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.

1.5. Hipotesis Unfinished removable orthodontic (retainer) treatment can lead to temporomandibular disorder type mylofacial pain.

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 bodys 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).

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 concaveshaped 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 crosssection 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.

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. Temporalis. Pterygoideus externus. 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 maxill 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 sideto-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
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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, at muscle. Its bres can be divided into two parts: the anterior bres that elevate the mandible (lower jaw) and close the mouth and the posterior bres 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 at quadrilateral muscle with deep and supercial 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 temporalis muscles, (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.

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. 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)
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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 (Soboeva 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
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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
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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
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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)

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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).
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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.
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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,Unskilledpatient 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
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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
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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)

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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)

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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).
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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 temporomuscles 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

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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; AchEacetylcholinesterase; AchRacetylcholine receptor (Dommerholt, 2006).

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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
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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

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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
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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, timedependent phenomenon (Svensson and Graven-Nielsen 2001), and indeed
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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).
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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 1520 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 (2.55mg 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 34 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 patients 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 strogens, are a group of steroid compounds, named for their importance in the estrous cycle, and functioning as
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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 estrogenlike 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).

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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 17estradiol. 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
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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
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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
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emerges in young adulthood (Warren & Fried, 2001) may implicate sex hormones in the pathophysiology of this condition. In particular, ER 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 ER in immune modulation (kubota, et al , 1998). Because ER is present in the immune cells in the human TMJ ,a likely target of 17 -estradiol in the human TMJ is ERpositive immune cell (Kang, et al, 2007). Furthermore ER- 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 ER in the increased incidence of TMJ inflammation Steroid hormones, particularly estrogen, act through their receptors (estrogen receptor- [Er] and estrogen receptor- [ER]) 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 [TNF-]).(Massart,2001) The cytokines IL-1 and IL-6 are present in the TMJ synovium during inflammation, and IL-1 and TNF- 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- 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 ER could lead to significant modifications in the physiological role of estrogen and consequently in TMJ derangements.

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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

46

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 ERalpha 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
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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-ke 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 its almost impossible to include sufficient omega-3s 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).

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CHAPTER 3 CONCEPTUAL MAPPING

TMJ General TMJ Anatomy Histology Physiology Pathology Prevalency TMJ Dissorder Type Mylofacial pain result of

Unfinished removeable orthodontic treatment

Women

>

Men

premature contact at prosterior tooth

because of trigger Hormonal system

30 years old Women

Occlusion disharmony

Decrease of Esterogen Fatique on 3 digestive muscle Over contraction and overload pressure at digestive muscle

masseter

temporalis

Pterygoideus medialis

Symtoms : hard to open the mouth

Miospasme

Inflamation

At Trigger point (digestive muscle)

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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 temporomuscles 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)
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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 movementthis 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
51

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
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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
53

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.

54

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.

55

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
56

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.
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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.

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