Ying 021611133157 Sharyna Emyra 021611133154

Fakultas Kedokteran Gigi

Universitas Airlangga

Surabaya

2018
 PREFACE

The writer wants to thank to Almighty Creator because of His bless and grace, he can
finish this paper. This paper titled “Temporo Mandibular Joint Disorder”. The writer wrote
it to fulfill the final assignment of Modul IV subject.

The writer also delivers his gratitude to Yuliati, drg., M. Kes as the lecture for the
subject of Modul, for the guidance to complete it. The writer realizes that this paper is far
from perfect in the arrangement or in the content of the paper. The writer hopes that the
suggestions from the reader can be a support to make her better in the next paper project.

Finally, the writer expects that it can be a medium for the reader to deepen the
knowledge about the temporo mandibular joint disorder.

Surabata, May 17th, 2018

The Writer

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Preface …………………………………………………………………………………… 1

Contents ………………………………………………………………………………….. 2

CHAPTER 1 : INTRODUCTION

1.1 Background …………………………………………………………………... 3

1.2 Problem ………………………………………………………………………..3

1.3 Purpose ……………………………………………………………………….. 3-4

1.4 Method …………………………………………………………………………4

1.5 Hypothesis ……………………………………………………………………...4

CHAPTER 2 : THEORITICAL STUDY

2.1 Anatomy and Histology of Temporo Mandibular Joint ………………………. 5-7

2.2 Physiology of Muscle and Nerve ………………………………………………7-

14

2.3 Contraction and Relaxation of Muscle ………………………………………..14-

16

2.4 Physiology of TMJ Movement ……………………………………………….16-

19

2.5 Risk Factors Contributed to Temporomandibular Joint Disorder Associated With

Pain ………………………………………………………………………………20-21

2.6 Management and Treatment of Temporo Mandibular Joint …………………21-24

2.7 Damage To Hard Tissue ……………………………………………………..24-28

2.8 Radiology of Temporo Mandibular Joint Disorder …………………………..28-30

CHAPTER 3 : CONCEPTUAL MAPPING …………………………………………..31

CHAPTER 4 : DISCUSSION …………………………………………………………..32-

37

CHAPTER 5 : CLOSING

5.1 Conclusion …………………………………………………………………….38

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 5.2 Solution ………………………………………………………………………..38

Bibliography ……………………………………………………………………………39-41

CHAPTER 1
INTRODUCTION
1.1 Background
Temporomandibular joint is the only joint that can be handled by dentists. It is very
important for us to learn about this joint because there are a lot of cases that can be caused by
temporomandibular joint disorder.

Temporomandibular joint is formed by bones, muscles, ligaments, nerves, etc. This

joint makes it possible for us to open and close the mouth. When the joint and surrounding
muscles and ligaments are malfunctioned in some way, it is called temporomandibular joint
disorder. It can be caused by bad habits such as bruxism, clenching, etc, disc displacement,
the degenerative joint, etc.

A 48-year-old man came to RSGM with a complaint of stiffness, cramp and pain
around the cheeks area after waking up from his sleep. After the clinical examination, it was
found out abrasion on the surfaces of the posterior teeth and palpation at the TMJ. There was
clicking sound when opening and closing the mouth.

1.2 Problem Statement

1. What are the anatomic structures and histologic of temporo mandibular joint?
2. What are the physiology of muscle and nerve?
3. How is the process of contraction and relaxation of muscle?
4. What are the physiology of temporo mandibular joint movement?
5. What are the factors causing temporo mandibular joint disorders accompanied
with pain?
6. What is the radiology of temporo mandibular joint disorder?
7. What is the management and treatment of temporo mandibular joint disorder?

1.3 Purposes

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 1. Students are able to describe the anatomic structures and histologic of temporo
mandibular joint
2. Students are able to describe the physiology of muscle and nerve
3. Students know the process of contraction and relaxation of muscle
4. Students understand the physiology of temporo mandibular joint movement
5. Students know the factors causing temporo mandibular joint disorders
accompanied with pain
6. Students are able to describe the radiology of temporo mandibular joint disorder
7. Students know the management and treatment of temporo mandibular joint
disorder

1.4 Methods

Research is done based on journals and textbooks that we get from both mass and
electronic media.

1.5 Hypothesis

The patient feels pain because of temporomandibular joint disorder. We conclude that
there is temporomandibular joint disorder because of some symptoms that are experienced by
the patient, for example ‘clicking’ sound, pain around the cheeks and muscle pain.

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 CHAPTER 2

LITERATURE STUDY

2.1 Anatomy and Histology of Temporomandibular Joint

Temporomandibular joint or TMJ is a diarthrodial synovial paired joint. This means

that the joint has to function in pairs and the joint movement will involve both joint
compartments. TMJ comprises mandibular condyle, glenoid fossa (mandibular fossa or
articular fossa), articular eminence (articular tubercle), articular disc, capsule (which is lined
by synovial membrane) and ligaments. Each joint involves the articular eminence and glenoid
fossa above and mandibular condyle below. The articular disc divides the joint space into the
upper and lower compartments (Drake.R, 2010).

a) Articular disc

Articular disc has been referred to as meniscus. Rees (1954) has described the
articular disc as like a jockey’s cap which overlaps the condylar head, with the border
of the cap forming its attachment to the condyle and the peak attached to the tendon of
the lateral pterygoid muscle. The articular disc is firmly attached to the head of the
condyle medially and laterally where 10 it bends with the capsule. Rees (1954)
described the meniscus as having four parts. The anterior band is moderately thick but
narrow antero-posteriorly. The posterior band is the thickest and widest, whereas the
intermediate zone is the thinnest. The interposition of the thin intermediate zone
between the anterior and posterior bands gives the disc more flexibility. The bilaminar
zone comprised of loose fibro-elastic tissue forming its upper part and inextensible
collagenous tissue forming its lower part (Drake.R, 2010).

b) Mandible

The mandible is the largest and strongest bone of the face. Its body is curved like a
horseshoe with two major projections; posterior is the head of the condyle or
condyloid process, and just anterior to this is the coronoid process. The head of the
condyle, which articulates with the glenoid fossa of the skull, via the meniscus, is
knuckle-shaped and convex in all directions. It is longer (1 5-20 millimeters) in its
horizontal length than its anteroposterior width (8-1 0 meters) (Drake.R, 2010).

c) Glenoid Fossa

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 The glenoid fossa accepts the condylar process of the mandible and is formed by the
articular tubercle anteriorly and by the postglenoid tubercle posteriorly of the zygoma
portion of the temporal bone. The articular surface is smooth, oval, and deeply
concave containing the articular disc or meniscus. According to Gray's Anatomy,
there is a nonarticular portion of the fossa in which a small part of the parotid gland is
found. The fossa is composed of a thin compact bone, whereas the articular tubercle
and condyle process is of a spongy bone under a thin compact bone. These
articulating surfaces are covered with an avascular white fibrous tissue containing
predominantly collagen fibers and a variable amount of cartilage cells. This fibrous
tissue is called fibrocartilage. This fibrocartilage is thinner anteriorly, increasing in
thickness as it continues to the posterior wall of the articular eminence. The roof of
the fossa is quite thin and is translucent. This is evidence that the articular fossa,
although containing the posterior rim of the disc and condyle, is not a functional part
of the craniomandibular articulation; the function in this articulation is always
between condyle and disc on one hand and anteriorly with the articular eminence on
the other. The articular tubercle is convex in an anteroposterior direction and concave
mediolaterally. This coincides with the slope of the condyle. Its anterior border does
not have the steep slope as posteriorly, but has a gentle rise from the infratemporal
surface of the cranial base. This allows a condylar movement which will be reviewed
later. Hyaline cartilage, as we know, provides an extremely smooth and wear-resistant
surface. Bathed in synovial fluid, hyaline cartilage provides an almost friction-free
environment. The TMJ, however, demonstrates a preponderance of fibrous cartilage
and lacks hyaline which is further proof that the fossa is not a stress-bearing structure.
Fibrocartilage provides for great tensile strength and resists long-term effects of
pressure and friction. Other structures that have similarity of design for minimal
pressure, friction, and the presence of a meniscus are the articulations of the clavicle
and intervertebral disc. The stress-bearing elements of the TM articulation is the
articular eminence and its meniscus (Drake.R, 2010).
d) Meniscus
The meniscus of articular disc is an oval fibrous plate of great firmness. The disc is
concave on its inferior surface and oval in shape. The upper or superior surface is
saddle-shaped or concave convex accommodating the form of the articular fossa and
tubercle. Of variable thickness with clearly defined fibrous bands, the disc resembles
a baseball cap. A thinner intermediate zone separates the anterior band from the

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 posterior band. This posterior band (cap) occupies the deepest part of the fossa and
continues posteriorly into a thick layer of the loose connective tissue to fuse with the
posterior wall of the articular capsule, the retrodiscal pad. The disc extends forward in
front of the condyle, is fused with the capsule, and allows the attachment of the upper
fibres of the lateral pterygoid muscle to the disc (visor). Posteriorly, the disc and
capsule are connected by a pad of loose vascularized and innervated connective
tissue. This loose connection gives the disc the necessary freedom of anterior
movement. The disc and capsule are independently attached to the lateral and medial
poles of the condyle, inferiorly. This direct and firm attachment of the disc to the
poles of the condyle assures simultaneity of movements by mandible and disc
(Sharawy, 2009).
e) Fibrous Capsule
The capsule attaches to the articular tubercle above and in front and to a bony fissure
behind (the squamotympanic fissure) and along the circumference of the mandibular
fossa. The capsule, above the articular disc, forms a loose envelope and becomes taut
below the disc as it attaches to the neck of the mandible.''The anterior medial and
posterior portion is quite loose and thin whereas the lateral capsule is taut and strong,
as it is strengthened by the temporomandibular ligament (Sharawy, 2009).

2.2 Physiology of Muscle and Nerve

The muscles of mastication are a group of muscles associated with movements of the
jaw (temporomandibular joint). They are one of the major muscle groups in the head – the
other being the muscles of facial expression. (Rowicki, T; Zakrzewska, J.,2006)

There are four muscles of mastication – the masseter, temporalis, medial pterygoid
and lateral pterygoid. Embryologically, the muscles of mastication develop from the first
pharyngeal arch. Consequently they are innervated by a branch of the trigeminal nerve (CN
V), the mandibular nerve. (Rowicki, T; Zakrzewska, J.,2006)

2.2.1 Joints

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  Capsule - The capsule is a fibrous membrane that surrounds the joint and attaches
to the articular eminence, the articular disc and the neck of the mandibular
condyle.
 Articular disc - The articular disc is a fibrous extension of the capsule that runs
between the two articular surfaces of the temporomandibular joint. The disc
articulates with the mandibular fossa of the temporal bone above and the condyle
of the mandible below. The disc divides the joint into two sections, each with its
own synovial membrane. The disc is also attached to the condyle medially and
laterally by the collateral ligaments. The anterior disc attaches to the joint capsule
and the superior head of the lateral pterygoid. The posterior portion attaches to the
mandibular fossa and is referred to as the retrodiscal tissue. ( Rowicki, T;
Zakrzewska, J.,2006)
 Retrodiscal tissue - Unlike the disc itself, the retrodiscal tissue is vascular and
highly innervated. As a result, the retrodiscal tissue is often a major contributor to
the pain of Temporomandibular Disorder (TMD), particularly when there is
inflammation or compression within the joint. (Rowicki, T; Zakrzewska,
J.,2006)

Figure 1 : Temporomandibular Joint (Rowicki, T; Zakrzewska, J.,2006)

2.2.2 Ligaments

The ligaments give passive stability to the TMJ.

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  The temporomandibular ligament is the thickened lateral portion of the capsule,
and it has two parts, an outer oblique portion and an inner horizontal portion.

Figure 2 : Temporomandibular Ligament and Joint Capsule Lateral View (Rowicki, T;

Zakrzewska, J.,2006)

 The stylomandibular ligament runs from the styloid process to the angle of the
mandible.
 The sphenomandibular ligament runs from the spine of the sphenoid bone to the
lingula of mandible. (Rowicki, T; Zakrzewska, J.,2006)

Figure 3 : Temporomandibular Ligament and Joint Capsule Medial View (Rowicki, T;

Zakrzewska, J.,2006)

2.2.3 Muscles

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 Masseter
The masseter muscle is the most powerful muscle of mastication. It is
quadrangular in shape, and can be split into two parts; deep and superficial.The
entirety of the muscle lies superficially to the pterygoids and temporalis, covering
them. (Miloro, M; Ghali, GE; Larsen, P; Waite, P, 2004)

Attachments: The superficial part originates from maxillary process of the

zygomatic bone. The deep part originates from the zygomatic arch of the temporal
bone. Both parts attach to the ramus of the mandible.
Actions: Elevates the mandible, closing the mouth.
Innervation: Mandibular nerve (V3).

Figure 4 : Masseter muscle Ghali, GE; Larsen, P; Waite, P,2004)

 Temporalis
The temporalis muscle originates from the temporal fossa – a shallow depression
on the lateral aspect of the skull. The muscle is covered by tough fascia which can
harvested surgically and used to repair a perforated tympanic membrane (an
operation known as a myringoplasty). ( Kuttila, S; Kuttila, M; Le Bell, BY;
Alanen, P; Suonpaa, J.,2005)

Attachments: Originates from the temporal fossa. It condenses into a tendon,

which inserts onto the coronoid process of the mandible.
Actions: Elevates the mandible, closing the mouth. Also retracts the mandible,
pulling
the jaw posteriorly.
Innervation: Mandibular nerve (V3).

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 Figure 5 : Temporalis muscle Ghali, GE; Larsen, P; Waite, P,2004)

 Medial pterygoid
The medial pterygoid muscle has a quadrangular shape, with two heads; deep and
superficial. It is located inferiorly to the lateral pterygoid. (Miloro, M; Ghali, GE;
Larsen, P; Waite, P, 2004)

Attachments: The superficial head originates from the maxilla. The deep head
originates from the lateral pterygoid plate of the sphenoid bone. Both parts attach
to the ramus of the mandible, near the angle of mandible.
Actions: Elevates the mandible, closing the mouth.
Innervation: Mandibular nerve (V3).

 Lateral pterygoid
The medial pterygoid muscle has a quadrangular shape, with two heads; deep and
superficial. It is located inferiorly to the lateral pterygoid.

Attachments: The superficial head originates from the maxilla. The deep head
originates from the lateral pterygoid plate of the sphenoid bone. Both parts attach
to the ramus of the mandible, near the angle of mandible. ( Langendoen, J;
Müller, J; Jull, GA,,1997)
Actions: Elevates the mandible, closing the mouth.
Innervation: Mandibular nerve (V3).

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 Figure 6 : Medial and lateral pterygoid ( Langendoen, J; Müller, J; Jull,
GA,,1997)

2.2.4 Nerve
The trigeminal nerve is the principal sensory nerve for the head and is the
motor nerve for the muscles of mastication and several small muscles, especially for
muscles that surround temporomandibular joint in this case. Functionally as well as
structurally, the trigeminal ganglion is comparable to the dorsal root ganglion of a
spinal nerve. At the lower border of the trigeminal ganglion, three major nerve
bundles arise. These are the three major divisions of the trigeminal nerve: the
ophtalmicus (V), maxillary (V) amd mandibular (V). The ophtalmicus and maxillary
divisions are entirely sensory, the mandibular division is both sensory and motor.
(Barr and Kieman, 1988)
The sensory trigeminal nerve is responsible for sensation from the skin of the
face and forehead, the scalp as far back as the vertex of the head, the mucosa of the
oral and nasal cavities and the   paranasal sinuses and the theeth. The trigeminal nerve
also contributes sensory fibers to most of the duramater. The scalp of the back of the
head and an area of skin at the angle of the jaw are supplied by the second and third
cervical nerves.(Sheppard and Reed, 1976)
The motor trigeminal nerve supplies the muscles of mastication (masseter,
temporalis, and lateral and medial pterigoid muscles) and several smaller muscles.
Afferents for reflexes come mainly from the sensory trigeminal nuclei, including the
mesencephalic nucleus. In addition to stretch reflex there is also a   jawopening reflex
in which the contractions of the masseter, temporalis and medial pterygoid muscles

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are inhibited as a result of   painful pressure applied to the teeth. (Sheppard and Reed,
1976)
The ophtalmicus division of the trigeminal nerve has three branches, the
lacrimalis, the frontalis and the nasociliary nerve. The lacrimalis nerve supplies the
lacrimal gland, conjunctiva and the skin of the lateral upper eyelied. The frontalis
nerve divide into the supraorbital and supratrochlear nerves. The supraorbital nerve
supplies skin of the forehead and anterior scalp, with small branches to the upper
eyelid and fontal sinus. The supratrochlear nerve supplies skin of the medial parts of
the forehead and upper eyelid. The nasociliary nerve to skin of the lower half of the
nose, the root of the nose and lowe eyelid. (Sheppard and Reed, 1976)
The maxillary division, after leaving the trigeminal ganglion, gives off a
meningeal branch to the duramater prior to passing through the foramen rotundum. In
the pterygopalatina fossa, the maxillary nerve gives off pterygopalatine, posterior
superior alveolar and zygomatic branches. The zygomatic supplies skin overlying the
lateral surface of the zygoma and skin over the anterior of the temporal muscles. The
posterior superior alveolar nerve, sends one terminal branch to the gingival of the
three posterior molar teeth and two terminal branches to the molar and premolar teeth
and to the mucous membrane of the maxillary sinus. The branches pterygopalatine
nerve arise some nerve else, they are   pharyngeal, lesser palatine, greater palatine,
posterior superior lateral nasal and nasopalatine. (Ogus and Toller, 1981)
The mandibular division of the trigeminal nerve exits from the skull at the
foramen ovale. The anterior division of the mandibular nerve contains a single
sensory branch, the general somatic afferent buccal nerve supplying skin of the check,
buccal mucosa, and gingival of premolar and molar teeth. The posterior division of
the mandibular nerve gives off four sensory branches:
1. The auriculotemporal nerve, which passes through the parotid gland to skin in
front of the ear and scalp, and sends branches to the temporomandibular joint.
2. The lingual nerve, which conveys general sensation from the anterior two
thirds of the tongue, lingual gingival of the mandibular teeth and the floor of
the mouth
3. The inferior alveolar nerve, which conveys sensation from molar and premolar
teeth

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 4. The mental nerve, which supplies skin of the chin, lip and mucosa of the lower
lip. The continuation of the inferior alveolar nerve within bone in the incisive
nerve to the remaining canine ang incisor teeth. (Barr and Kieman, 1988)

2.3 Contraction And Relaxation Of Muscle

2.3.1 Muscle Contraction

Contraction is the step in which the muscle fiber develops tension and may
shorten (muscles often “contract,” or develop tension, without shortening, as we see
later). How a muscle fiber shortens remained a mystery until sophisticated techniques
in electron microscopy enabled cytologists to see the molecular organization of
muscle fibers. In 1954, two researchers at the Massachusetts Institute of Technology,
Jean Hanson and Hugh Huxley, found evidence for a model now called the sliding
filament theory. This theory holds that the thin filaments slide over the thick ones and
pull the Z discs behind them, causing the cell as a whole to shorten (Saladin, 2003).
A muscle contraction occurs when a muscle fibre generates tension through
the action of actin and myosin cross-bridge cycling. Though the term contraction
implies a shortening or reduction, when used as a scientific term referring to the
muscular system contraction refers to the generation of tension by muscle fibers with
the help of motor neurons. Locomotion in most higher animals is possible only
through the repeated contraction of many muscles at the correct times. Contraction is
controlled by the central nervous system (CNS), which comprises the brain and spinal
cord. Voluntary muscle contractions are initiated in the brain, while the spinal cord
initiates involuntary reflexes (Eisenberg and Hill, 1985).
Muscle contraction occurs when the actin and myosin filaments in muscle are
driven past each other by a cyclic interaction of adenosine triphosphate (ATP) and
actin with crossbridges that extend from myosin. Current biochemical studies suggest
that, during each adenosine triphosphatase cycle, the myosin cross-bridge alternates
between two main conformations, which differ markedly in their strength of binding
to actin and in their overall structure. Binding of ATP to the cross-bridge induces the
weak-binding conformation, whereas inorganic phosphate release returns the cross-
bridge to the strong-binding conformation. This cross-bridge cycle is similar to the

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kinetic cycle that drives active transport and illustrates the general principles of free
energy transduction by adenosine triphosphatase systems (Eisenberg and Hill, 1985).

General mechanism of muscle contraction

The initiation and execution of muscle contraction occur in the following sequential
steps (Guyton and Hall, 2006).
1. An action potential travels along a motor nerve to its endings on muscle fibers.
2. At each ending, the nerve secretes a small amount of the neurotransmitter
substance acetylcholine.
3. The acetylcholine acts on a local area of the muscle fiber membrane to open
multiple “acetylcholinegated” channels through protein molecules floating in
the membrane.
4. Opening of the acetylcholine-gated channels allows large quantities of sodium
ions to diffuse to the interior of the muscle fiber membrane. This initiates an
action potential at the membrane.
5. The action potential travels along the muscle fiber membrane in the same way
that action potentials travel along nerve fiber membranes.
6. The action potential depolarizes the muscle membrane, and much of the action
potential electricity flows through the center of the muscle fiber. Here it
causes the sarcoplasmic reticulum to release large quantities of calcium ions
that have been stored within this reticulum.
7. The calcium ions initiate attractive forces between the actin and myosin
filaments, causing them to slide alongside each other, which is the contractile
process.
8. After a fraction of a second, the calcium ions are pumped back into the
sarcoplasmic reticulum by a Ca++ membrane pump, and they remain stored in
the reticulum until a new muscle action potential comes along; this removal of
calcium ions from the myofibrils causes the muscle contraction to cease.

2.3.2 Muscle Relaxation

When its work is done, a muscle fiber relaxes and returns to its resting length. This is
achieved by these steps (Saladin, 2003) :
1. Nerve signals stop arriving at the neuromuscular junction, so the synaptic
knob stops releasing ACh.

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 2. As ACh dissociates (separates) from its receptor, acetylcholinesterase breaks it
down into fragments that cannot stimulate the muscle. The synaptic knob
reabsorbs these fragments for recycling. All of this happens continually while
the muscle is being stimulated, too; but when nerve signals stop, no new ACh
is released to replace that which is broken down. Therefore, stimulation of the
muscle fiber by ACh ceases.
3. Active transport pumps in the sarcoplasmic reticulum (SR) begin to pump
Ca2+ from the cytosol back into the cisternae. Here, the calcium binds to a
protein called calsequestrin and is stored until the fiber is stimulated again.
Since active transport requires ATP, you can see that ATP is needed for
muscle relaxation as well as for muscle contraction.
4. As calcium ions dissociate from troponin, they are pumped into the SR and are
not replaced.
5. Tropomyosin moves back into the position where it blocks the active sites of
the actin filament. Myosin can no longer bind to actin, and the muscle fiber
ceases to produce or maintain tension.

2.4 Physology of Temporo Mandibular Movement

There are mandible movements that are regulated by temporomandibular joint.

2.4.1 Depression of the Mandible

During simple depression of the mandible (central opening movement) from it

is rest position, both condyles move forward, the menisci moving with them. It is
generally agreed by many authorities (Prentiss, Lord, Chissin, Brodie, Higley,
Stimson, Sicher, and others) that  both condyle heads are pulled forward in this initial
opening movement  by the external pterygoid muscles. While the condyle is being
pulled forward in opening the jaw by the inferior head of the external pterygoid, the
meniscus is being pulled forward by the superior head of the external pterygoid
muscle. When the condyle approaches the articular eminence it rides forward on the
thinner   portion of the meniscus-an arrangment which makes allowances for the
downward protuberance of the eminence. When in “rest position” each condyle rests
upon a thick posterior   portion of the meniscus which fills the space between the
condyle and the deeper portion of the glenoid fossa. Anterioly, the meniscus is much

16
thinner at the portion which approximates the dorsal area of the articular eminence
and the frontal area of the condyle. (Wheeler, 1984)

The relative thickness of the meniscus anteroposteriorly, plus the

compensating activity of the two heads of the external pterygoid muscle, allows the
condyles of the mandible to move forward with a glinding movement on a “single
plane” regardless of the irregularity of the surface of the glenoid fossa and of that of
the articular eminence. The “plane” has an inclination downward when the head is
held erect. It is interesting to note that the inclined plane of the condylar glide when
the mandible is depressed is seemingly parallel to the occlusal plane of the molars and
the lower border of the body of the mandible when the jaws are closed (Wheeler,
1984). During the central opening movement of the mandible, the axis of movement
is not in the condyle heads, since these move forward immediately, even tho ugh the
initial movement forward is slight. (Wheeler, 1984)

Apparently the area of rotation approaches the attachment of the

temporomandibular ligament laterally and distally to the neck of the condyle. This is a
logical conclusion   because of the suspensory character of this strong ligament and
the general direction of its fibers. The central opening movement of the mandible
(depression) in conjuction with the central closing movement (elevation) provides the
action commonly termed “simple hinge movement”. As far as the relation of the
dental arches is concerned in this opening and closing movement, the action is
comparable to the action of a simple hinge. The occlusal surfaces of the maxillary
teeth may   be considered as the upper extension of the hinge, and the occlusal
surfaces of the mandibular teeth as the lower extension in the central opening
movement. (Wheeler, 1984)

Owing to the involved design of the articulation and the need for jaw support,
the rotation point or axis of the hinge cannot be centered in the condyles as many
believes. The uneven shape of the condyle, added to its forward movement
immediately upon jaw opening, would defeat this argument. The jaw has body and
weight and must be suspended by ligamentous attachment in some area. The design
and location of the temporomandibular ligament makes it the logical choice among
condyle attachment to accomplish ligamentous suspension of the   jaw in the initial
opening movement. The attachment superiorly is forward, wrapped around the

17
zygomatic “bar” of the temporal bone; inferior, it is down and back, and is strongly
attached posteriorly in a limited area to the neck of the condyle, below the condyle
itself (Wheeler.1984). When the jaw is opened no more than necessary for ordinary
use in mastication (10-12mm, maximum), the action of placing the teeth of one arch
in and out of contact with the teeth of the opposing arch in a sagittal plane may be
called a hinge movement, reegardless of our inability to pinpoint the “hinge axis”.
(Wheeler, 1984)

2.4.2 Elevation of the Mandible

The mandible is elevated by the temporal muscles, the masseter muscles and

the internal pterygoid muscles. The temporal muscle has anterior and posterior fibers.
The anterior fibers exert an upward pull; the posterior fibers pull upward and
backward (Wheeler.1984). The masseter muscle has two sets of fibers: superficial and
deep fibers. The superficial fibers exert a pull upward and foward on the mandible.
The deep fibers exert a pull vertically upward (Wheeler.1984). The internal pterygoid
muscle has two heads, each of which pulls in the same general direction. Together
they exert a pull on the mandible which is upward, foward and inward
(Wheeler.1984). When the temporal, masseter and internal pterygoid muscles of the
sides contract simultanecously, the mandible is elevated and returns the teeth to
occlusion (Wheeler.1984). When the teeth are brought into centric occlusion, both
condyles of  the mandible are moved a short distance posteriorly to their rest position
(Wheeler.1984).

2.4.3 Protusion of the mandible

The mandible cannot be protruded unless the cusps of the teeth are
disengaged. Therefore, the mandible must be depressed slightly, the condyles moving
forward before the protrusive movement is begun (Wheeler, 1984). The muscles
which promulgate the protrusive movement which brings about the protrusive
occlusal relation of the teeth are the external pterygoid muscles, which are assisted by
the anterior fibers of the temporal muscles. The pterygoid pull forward on the
condyles and the temporal pull upward with a counter action on the coronoid
processes; this prevent further depression of the mandible during the protrusive
movement. The tonus and counterbalancing action of other fibers of the temporal as
well as some other muscles may come into play during the   protrusive movement.

18
During this movement the condyles are pulled forward with their menisci, but their
forward movement is quite limited (Wheeler.1984).

2.4.4 Retraction of the Mandible

In retraction, the mandible returns along the same path it traveled in the
protrusive movement. The retractive movement is, therefore, just the reverse of the
protrusive movement (Wheeler.1984). The jaw is pulled back by the action of the
temporal muscle, the posterior fibers principally. The codyles with their menisci are
returned to rest position. If it is the purpose of this movement to bring the teeth   back
into centric occlusion, the masseter and the internal pterygoid muscles join the
activity of the temporals in the culmination of the act (Wheeler.1984). The mandible
may be retracted a very small degree posteriorly to centric occlusal relation of the
teeth. This movement is nonfuctional and consequently very limited. Movement of
the condyles distally is resisted by the posterior wall of the glenoid cavity; the
movement is limited to the compressibility of the soft tissues intervening between the
bony parts (Wheeler.1984).

2.4.5 The lateral of the Mandible

The lateral movement (right and left) of the mandible are asymmetrical
movements; the right and left condyles do not follow similar paths. These movements
are made possible by the ability of one temporomandibular joint to move
independently of the other. Each internal pterygoid muscle exerts a medial pull on the
mandible, since it does not operate on a line with the forward or   protrusive
movement of the jaw. Its action pulls the condyle inward as well as forward. The right
lateral movement of the mandible is affected, therefore, by a slight depressive
movement of the mandible, both external pterygoid operating, which action depresses
the mandible and moves both condyles forward. At this point the left internal
pterygoid contracts indepently, the right internal pterygoid and other muscles
relaxing. The activity of the left internal pterygoid pulls the left condyle forward and
inward in a circular path which rotates about a point in the right condyle, the right
condyle turning on the pivontal point. (Wheeler, 1984)

This action results in the rotation of the mandible about the pivontal point in
the right condyle, moving the mandible to the right. In the return movement, the
condyles retrace their   path. The mandible is returned to rest position, or the teeth into

19
 centric occlusion, through the activity of the left temporal muscle (mainly posterior
fibers), other muscles of mastication of both sides joining forces as the teeth approach
central occlusion with final masticatory thrust. The left lateral movement of the
mandible is affected in the same manner. In this instance the right condyle is pulled
forward and inward while the left condyle pivots. The right internal pterygoid muscle
contraction dcauses the movement of the mandible to the left. The right temporal is
the muscle mainly operative which affects the return of the mandible to centric
relation with the assistance of the other mucles in balance with it (Wheeler.1984)

2.5 Risk Factors Contributed to Temporomandibular Joint Disorder Associated With

Pain

The causes of Temporomandibular Disorders (TMD) are multifactorial. Factors that

increase the risk of temporomandibular disorders are called “Predisposing factors” and those
causing the onset of temporomandibular disorders are called “Initiating factors”. Meanwhile
the factors that interfere with healing or enhance the progression of temporomandibular
disorder are called “Perpetuating factors” (Athanasiou, 2003). Perpetuating factors may
include the following:

1. Behavioral factors (grinding, clenching and abnormal head posture)

2. Social factors (affect perception and influence of learned response to pain)
3. Emotional factors (depression and anxiety)
4. Cognitive factors

The etiology of TMD is multidimensional: biomechanical, neuromuscular, bio-

psychosocial and biological factors may contribute to the disorder. Occlusal overloading and
parafunctions (bruxism) are frequently involved as biomechanical factors; increased levels of
estrogen hormones are considered biological factors affecting the temporo-mandibular-joint.
Among bio-psychosocial factors, stress, anxiety or depression were frequently encountered
(Andrea et al, 2015).
Occlusal factor is the main factor that cause TMD associated with pain. For example,
posterior cross-bite, overjet greater than 5mm, maximum intercuspal sliding greater than
2mm and edge-to-edge bite are common malocclusions that involve in development of TMD.
Besides that, sagittal relation Class II, anterior open bite or missing teeth problem can

20
contribute as occlusal factors as well (Andrea et al, 2015). Eminence ratio (antero-posterior
length of the disk in relation to the length of the articular eminence) is one of the factors
causing temporomandibular disorder. In a patient with a flat eminence, posterior rotation of
the disk on the condyle during opening is not very frequent. As the steepness increases, more
rotational movement is required between the disk and condyle during translation of the
condyle. Therefore patients with steep articular eminences may undergo ligament elongation
that leads to disk derangement disorders (Sharma et al, 2011).

Iatrogenic injuries can act as both initiating as well as predisposing factors. This can
occur during any dental procedure in which there is prolonged opening like orthodontic
treatment, single-sitting root canal treatment or because of factors like relapse which causes a
functional imbalance between the temporomandibular joints, muscles and occlusion.

Association between psychological factors and TMD are always being discussed in
literature. Stress, anxiety and other psychological factors can induce muscle hyperactivity and
muscle fatigue that lead to muscle spasms, occlusal disharmony or even degenerative
arthritis. TMD symptoms, escpecially pain, are also a factor in the development of depression
and psychic diseases (Ferrando et al, 2004).

On the other hand, it is hypothesized that the presence of estrogen receptors in

women’s TMJ changes metabolic functions increasing ligament laxity. Estrogen also
increases susceptibility to painful stimuli by modulating the limbic system. Studies in humans
have shown that painful symptoms increase by 30% among patients on menopause treatment
with estrogen replacement therapy and by 20% in women using oral contraceptives (Andrea
et al, 2015).

Macrotrauma such as injuries on head or neck is a predisposing and initiating factor

for TMD. Parafunctions are also one of the TMD causing factors. Excessive gum chewing,
teeth chewing, teeth clenching and bruxism have been studied for years as possible risk
factors for TMD. Bruxism will cause muscle dysfunction and even joint dysfunction, such as
disc displacement. This may result in condylar bone remodeling and articular cartilage
degradation (Fischer et al, 2006).

2.6 Management And Treatment Of TMJ Disorder

21
 Management Dislocation of TMJ include non-surgical therapy and surgical therapy, in
accordance with the indications: (Gross et al., 1995)
1.  Non-surgical therapy:
a. Medikamentosa
b. Reposition
c. Fixation and immobilization
d. Repair dental occlusion
2.  Dislocation Treatment with Surgical Procedure:
a. Open Reduction
b. Myotomy pteygoideus externus muscle, "Blocking" & Anchoring
c. Meniscectomy & Eminectomy
d. Condilotomy, Condilectomy

Management dislocation of TMJ (temporomandibular joint) depending on the

occurrence of dislocation. In acute circumstances, should be performed manually
repositioned before increases in muscle spasm. Whereas in recurrent chronic condition
required surgery and non-surgical others to avoid Redeployment.
Procedures manual therapy is a reduction method which has long been introduced.
Procedures stages are as follows: (Saleh, E. 2015)
1. If the possibility of fracture, X-ray photograph needs to be done first. If no
trauma, can be done directly handling process.
2. The patient is placed on a seat that is not backed and stick to the wall so that
the patient's back and head against the wall.
3. Before doing aid, bandage the thumb with a rather thick gauze to prevent
being bitten thumb because after being in the correct position then the jaws
will shut quickly and violently. Then use gloves.
4. Operator position is in front of the patient.
5. Put your thumb on the retromolar pad area (behind the last molar teeth) on
both sides of the mandible as high as elbows operator and the other fingers
holding the lower surface of the mandible (A).
6. Give pressure on the teeth of mandibular molars to free the condyles of the
locked position in front of the eminence artikulare (B).
7. Push the mandible backwards to restore it to its anatomic position (C & D).

22
 Figure 7 : Treatment of TMJ Disorder (Carlsson, 1999)

Picture 1. (Carlsson, 1999)

8. If it is not easy to be relocated, the operator can refer to do an X-ray photograph

9. May be giving intravenous midazolam (to loosen the muscles) and 1-2 mL of
1% lidocaine Intraarticular (to reduce pain). Injection is done on the left side
of the depressed area of the condyle displacement.
10. Installation Barton Head Bandage to prevent the relocation and avoid patient
opened his mouth too wide in 24-48 hours. Patients are also instructed to soft
food diet.
11. The drug delivery in the form of analgesics and muscle relaxants (if necessary)

In the treatment of TMJ dislocation cases, among others (Saleh, E. 2015) :

1. Medicamentosa:
Indication; relieve pain and muscle spasm that accompanies dislocation. An act is
done with the use of drugs, as follows:
a. analgesics: Pain is gone, lost muscle spasm, repositioning
b. Anti-inflammatory: Inflammation is gone, the pain is gone, lost muscle
spasm, spontaneous repositioning.
c.  Tranquillizer: Emotional disturbances
resolved, spasms disappeared, repositioning.
d. Sedativa: overcome nervous tension, spasms
disappeared, repositioning.

23
 e. Muscle relaxants: Relaxation acquired, repositioned.
f. Intra-articular injection of local anesthetic / pd intramuscular
masticatory muscles: Overcoming pain and muscle relaxation,
repositioning
2. Reposition :
Done with the intent to restore the position of the condyle to its original position,
either manually or assisted medical treatment.

Figure 8 : Manual reposition (Saleh, E. 2015)

3. Fixation and immobilization

The main purpose of resting the joint during the healing period after
repositioning. Another aim is to gain traction repositioning of the condyle
dislocation with the fractures of the condyles simple. This can be done either
extraoral or intraoral.
4. Improvements dental occlusion
The main purpose is to follow up of treatment TMJ Dislocation. Another aim
is to eliminate predisposing factors. And to covering occlusion relationship
between the teeth of the upper to the lower jaw and treatment of malocclusion.

2.7 Damage To Hard Tissue

24
2.7.1 Abrasion

Abrasion describes the wearing away of a substance or structur through

mechanical process. Dental abrasion is the pathologic wearing of teeth as a result of
abnormal processes, habit, or abrasive substance. The location and pattern of abrasion
may dependent upon the cause and the most common cause found is toothbrushing.
(Litonjua, 2003) Toothbrushing, which is a contemporary tooth cleaning routine
activity, has almost no or little effect on hard enamel, while much softer dentin is
more susceptible to toothbrushing abrasion. Incorrect oral hygiene habits can result in
severe wear of enamel. (Wu, 2017)

2.7.2 Attrition

Attrition describes the action of rubbing against something. Dental attrition is

defined as the physiologic wearing of teeth resulting from tooth to tooth contact as in
mastication. Clinically, the first manifestation is the tip or ridge or an incisal edge.
Attrition may lead to dentinal exposure. Some malfunctional such as bruxism and
clenching can contribute to attrition. (Litonjua, 2003) Bruxism is usually a response of
an individual to increased stress and is associated with lowering the levels of stress-
induced increase of nor-epinephrine turnover in brain. Stress as a lifestyle factor is
increasingly seen as a predisposing influence towards bruxism. It is most often seen
on the occlusal surfaces of posterior teeth, the incisal edges of anterior teeth. It is due
to mechanical wear that the contact points on the proximal surfaces turn into contact
areas which can lead to a reduction in the dental arch. Attrition of teeth was seen in
the older age group as a sign of the natural ageing phenomenon. (Jain, 2015)

Developmental anomalies, especially, amelogenesis imperfecta and

dentinogenesis imperfecta predispose teeth to rapid wear. This is because the enamel
is very thin in amelogenesis imperfect while in dentinogenesis imperfect the
attachment of the enamel and dentin is weak which results in easy separation. (Jain,
2015)

2.7.3 Bruxism
Bruxism is the medical term for the grinding, gnashing, chafing, rubbing of
the teeth, clenching of the jaw, especially during deep sleep. Bruxism has few causes-

25
malaocclusion, bruxism, TMJ and stress is an injury to the jaw due to incorrect
positions during the day but especially at night. Bruxism is the violent and noisy
rubbing of the lower teeth against the upper teeth lasting a few seconds. Bruxism is
one of the most common sleep disorder. Bruxism occurs predominantly during sleep,
always and only in those people who sleep lying face downwards on the bed, on their
stomach or on their hips, as they weight heavily with static load on their jaws (health
and sleeping position). (Slabach, 2007)
From some of the research done on children, we know there is a link between
bruxism and the body's survival mechanism to keep the airway open. If a child is
grinding his or her teeth at night, the first causative factor to look for is an obstructed
airway. Enlarged tonsils and adenoids are a common cause for airway obstruction in
children and even contribute to obstructive sleep apnea. Bruxism triggers a muscle in
the back of the throat to spasm and keep the airway open. It is hard to blame teeth-
grinding on stress in a young child This is particularly apparent in people suffering
from sleep-disordered breathing, the most severe cases being obstructive sleep apnea.
In adults the cause is usually not enlarged tonsils and adults, but a collapsible
windpipe that contributes to the sleep apnea. (Galiffa, 2010)

When the jaw is in the wrong position, the body attempts to correct it by
bruxism. The muscles of the jaw and face spasm and attempt to move the jaw to a
more comfortable position. As these muscles spasm, the teeth slide back and forth in
response to that muscle activity. This can occur particularly in a person whose facial
and jaw muscles are shortened-a muscle cramp in the jaw. The teeth grind to relieve
the spasms much like stretching to relieve a cramp in the calf muscles. (Galiffa, 2010)
After even a short period of grinding, the lower jaw can recede backward
causing a jaw joint disorder or TMJ disorder. The lower jaw fits in to a socket of the
upper jaw and is protected by a cartilage disc. If the lower jaw is allowed to retrude to
the back of the socket, a couple of things can occur (Galiffa, 2010) :
1. Compression of the nerves and blood vessels in the back of the jaw joint,
which can cause headaches, face, jaw and neck pain
2. Displacement of the cartilage disc, indicating a dislocation of the joint and
resulting in clicking, popping or grating noises upon opening and closing
of the jaw

26
 3. Further compromise of the airway, making obstructive sleep apnea even
more possible

Sleep clenching, which occurs while dreaming is anunconscious act together

while sleeping is not always dysfunctional; that is, it is needed for the eruption
process of teeth. (Galiffa, 2010)
The Clenching Syndrome (also called the TMJ Syndrome) is a cycle. It has a
beginning, which is always the same, and a final stage, which is always the same, if it
progresses to its end. A slight (subtle) looseness of the teeth is the first sign of sleep
clenching--something you can detect yourself. The final stage, which is advanced
periodontal disease (teeth that may have to be removed), is not experienced in every
person. Nevertheless, if one continues to clench, the cycle will continue reaching the
final stage. (Galiffa, 2010)
There are two parts of the clenching syndrome: occlusomuscular problems and
occlusodentition problems. The first is concerned with irritation of the muscles of
the head and neck with irritation to the TM joints and ear apparatus. The second deals
with damage to teeth and their supporting structures. (Galiffa, 2010)
Chewing on one side forced one side’s muscles to do more activities so it can
cause hyperactivities and hypercontraction. The uses one side of the body to prop the
whole body, usually one side of the face will prop the whole mass of the body. TMJ
are placed on both right and left side of the face that’s why if a person do this bad
habit, their TMJ is forced to prop a big mass so it is forced and can cause pain and
will become a disorder. (Galiffa, 2010)

2.7.4 Erosion
Dental erosion is the loss of dental hard tissue, associated with extrinsic and/or
intrinsic acid that is not produced by bacteria. Though the chemical process of dental
erosion is similar to that of caries, dissolution of hydroxyapatite by acids, the clinical
manifestations and management of dental erosion are fundamentally different from
caries because the erosive process does not involve acid of bacterial origin. Dental
erosion does not begin as a subsurface enamel lesion that is conducive to
remineralization, as in the caries process, but rather as a surface-softening lesion that
is susceptible to wear and resistant to remineralization by conventional therapies. It is
often widespread and may involve the entire dentition. Dental hard tissue loss

27
 associated with erosion is almost always complicated by other forms of tooth wear
such as attrition and abrasion. Dental erosion results in tooth surface softening, which
inevitably accelerates tissue loss caused by tooth-to-tooth contact while chewing and
grinding (attrition) or by abrasive wear while mechanically brushing or cleaning tooth
surfaces (abrasion). If dental erosion is not managed through effective interventions, it
may result in substantial loss of enamel and subsequent exposure of the underlying
dentin, which can, in turn, lead to dentin sensitivity, loss of vertical height and
esthetic problems. (Jaeggi T, Lussi A.,2006)
As described earlier, extrinsic and intrinsic acids are the predominant
etiological factors for dental erosion. Therefore, erosion risk assessment mainly
involves identification of these factors in a specific patient and an evaluation of their
roles in the development of dental erosion.
Risk factors for dental erosion include (Jaeggi T, Lussi A.,2006) :
1. Frequent use of acidic dietary products, especially soft drinks, fruit juices and
acidic foods
2. GERD, rumination, regurgitation and frequent involuntary vomiting
3. Prolonged use of chewable acidic medications, especially vitamin C and
aspirin
4. People in occupations involving hazards that include direct contact with acidic
substances, wine makers and tasters, swimmers, and battery workers
5. Sustained use of recreational drugs such as ecstasy
6. Low saliva flow rate and inadequate saliva buffering capacity
Patients with any of the above factors are at risk of developing dental erosion.
Though the current paradigm is for dental practitioners to look for these risk factors
after they see signs of erosion and erosive wear, identification of these factors before
the existence of any sign of erosion may be more important. Early intervention for the
prevention of dental erosion is a more effective therapeutic strategy than any attempt
to restore lost dental hard tissue due to erosion. A thorough evaluation of dietary
habits will be helpful in assessing the erosive potential of acidic foodstuffs. (Lussi A,
Schaffner M. Caries Res. 2000)

2.8 Radiology of Temporomandibular Joint Disorders

2.8.1 Rheumatoid arthritis

28
 Fifty percent of rheumatoid arthritis patients show some involvement from
TMJ. Patients complain of pain, swelling, and reduce mouth opening. This change is
most noticeable in the morning and usually occurs periodically. Conventional X-ray
techniques in the early stages of the disease are undiagnostic because of pathological
changes that begin with synovial tissue that cannot be seen in this examination. MRI
shows an excellent overview of early changes in the synovial part of the joint and is
very sensitive. Very sensitive is STIR. After progression of the disease, bone changes
and demineralization are seen in 50-80% of patients with articular surface applanation
and bone erosion. Erosion is usually on the anterior portion of the articular surface.
The articular surface by the development of the disease becomes irregular, erosion
and loss of the normal articular form. Material erosion can be found in the glenoidalis
fossa. Pain, swelling, reducing open mouth and crepitations are identical with those of
rheumatoid arthritis. (G. Steinhart, 2008)

Figure 9 : Panoramic features, indicating irregular erosion on the right and left sides of the
flat condyle on the articular eminent. (G. Steinhart, 2008)

2.8.2 Ankilosys
Ankilosys is a fusion of joints, usually rare but the result of trauma, head
fractures, especially condylus and birth injury, bleeding into the joints, and infection.
Ankilosys in TMJ can become fibrous or bone. Fibrous ankilosys cannot be diagnosed
by conventional X-ray methods because the fibrous tissue is transparent to
conventional images. Osseous ankylosys or bony ankylosys in articular joints can be
detected by conventional x-rays. MSCT is a gold standard in diagnosing TMJ
ankilosys. Types of Bone Ankylosis (Mariani PB, 2003) :

29
 Type I: flat and deformed condyl head near the upper joint space. The fibrous
attachment is seen in it. Difficulty in movement due to fibrosis in and around
joints.
Type II: a flat condyle close to the glenoid fossa, bone union on the outer
surface of the arteryic surface anteriorly and posteriorly and confined to a
narrow region.
Type III: ankylosis usually results from a dislocation of fractures pushed into
the condyle of the condyle with a mandibular ramus bone bridge to the
zygomatic arch. The condylet head is atrophy both free and also integrates
with the posterior aspect of the ramus.
Type IV: the trellis barrier of the wide mandibular ramus and zygomatic arch,
waves and takes up joint space and replaces the overall architecture of the
joint.

Figure 10 : Transverse CT scans show bony shift and bony fusion on the right TMJ. (Mariani
PB, 2003)

30
31
 CHAPTER 3
CONCEPTUAL MAPPING

Tooth Grinding

Soft Tissue Hard Tissue

Bruxism, Clenching Attrition at Cusp

Trauma Compression of TMJ

(compression of condyle)

Secretion of ATP, H+ &

sensitizing agent
(Substance P, CGRP, Synovial fluid & Synovial
bradykinin, Membrane decreases
prostaglandin)

Limited movement of
Nociceptor TMJ
Muscle

Disc dislocation
Permeability
increases

‘Clicking’
Na+ enters Pain

Action Somatic Area (At

Potential postcentral gyrus)

Stimulation towards
M. Spinalis Thalamus

32
 CHAPTER 4
DISCUSSION

Activities of the masticatory system can be divided into two types: Functional, which
includes chewing, speaking, and parafunctional, which includes clenching or grinding of the
teeth (referred to as bruxism). Parafunctional activity is also known as muscle hyperactivity.
The functional activities are very controlled muscle activities, which allow the masticatory
system to perform necessary functions with minimum damage to the structures of this system.
However, some interfering tooth contacts have inhibitory effects on functional muscle
activity. Therefore, functional activities are considered to be directly influenced by the
occlusion.
Occlusion affects the function of jaw muscles, which in turn affects the way the
temporomandibular joint (TMJ) functions. Hence, any changes in the patient’s occlusion will
have an effect on the TMJ structures and jaw muscles. (Mense, 2008)
Parafunctional activities like bruxism apparently are controlled by entirely different
mechanisms. The etiology of bruxism is not completely clear. Few morphological factors
such as dental occlusion and the anatomy of the bony structures of stomatognathic system
may be associated with bruxism. Other distinguishable etiologic factors of bruxism are:
Psychosocial factors such as stress and certain personality characteristics, central factors and
special neurotransmitters, patho-physiological factors (i.e., diseases, trauma, genetics,
smoking, alcohol, caffeine intake, illicit drugs and medications), sleep disorders (sleep apnea
and snoring), and dopaminergic system involvement. One thing seems certain: There is no
single factor that is responsible for bruxism. It is also rather evident that there is no single
treatment that is effective for eliminating or even reducing bruxism. (Mense, 2008)
We can say that the patient might be stress because elders are more vulnerable to
stress and depression. Stress can cause a bad habit called bruxism and clenching. It r esults
from a physiological and highly functional activity: Spontaneous Deglutition or Spontaneous
Swallowing. Normally, in the rest position and in the absence of disease, the jaw is centred,
balanced and suspended under the skull while muscles are relaxed, balanced and tonic,
condyles are symmetrical in their position in articular cavities, teeth are not in contact, and
enjoy the Benefits of inactivity . This precious gift of nature and health can only occur
whether the jaw is free to move and make contact with the teeth in the right position,
(maximum Intercuspidation occlusion), in anatomical and functional harmony with the other

33
chewing elements. In wrong sleeping position ( sleep stomach, face down) the weight of the
head pushes the mandibula to lateral occlusion and exerts non-stop compression ( for many
hours) on the teeth, gum, periodontium and TMJ , therefore obstructing blood circulation and
moving the teeth to a lateral bad occlusion position(TMJD). In order to swallowing,
masticatory muscles must activate themselves to centre the jaw and then they must bring the
teeth from forced lateral malocclusion to centred occlusion (maximum Intercuspidation
occlusion), rubbing , grinding teeth between them, this is the cause of nocturnal bruxism and
negative trophic action on the gum , periodontium and TMJ disfunction. Throughout the
night the Neuromuscular component, instead of being relaxed, has pledged to oppose the
thrust of the weight that lies heavily on the jaw. This is the real reason for the bruxism is
especially active during sleep. The teeth are pushed sideways for hours, months, years move
sideways, their movement generates a bad occlusion. Malocclusion, in which the upper and
lower teeth occlude in a disharmonic way, through premature contact of back tooth the
relationship disharmony between the teeth and the imbalance of the jaw, can also cause
bruxism during the day in an attempt to reposition the teeth. The rubbing causes tooth facet
wear but also mobility and parodontal disease pyorrhoea . Compression lasting all night on
the teeth, face and mandibular joints, prevents the circulation of blood in all components, in
particular in support of the teeth (periodontium). The ischemia and dystrophy, which might
ensue cause suffering to all the anatomical components of chewing. The joints , which are
under pressure all night , are subject to structural and functional damage , hence they deform.
This explains why bruxism is often associated to limitations, pain, buzzing and crackling,
clicks, teeth chafing, gnashing of teeth, teeth grinding and dysfunction of the jaw joint, TMJ,
persistent face pimples, headache, migraine, hum, tinnitus, cervical and lumbar pain from
postural problems, gingivitis, periodontitis, pyorrhoea. Stress and psychological problems are
not the cause but pro-factors. (Shibuya, 2007)
Most functional activity occurring in jaws consists of well-controlled, rhythmic
contraction and relaxation of the muscles. This rhythmic activity permits adequate blood
flow, which supplies oxygen to the tissues and eliminates by-products accumulated at the
cellular level. Bruxism, by contrast, results in sustained muscle contraction for long periods.
This type of activity reduces oxygenation within the muscle tissues as there is reduced blood
flow. As a result, the levels of carbon dioxide and cellular waste by-products increase within
the muscle tissue creating the symptoms of fatigue, pain, and spasms. (Mense, 2008)
Muscle pain is evoked by specialized nerve endings (nociceptors). Important stimuli
for muscle pain are adenosintriphosphate (ATP) and a low tissue pH. Excitation of muscle

34
nociceptors leads to hyperexcitability of spinal sensory neurons (central sensitization). Low
frequency activity in muscle nociceptors is sufficient to induce central sensitization. (Mense,
2008)
Muscle pain is produced by the activation of specific receptors (so-called
nociceptors): these receptors are specialized for the detection of stimuli that are objectively
capable of damaging tissue and that are subjectively perceived as painful. They consist of
free nerve endings and are connected to the central nervous system (CNS) by way of
unmyelinated (group IV) or thinly myelinated (group III) fibers. They can be sensitized and
activated by strong mechanical stimuli, such as trauma or mechanical overloading, as well as
by endogenous inflammatory mediators including bradykinin (BK), serotonin, and
prostaglandin E2 (PGE2).(Mense, 2008)
Two activating chemical substances are particularly important for the generation of
muscle pain: adenosine triphosphate (ATP) and protons (H+ ions). These chemical irritants
activate nerve endings by binding to receptor molecules located in the membrane of the nerve
ending. ATP activates muscle nociceptors mainly by binding to the P2X3 receptor molecule,
H+ mainly by binding to the receptor molecules TRPV1 (transient receptor potential
vanilloid 1) and ASICs (acid-sensing ion channels). These receptor molecules are channel
proteins that span the membrane of the nerve ending and mainly permit Na+ ions to enter the
neuron. These Na+ ions then induce neural excitation. (Mense, 2008)
ATP is found in all cells of the body and is released whenever bodily tissues of any
type are injured. Muscle nociceptors contain neuropeptides, including substance P (SP) and
calcitonin-gene-related peptide (CGRP). These peptides are released when nerve endings are
activated and induce local edema by dilating the local blood vessels and increasing their
permeability. Thus, a nociceptor can alter the microcirculation in its immediate neighborhood
by releasing neuropeptides. Endogenous substances such as BK and E2 prostaglandins are
released by muscle lesions of all kinds. BK is synthesized from plasma proteins by the action
of the enzyme kallikrein, while prostaglandins are synthesized from arachidonic acid by the
action of cyclooxygenase. These two activating substances increase the sensitivity of
nociceptors to external stimuli (peripheral sensitization). (Mense, 2008)

Because ATP is released in any kind of tissue injury, it can be considered a universal
pain-inducing substance. ATP is found in particularly high concentration in muscle cells; it
can cause pain in muscle trauma (e.g., a bruise or tear of muscle fibers) as well as in other
types of pathological change in muscle (e.g., necrotizing myositis) .The neuropeptides stored

35
in muscle nociceptors are released not only when peripheral stimuli activate the nerve
endings, but also when spinal nerves are compressed. In this type of neuropathic pain, action
potentials are generated at the site of compression and spread not only centripetally, i.e.,
toward the central nervous system, but also centrifugally, i.e., toward the nociceptive endings,
where they induce the release of vasoactive neuropeptides. In this way, neurogenic
inflammation comes about, characterized by hyperemia, edema, and the release of
inflammatory mediators. The inflammatory mediators sensitize the muscle nociceptors and
thereby increase neuropathic pain. (Mense, 2008)

The sensitization of the muscle nociceptors by endogenous mediators such as BK and

PGE2 is one of the reasons why patients with muscle lesions suffer from tenderness to
pressure on the muscle, and from pain on movement or exercise. It is also the reason why
many types of muscle pain respond well to the administration of non-steroidal anti-
inflammatory drugs (NSAID), which block prostaglandin synthesis. Sensitization manifests
itself clinically in two closely related phenomena: stimuli that normally do not cause pain are
perceived as painful (allodynia), while stimuli that are normally painful cause more severe
pain than before (hyperalgesia). The principal mechanism for allodynia and hyperalgesia,
however, is thought to be located in the central nervous system. (Mense, 2008)

The increased excitability of spinal neurons and the spread of excitation within the
CNS are the first steps in the process of chronification of muscle pain. The endpoint of
chronification consists of structural remodeling processes in the CNS that open up new
pathways for nociceptive information and cause pain to persist over the long term. Patients
with chronic muscle pain are difficult to treat, because the functional and structural changes
in the CNS need time to regress. The fact that not all muscle pain becomes chronic implies
that chronification requires not only the mechanisms just discussed, but also other ones.
(Mense, 2008)

Muscle spasm can be defined as persistent, involuntary muscle contraction (not

including spasticity, a phenomenon of central nervous origin). The main reason why pain
arises in muscle spasm is muscle ischemia, which leads to a drop in pH and the release of
pain-producing substances such as bradykinin, ATP, and H +.The vicious-circle concept of
muscle spasm – muscle pain causes spasm, which causes more pain, etc. – should now be
considered obsolete. Most studies have shown that muscle pain lowers the excitability of the
α-motor neurons innervating the painful muscle (a "pain adaptation" model). (Mense, 2008)

36
 Muscle spasm can be precipitated by, among other things, pain in another muscle.
Thus, a spasm-like increase EMG activity in the trapezius muscle has been described in
response to painful stimulation of the biceps brachii muscle. Another source of muscle
spasms is pathological changes in a neighboring joint. These sources of pain must be
deliberately sought. (Mense, 2008)
Clicking jaw, also referred to as popping jaw or TMJ (temporomandibular joint)
syndrome/dysfunction is a symptom associated with inflammation of the temporomandibular
joint or uncoordinated action of the facial muscles. This situation can occur in the morning,
at midnight, or at night when there was a motion to open the mouth. Clicking can also occur
during the motion to close the mouth as in the motion to open the mouth. (Mense, 2008)
In addition, the incidence of sound in the joint is a TMJ dysfunction that can be
divided into two types, namely rubbing sound, and clicking sound. In most cases clicking
noise on TMJ 70-80% is caused by disk displacement with varying degrees and directions,
but mostly in the anteromedial direction. This phenomenon can be described as an
interference against the translatoric motion of the condyle and meniscus (discus) during
movement closing and opening the mandible. The superior lining of the condyle allows the
interference between the condyle and the meniscus as they move. Normally, muscle activity
is such that the flexible meniscus moves smoothly between the condyle and eminentia. If the
initial position of the condyle changes (eg due to changes in the occlusion pattern), the
direction of movement may change and the posterior zone is thicker while trapped between
the condyle and eminentia. (Liebgott, 1994)
Neuromuscular responses usually produce the adaptation motion required to complete
open mouth motion. Deviation drift to avoid clicking will occur and a further barrage of
clicking and adaptation moves occur, in the clique group there is a deviation of movement
pattern than in healthy group. In the absence of pain fibers in the meniscus, making clicking
rarely causes pain, but if resistance increases (eg, viscosity of synovial fluid), continuing the
opening motion may result in tearing of muscle fibers (pterygoidal lateralis), resulting in pain
and stiffness as accompanying symptoms. (Liebgott, 1994)
Clicking generally occurs during motion opening the mouth, but can also occur just
before closing the mouth when the discus moves backward in the direction that has changed.
Clicking can be removed by opening or closing the mandible on the reticular axis or by
placing the bite plane in contact with the lower incisors just before the motion closes.
Changes in the occlusion pattern is one of the causes of clicking. Another cause is the

37
excessive and sudden movements of the mandible that result in the discs or clenching of the
prolonged teeth so that the opening changes with muscle fatigue. Clicking can also occur
intermittently in adolescence due to adaptation movement when growth is underway, this
condition can be avoided by closing and opening on the axis of retrusion. Watt classifies the
sound of joints into clicks and crepitus, then both are grouped into soft and hard depending
on the quality. Furthermore it is also classified into initial, intermediate and terminal,
depending on the position of the jaw at the time of clicking. (Watt, 1980) Hard clicking may
indicate a common abnormality of the joint followed by a hard crepit indicating a specific
defect in the joint surface. (Liebgott, 1994)
Bruxism is the medical term for the grinding, gnashing, chafing, rubbing of the teeth,
clenching of the jaw, especially during deep sleep. We know there is a link between bruxism
and the body's survival mechanism to keep the airway open. If a child is grinding his or her
teeth at night, the first causative factor to look for is an obstructed airway. Enlarged tonsils
and adenoids are a common cause for airway obstruction in children and even contribute to
obstructive sleep apnea. Bruxism triggers a muscle in the back of the throat to spasm and
keep the airway open. It is hard to blame teeth-grinding on stress in a young child. Most
children do not have the level of emotional stress that adults do. Adults with compromised
airways also brux to keep the airway open. This is particularly apparent in people suffering
from sleep-disordered breathing, the most severe cases being obstructive sleep apnea.
(Mense, 2008)
In adults the cause is usually not enlarged tonsils and adults, but a collapsible
windpipe that contributes to the sleep apnea. When the jaw is in the wrong position, the body
attempts to correct it by bruxism. The muscles of the jaw and face spasm and attempt to move
the jaw to a more comfortable position. As these muscles spasm, the teeth slide back and
forth in response to that muscle activity. This can occur    particularly in a person whose
facial and jaw muscles are shortened-a muscle cramp in the jaw. The teeth grind to relieve the
spasms much like stretching to relieve a cramp in the calf muscles. (Mense, 2008)
After even a short period of grinding, the lower jaw can recede backward causing a
jaw joint disorder or TMJ disorder. The lower jaw fits in to a socket of the upper jaw and is
protected by a cartilage disc. If the lower jaw is allowed to retrude to the back of the socket, a
couple of things can occur: - Compression of the nerves and blood vessels in the back of the
jaw joint, which can cause headaches, face, jaw and neck   pain - Displacement of the
cartilage disc, indicating a dislocation of the joint and resulting in clicking, popping or

38
grating noises upon opening and closing of the jaw - Further compromise of the airway,
making obstructive sleep apnea even more possible. (Mense, 2008)

39
 CHAPTER 5
CLOSING

5.1 Conclusion
It can be concluded that the patient is having a temporo mandibular joint disorder
which causes ‘clicking’ sound when opening and closing the mouth due to bruxism, which
explains the abrasion on the surfaces of the posterior teeth and palpation at the TMJ. This can
be occured due to possible stress and wrong sleep position that causes stiffness, cramp and
pain around the cheeks area after waking up from his sleep.

5.2 Solution
In order to prevent from temporo mandibular joint disorder to happen, it is advised for
the patient sleep without laying on one side only and keep himself away from getting too
stress. For the treatment of tmj, patient can either take non-surgical treatment such as
reposition or repair dental occlusion, or the surgical treatment such as open reduction or
condilotomy.

40
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