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CHAPTER 1 INTRODUCTION1.1 Background Temporomandibular joint is the only joint that can be handled by dentists. It is very important for us to learn about this joint because there are a lot of cases that can be caused by temporomandibular joint disorder. Temporomandibular joint is formed by bones, muscles, ligaments, nerves, etc. This joint makes it possible for us to open and close the mouth. When the joint and surrounding muscles and ligaments are malfunctioned in some way, it is called temporomandibular joint disorder. It can be caused by bad habits such as bruxism, clenching, etc, disc displacement, the degenerative joint, etc. 46 year old female patient came to the dentist with a complaint that this 1 year, she has been feeling stiffness, dull, clicking sound as well as pain in the left and right cheek area when she opens her mouth, especially on mornings when she wakes up, whereas there is no dental cavities 1.2 1.3 1.4 1.5 Problem Statement Purposes Objectives Methods Our research is based on journals and textbooks that we get both from mass and electronic media. 1.6 Hypothesis The patient feels pain because of there is a temporomandibular joint disorder. We conclude that there is temporomandibular joint disorder because of some symptoms that are experienced by the patient like clicking sound, pain on the right and left cheeks, also muscle pain. CHAPTER 2 LITERATURE STUDY 2.1 Anatomical View of Temporomandibular Joint The temporomandibular joint, or TMJ, is the articulation between the condyle of the mandible and the squamous portion of the temporal bone. There are two TMJs, one on either side, working in unison. The name is derived from the two bones which form the joint : the upper temporal bone which is part of the cranium ( skull ), and the lower jaw bone called the mandible . The unique feature of the TMJs is the articular disc . The disc is composed of fibrocartilagenous tissue (like the firm and flexible elastic cartilage of the ear) which is positioned between the two bones that form the joint. The TMJs are one of the only synovial joints in the human body with an articular disc , another being the sternoclavicular joint . The disc divided each joint into two. The lower joint compartment formed by the mandible and the articular disc is involved in rotational movement-this is the initial movement of the jaw when the mouth opens. The upper joint compartment formed by the articular disk and the temporal bone is involved in translational movements, this is the secondary gliding motion of the jaw as it is opened widely. The part of the mandible which mates to the under-surface of the disc is the condyle and the part of the temporal bone which mates to the upper surface of the disk is the glenoid (mandibular) fossa. Temporomandibular joint divided into two components, there are active component and passive component. Passive component Passive components are bone, articular capsule, ligament, and articular disc. Bone component in passive component is fossa mandibularis, capitulum mandibula (condyle/ processus condyloideus), tuberculum articulare (articulare eminence). Fossa mandibularis is the squamous portion of the temporal bone (concave). Anterior boundary of fossa mandibular is a convex bony eminence (tubercle) or articular eminence. It is quite thick to arrest the strength, instructing movement of condyle when the position of mandibular to anterior. Processus condyloideus is the posterior portion of the ramus mandibula that extends upward. The condyle is elliptically shaped with its long axis oriented mediolaterally.Length of mediolateral is 15-20 mm, and length of anteroposterior is 8-10 mm. the medial pole generally more prominent than lateral. The articular surface of the temporal bone is composed of the concave articular fossa and the convex articular eminence. Capsule articularis or capsular ligament is fibrous structure surrounds the entire temporomandibular joint. Superior of capsule is patch with temporal, the borders of the articular surface of the mandibular fossa and articular eminence. Inferior of articular capsule is patch to the collum mandibula. The function of capsular ligament is to resist any medial, lateral or inferior force that tend to separate or dislocate the articular surface and to retain the synovial fluid. Ligament of temporomandibular divided into collateral ligament, temporomandibular ligament, sphenomandibualr ligament, stylomandibular ligament. Collateral (discal) ligament lies from medial and lateral borders of the disc to the poles of the condyle. It consist of the medial discal ligament and the lateral discal ligament. It composed of collagenous connective tissues. The function is allow the disc move passively with the condyle as it glides from the anterior to the posterior and permit the disc to be rotated anterior to posterior on the articular surface of the condyle. These ligaments are responsible for the hinging movement between the condyle and the articular disc. They have a vascular supply and innervated. Temporomandibular ligament lies at the lateral aspect of capsular ligament. It composed of two parts, they are outer oblique portion and inner horizontal portion. Outer oblique portion from the outer surface of the articular tubercle and zygomatic process posteroinferior to the outer surface of the condylar neck. It resists excessive dropping of the condyle so limiting the extent of mouth opening. Inner horizontal portion from the outer surface of the articular tubercle and zygomatic process posteriorlyand horizontally to the lateral pole of the condyle and posterior part of the articular disc. It limits posterior movement of the condyle and disc. Sphenomandibularis ligament is an accessory ligament. It lies from the spine oh the sphenoid bone and extends downward to lingual mandibula. Stylomandibular ligament is the second accessory ligament. It lies from the styloid processand extends downward and forward to the angle and posterior border of the ramus mandibula. It limits excessive protrusive movement of the mandible. Articular disc is composed of dense fibrous connective tissue devoid of any blood vessels or nerve fibers. In sagital plane can be divided into three regions according to thickness, anterior border, posterior border(slightly thicker than anterior border), and central area is the tinnest, in normal condition, the condyle lies in intermediate zone. The disc is generally thicker medially than laterally, it increased space between the condyle and the articula fossa toward to the medial of the joint. The shape of the disc is determined from the morphology of the condyle and mandibula fossa. During movement the disc is flexible, and can adapt to the functional demands of the articular surface, but it cannot be reversible in its function. The disc maintain its morphology unless destructive forces or structural changes occurs. Its morphology can be irreversibly altered. It can be happened the biomechanical changes during its function. The temporomandibular joint considered as a ginglymoarthrodial joint in two movement, they are hinging movement (gingly joint) and gliding movement (arthrodial joint). It is formed by mandibular condyle fitting into mandibular fossa and the two bones is separated by articular disc. It is classified as a compound joint ( at least 3 bones ) and functionally the articular disc served as a non-ossified bone. The temporomandibular joint is divided into superior cavity (gliding action between condyle and articular eminence) and inferior cavity (hinge action between undersurface of the disc and the rotating surface of the condyle) by the articular disc. Retrodiscal tissue is a loose connective tissue region that highly vascularized and innervated. The articular disc is attached posteriorly to this region. In superior there are superior retrodiscal lamina, it contains of many elastic fibers. It attaches the disc posteriorly to the tymphanic plate. Inferior retrodiscal lamina contains of collagenous fibers. It attaches the inferior border of the posterior edge of the disc to the posterior margin of the articular surface of the condyle. The remaining body of the tissue is attached posteriorly to a large venous plexus, it fills with blood as the condyle moves forward. Anterior region of the disc is attached to the capsular ligament, in superior there are anterior margin of the articular surface of the temporal bone and in inferior there are anterior margin of the articular surface of the condyle. It composed of collagenous fibers. Anteriorly the disc is also attached by tendonous fibers to the superior lateral pterygoid muscle. The articular surface of the mandibular fossa and condyle are lined with dense fibrous connective tissue. It affords several advantages over hyaline cartilage , they are less susceptible to the effects of aging, less likely to break down over time, and a better ability to repair. The internal surface of the joint cavity are surrounded by specialized endothelial cells that form a synovial lining, it produces synovial fluid. The synovial fluid serves two purposes, they are : acts as medium for providing metabolic requirement, since the articular surfaces of the joint are nonvascular, and as a lubricant during its function. Two mechanism of the lubrication is boundary lubrication and weeping lubrication. Boundary lubrication is prevents friction in the moving joint. Weeping lubrication is eliminates friction in the compressed but not in moving joint. So the temporo mandibular joint is a synovial joint. Active component Active component consist of masticatory mascle and additional muscle. Masticatory muscle contains of masseter muscle, temporalis The superficial portion may also aid in protruding the mandible and biting force. the deep portion is stabilize the condyle against articular eminence. Its origo in 1/3 dorsal of the inferior border of the zygomatic arch and medial surface of the zygomatic arch.muscle. Masseter muscle is a rectangular muscle. Its insertio extends downward and backward to the tuberositas masseterica. If only portions contract. pterygoid medial muscle and pterygoid medial muscle. they are : Superficial head (caput superficial). Profundus head (caput profundus). Contraction of masseter cause the mandible is elevated and the teeth are brought into contact. Contraction of the muscle elevates the mandible and the teeth brought into contact. The second masticatory muscle is temporalis muscle. the contraction can cause the mandible is raised vertically Middle portion : The fibers run obliquely across the lateral aspect of the skull (forward as they pass downward ). This muscle give the efficient mastification strength. According to fiber direction and ultimate function. There is two portions or head (caput). It is origo in processus zygomaticus ossis maxillae and 2/3 ventral of the inferior border of zygomatic arch. because it can causes . it can be divided into 3 distinct areas : Anterior portion : The fibers are directed almost vertically. the contraction can cause elevate and retrude the mandible Posterior portion : Run almost horizontally. the mandible is moved according to the direction of those fibers that are activated. Its origo in temporal fossa. Its insertio in processus coronoideus and ramus mandibula. Its insertio extends downward and forward to ramus mandibula and lateral surface of processus coronoideus. coming forward above the ear to join other temporalis fibers as they pass under the zygomatic arch. The function is controversial. Its fibers extend downward between zygomatic arch and the lateral surface of the cranial. Temporalis muscle is a fan shaped muscle. it can be able to coordinate the movement of closing mouth. becoming active only in conjunction with the elevator The right and left inferior contracts simultaneously can cause the condyles are pulled down the articular eminence and the mandible is protruded . the disc and the neck of the condyle (fovea pterygoid). Pterygoid lateral muscle is the fourth muscle in mastificatory muscle. extending almost horizontally. it forms a muscular sling to support the mandible. This muscle fiber angulation is various. Pterygoid medial muscle consist of two head (caput). backward and outward to insert on the articular capsule. they are : Caput superficial : its origo in facies medialis lamina lateralis. processus pterygoideus (fossa pterygoideus). The third muscle of mastification is pterygoid medial muscle. The nilateral contraction can cause mediotrusive movement of the mandible.elevation and only slight retrusion. the superior remains inactive. It is also active in protruding the mandible. Caput inferior: its origo in facies lateralis lamina lateralis processus pterygoideus extends backward. they are : Caput superior : its origo in facies infratemporalis ala magna ossis sphenoidalis. It consists 2 heads or bellies with different function. The contraction can cause mandible is elevated and the teeth are brought into contact. Caput profundus : its origo in processus pyramidalis ossis palatine and tuber maxillae Extend downward. upward and outward to insert on the neck of the condyle (fovea pterygoid). backward and outward to insert along the medial surface of the mandibular angle (tuberositas pterygoidea). The function of pterygoid lateral muscle are : The superior lateral pterygoid is active during power stroke can cause closure mandible against resistance ( chewing and clenching ) While the inferior active during opening. With the masseter. and processus pyramidalis ossis palatine. It is formed by collagen and elastic (only a little amount) fibers. The second layer is the cell rich layer. It contains a lot of water inside because of the water absorption of the glycosaminoglycan. ground substance. it is classified to slidingginglimoid joint. but on the inferior. The fourth layer is the real bone. cells. TMJ is formed by mandibular fossa. It is covered by thin fibrous layer. The form of the cells are flatened (fibrous like). Actually. It surrounded by an articular capsule. Synovial membrane is the capsule’s membrane. The intima layer is formed by 1-4 cells layer. there’s no blood vessel (avascular) and inelastic. and rounded (Chondrosite like). vascular elements. The condylar head formed by thick fibrous connective tissue. used to distribute foods into the disk. Because it’s movement (sliding and rotation). and the bone is proliferating. The third layer contains fibrous and collagen fibers. Mandibular fossa is a part of the temporal bone. Blood vessels are found on the periferal side. The condyle has 4 layers. The articular disc separates the upper and lower synovial cavity. and condyle. On the superior lamellae. It produces the synovial fluid. and blood vessels. Becaues it contains 2 bones and surrounded with a capsule and it’s joint cavity filled by synovial fluid. and cells. articular disk. There are 2 layers : intima and subintima layer.2 Histological View of Temporomandibular Joint TMJ is one of synovial joints. it is the capsule of the joint but it is placed in the joint itself. .- The inferior functions with the mandibular depressorscan cause the mandible is lowered and the condyles gide forward and downward on the articular eminences 2. Sub intima layer is formed by loose connective tissue. there are a lot of blood vessels. The first layer is formed by a lot of collagen fibers and a little elastic fibers. the mandibular division is both sensory and motor. three major nerve bundles arise. including the mesencephalic nucleus. The trigeminal nerve also contributes sensory fibers to most of the duramater. the lacrimalis. especially for muscles that surround temporomandibular joint in this case. the frontalis and the nasociliary nerve.(Sheppard and Reed. (Barr and Kieman. In addition to stretch reflex there is also a jawopening reflex in which the contractions of the masseter. The scalp of the back of the head and an area of skin at the angle of the jaw are supplied by the second and third cervical nerves.2 Nerve The trigeminal nerve is the principal sensory nerve for the head and is the motor nerve for the muscles of mastication and several small muscles. At the lower border of the trigeminal ganglion. These are the three major divisions of the trigeminal nerve: the ophtalmicus (V ). the mucosa of the oral and nasal cavities and the paranasal sinuses and the theeth. the scalp as far back as the vertex of the head.(Sheppard and Reed. temporalis.3. 1976) The motor trigeminal nerve supplies the muscles of mastication (masseter. The .3 Muscles and Nerve inTemporomandibular Joint 2. and lateral and medial pterigoid muscles) and several smaller muscles. maxillary (V ) amd mandibular (V ). 1988) The sensory trigeminal nerve is responsible for sensation from the skin of the face and forehead. Functionally as well as structurally.3. temporalis and medial pterygoid muscles are inhibited as a result of painful pressure applied to the teeth. the trigeminal ganglion is comparable to the dorsal root ganglion of a spinal nerve. The ophtalmicus and maxillary divisions are entirely sensory.2. Afferents for reflexes come mainly from the sensory trigeminal nuclei. 1976) The ophtalmicus division of the trigeminal nerve has three branches.1 Muscle 2. The branches pterygopalatine nerve arise some nerve else. posterior superior alveolar and zygomatic branches. greater palatine. lesser palatine. the maxillary nerve gives off pterygopalatine. posterior superior lateral nasal and nasopalatine. In the pterygopalatina fossa. the root of the nose and lowe eyelid. they are pharyngeal. The nasociliary nerve to skin of the lower half of the nose. The frontalis nerve divide into the supraorbital and supratrochlear nerves.lacrimalis nerve supplies the lacrimal gland. The supraorbital nerve supplies skin of the forehead and anterior scalp. conjunctiva and the skin of the lateral upper eyelied.sciencedaily. 1981) . sends one terminal branch to the gingival of the three posterior molar teeth and two terminal branches to the molar and premolar teeth and to the mucous membrane of the maxillary sinus.com) The maxillary division. with small branches to the upper eyelid and fontal sinus. The supratrochlear nerve supplies skin of the medial parts of the forehead and upper eyelid. The zygomatic supplies skin overlying the lateral surface of the zygoma and skin over the anterior of the temporal muscles. (Burket) The Ophtalmicus nerve and divisions (www. after leaving the trigeminal ganglion. (Ogus and Toller. The posterior superior alveolar nerve. gives off a meningeal branch to the duramater prior to passing trough the foramen rotundum. 4. The auriculotemporal nerve. The inferior alveolar nerve. The posterior division of the mandibular nerve gives off four sensory branches: 1. which conveys general sensation from the anterior two thirds of the tongue. and sends branches to the temporomandibular joint. The anterior division of the mandibular nerve contains a single sensory branch. The continuation of the inferior alveolar nerve within bone in the incisive nerve to the remaining canine ang incisor teeth. which conveys sensation from molar and premolar teeth The mental nerve. lingual gingival of the mandibular teeth and the floor of the mouth 3. and gingival of premolar and molar teeth. 1988) . buccal mucosa. which passes through the parotid gland to skin in front of the ear and scalp. 2. which supplies skin of the chin. the general somatic afferent buccal nerve supplying skin of the check.com) The mandibular division of the trigeminal nerve exits from the skull at the foramen ovale. (Barr and Kieman.The mandibularis nerve distribution (www. The lingual nerve. lip and mucosa of the lower lip.sciencedaily. when used as a scientific term referring to the muscular system contraction refers to the generation of tension by muscle fibers with the help of motor neurons. 2008). causing the cell as a whole to shorten (Saladin. which comprises the brain and spinal cord. Voluntary muscle contractions are initiated in the brain.1 Muscle Contraction Contraction is the step in which the muscle fiber develops tension and may shorten (muscles often “contract. Current biochemical studies suggest that. found evidence for a model now called the sliding filament theory. How a muscle fiber shortens remained a mystery until sophisticated techniques in electron microscopy enabled cytologists to see the molecular organization of muscle fibers. Locomotion in most higher animals is possible only through the repeated contraction of many muscles at the correct times. as we see later).2. during each adenosine triphosphatase cycle. Though the term contraction implies a shortening or reduction. two researchers at the Massachusetts Institute of Technology. . This theory holds that the thin filaments slide over the thick ones and pull the Z discs behind them. 2003).4 The contraction and Relaxation of the Muscle 2. Muscle contraction occurs when the actin and myosin filaments in muscle are driven past each other by a cyclic interaction of adenosine triphosphate (ATP) and actin with crossbridges that extend from myosin. while the spinal cord initiates involuntary reflexes (Etja. Contraction is controlled by the central nervous system (CNS).” or develop tension.4. A muscle contraction occurs when a muscle fibre generates tension through the action of actin and myosin cross-bridge cycling. In 1954. Jean Hanson and Hugh Huxley. without shortening. the myosin cross-bridge alternates between two main conformations. The action potential depolarizes the muscle membrane. This cross-bridge cycle is similar to the kinetic cycle that drives active transport and illustrates the general principles of free energy transduction by adenosine triphosphatase systems (Eisenberg and Hill. 2. 3. 1. The acetylcholine acts on a local area of the muscle fiber membrane to open multiple “acetylcholinegated” channels through protein molecules floating in the membrane. 4. the nerve secretes a small amount of the neurotransmitter substance acetylcholine. This initiates an action potential at the membrane. At each ending. Opening of the acetylcholine-gated channels allows large quantities of sodium ions to diffuse to the interior of the muscle fiber membrane. whereas inorganic phosphate release returns the cross-bridge to the strong-binding conformation. An action potential travels along a motor nerve to its endings on muscle fibers. 1985). Here it causes the sarcoplasmic reticulum to release . 2006). Binding of ATP to the cross-bridge induces the weak-binding conformation. and much of the action potential electricity flows through the center of the muscle fiber.which differ markedly in their strength of binding to actin and in their overall structure. 5. The action potential travels along the muscle fiber membrane in the same way that action potentials travel along nerve fiber membranes. 6. General mechanism of muscle contraction The initiation and execution of muscle contraction occur in the following sequential steps (Guyton and Hall. and they remain stored in the reticulum until a new muscle action potential comes along. 1995) Sliding filament mechanism of muscle contraction . 8. causing them to slide alongside each other. After a fraction of a second. Figure2. 7. The calcium ions initiate attractive forces between the actin and myosin filaments.: Mechanism of Ca ++ release (Guyton. this removal of calcium ions from the myofibrils causes the muscle contraction to cease.large quantities of calcium ions that have been stored within this reticulum. which is the contractile process. the calcium ions are pumped back into the sarcoplasmic reticulum by a Ca++ membrane pump. This SNARE complex interacts with both NSF (N-ethylmaleimide Sensitive Fusion protein) and SNAP (Soluble NSF Attachment Proteins) to form a fusion complex. titin and nebulin (Etja. T tubules ( found DHP receptor). The release of the acetylcholine from the vesicles into the fissure through eksositosys stage. Skeletal muscle filament consists of actins. Due to the docking process. The vesicle will undergo docking on the side of the membrane. 2008). thus. Ca+ voltage gated channel will be activated.Sliding filament is a movement of contractile protein (filament) of skeletal muscle. Skeletal muscle filament is a muscle fibers could contraction when skeletal muscle movement. sarcoplasma. The pre-synaptic membrane consists of neurotransmitter acetylcholine (Ach) held in the form of vesicles. The influx will activate the vesicles to move the side of the membrane. The opening of this channel will cause the occurrence calcium influx. The terminal bulb has a membrane called pre-synaptic membrane (at the muscular cell) and synaptic fissure (fissure between two membranes) forming neuromuscular junction. Sliding filament the process of impulse transmitting until the occurrence of sliding filament are as follows: There is an enlargement which is usually called as bouton terminale or terminal bulb. The Ach released will bind with the . thus. the acetylcholine contained inside the vesicle will be released into the synaptic fissure called as the exositocys stage.Skeletal muscle composed by sarcolemma. contractile protein. Synaptic vesicles move down the axon and bind to release sites on the pre-synaptic membrane via vesicle-membrane proteins (v-SNARE) and target-membrane proteins (t-SNAREs). myosin. If there is a potential action. and cysterna (found ryanodine receptor). The synaptic fissure has the thickness of 20 to 30 nanometers. 2008). The fissure is filled with basic substance of gelatin diffused with extra cell fluid (Etja. will then be hydrolyzed by acetyl cholinesterase enzyme which is in enough amount at the synaptic fissure. Relaxation is . that cause the part of the active actins to open and bind with myosin. thus. which later stimulates the excretion of ryanodine receptor. and each of 1 beta. which happens along the sarkolema or muscle cell membrane and T tubulus. potential action will be propagated (spread) to all directions accordingly to the cell excitable characteristic. 2. if the The depolarization reaches a certain limit value (firing level). and soon after that will influx the Na+. The excretion of the receptor will stimulate the excretion of Ca2+ from the cistern. gamma and delta. These sub-units are arranged to form a circle which is ready to bind the Ach (Etja. Ach will be broken into koline and lactate acid.2 Muscle relaxation Ca2+ is the primary regulator of force generation by crossbridges in striated muscle activation and relaxation. we can say that. The ACh which is still stick to the AChR. The AChR is located in the hollows of post-synaptic membrane. The occurrence of the depolarization will cause the opening of DHP receptor which form channel. 2003). The hydrolysis process will be done to prevent the continuing potential action which will cause the continuous contraction (Murray. which at the end causes contraction. The bind between Ach and AChR will cause the opening of the natrium gate at the muscular cell. which later will bind with troponim C. the potential action at muscle cell will potentially occurred. Colin will re-enter to the pre-synaptic membrane to form back Ach.4. Besides. 2008). which stimulates the excretion of Ca2+ from the T tubulus.acetylcholine receptor (AChR) which is in the post-synaptic membrane. the influx of the Na+ will cause the depolarization at the post-synaptic membrane. AChR consists of 5 subunit protein. and at the end will cause contraction (Etja. namely 2 alpha. 2008). Here. The synaptic knob reabsorbs these fragments for recycling. . Since active transport requires ATP. As calcium ions dissociate from troponin. have been used to explore the cascade of kinetic events leading to mechanical relaxation (Poggesi et al. stimulation of the muscle fiber by ACh ceases. from whole muscle organs and intact muscle fibres down to single myofibrils. 4. Therefore. too. 1. 2. Nerve signals stop arriving at the neuromuscular junction. they are pumped into the SR and are not replaced. 2003).as necessary as contraction and while the kinetics of Ca2+ induced force development has been investigated extensively. the calcium binds to a protein called calsequestrin and is stored until the fiber is stimulated again. 2004). those of force relaxation have been both studied and understood less well. As ACh dissociates (separates) from its receptor. Active transport pumps in the sarcoplasmic reticulum (SR) begin to pump Ca2+ from the cytosol back into the cisternae. This is achieved by these steps (Saladin. 3. you can see that ATP is needed for muscle relaxation as well as for muscle contraction. A number of experimental models. so the synaptic knob stops releasing ACh. acetylcholinesterase breaks it down into fragments that cannot stimulate the muscle. General mechanism of muscle relaxation When its work is done. All of this happens continually while the muscle is being stimulated. a muscle fiber relaxes and returns to its resting length. but when nerve signals stop. no new ACh is released to replace that which is broken down.. plus the compensating activity of the two heads of the external pterygoid muscle.5. and others) that both condyle heads are pulled forward in this initial opening movement by the external pterygoid muscles(Wheeler. Stimson. the meniscus is being pulled forward by the superior head of the external pterygoid muscle.1984). It is generally agreed by many authorities (Prentiss. The relative thickness of the meniscus anteroposteriorly. Tropomyosin moves back into the position where it blocks the active sites of the actin filament. Lord. 1. Chissin. When the condyle approaches the articular eminence it rides forward on the thinner portion of the meniscus-an arrangment which makes allowances for the downward protuberance of the eminence(Wheeler. When in “rest position” each condyle rests upon a thick posterior portion of the meniscus which fills the space between the which fills the space between the condyle and the deeper portion of the glenoid fossa. Sicher. the menisci moving with them. Depression of the Mandible During simple depression of the mandible (central opening movement) from it is rest position.1984).1984). Myosin can no longer bind to actin. and the muscle fiber ceases to produce or maintain tension. both condyles move forward. the meniscus is much thinner at the portion which approximates the dorsal area of the articular eminence and the frontal area of the condyle(Wheeler. Higley. The “plane” has an inclination downward when the head is held erect.5 Temporomandibular Joint Movement There are mandible movements that are regulated by temporomandibular joint. Brodie. 2. It is interesting to note that the inclined plane of the condylar glide when the mandible is . Anterioly. While the condyle is being pulled forward in opening the jaw by the inferior head of the external pterygoid. allows the condyles of the mandible to move forward with a glinding movement on a “single plane” regardless of the irregularity of the surface of the glenoid fossa and of that of the articular eminence. it is down and back. inferior. The attachment superiorly is forward.depressed is seemingly parallel to the occlusal plane of the molars and the lower border of the body of the mandible when the jaws are closed(Wheeler. would defeat this argument. below the condyle itself(Wheeler. The central opening movement of the mandible (depression) in conjuction with the central closing movement (elevation) provides the action commonly termed “simple hinge movement”. even tho ugh the initial movement forward is slight. the axis of movement is not in the condyle heads. The jaw has body and weight and must be suspended by ligamentous attachment in some area. The design and location of the temporomandibular ligament makes it the logical choice among condyle attachment to accomplish ligamentous suspension of the jaw in the initial opening movement.1984). The occlusal surfaces of the maxillary teeth may be considered as the upper extension of the hinge. Owing to the involved design of the articulation and the need for jaw support. Apparently the area of rotation approaches the attachment of the temporomandibular ligament laterally and distally to the neck of the condyle. wrapped around the zygomatic “bar” of the temporal bone. the action is comparable to the action of a simple hinge. since these move forward immediately. The uneven shape of the condyle. and the occlusal surfaces of the mandibular teeth as the lower extension in the central opening movement. . and is strongly attached posteriorly in a limited area to the neck of the condyle. During the central opening movement of the mandible. As far as the relation of the dental arches is concerned in this opening and closing movement.1984). This is a logical conclusion because of the suspensory character of this strong ligament and the general directionof its fibers. the rotation point or axis of the hinge cannot be centered in the condyles as many believes. added to its forward movement immediately upon jaw opening. 1984). The pterygoid pull forward on the condyles and the . Together they exert a pull on the mandible which is upward. The deep fibers. Elevation of the Mandible The mandible is elevated by the temporal muscles. maximum). the posterior fibers pull upward and backward(Wheeler. both condyles of the mandible are moved a short distance posteriorly to their rest position (Wheeler. which are assisted by the anterior fibers of the temporal muscles. reegardless of our inability to pinpoint the “hinge axis”. the mandible must be depressed slightly.1984). the masseter muscles and the internal pterygoid muscles. The anterior fibers exert an upward pull.1984). The superficial fibers exert a pull upward and foward on the mandible. The internal pterygoid muscle has two heads. Protusion of the mandible The mandible cannot be protruded unless the cuspsof the teeth are disengaged. The deep fibers exert a pull vertically upward(Wheeler. When the temporal. the mandible is elevated and returns the teeth to occlusion(Wheeler. 2. Therefore. The muscles which promulgate the protrusive movement which brings about the protrusive occlusal relation of the teeth are the external pterygoid muscles.1984). each of which pulls in the same general direction. masseter and internal pterygoid muscles of the sides contract simultanecously. 3.When the jaw is opened no more than necessary for ordinary use in mastication (10-12mm.1984). The masseter muscle has two sets of fibers: sepurficial and deep fibers. When the teeth are brought into centric occlusion. the action of placing the teeth of one arch in and out of contact with the teeth of the opposing arch in a sagittal plane may be called a hinge movement. foward and inward(Wheeler.1984).The temporal muscle has anterior and posterior fibers. the condyles moving forward before the protrusive movement is begun(Wheeler. 1984). The retractive movement is. The jaw is pulled back by the action of the temporal muscle. 5. therefore. the movement is limited to the compressibility of the soft tissues intervening between the bony parts(Wheeler. These movements are made possible by the ability of one temporomandibular other(Wheeler.1984). The tonus and counterbalancing action of other fibers of the temporal as well as some other muscles may come into play during the protrusive movement. The mandible may be retracted a very small degree posteriorly to centric occlusal relation of the teeth. the masseter and the internal pterygoid muscles join the activity of the temporals in the culmination of the act(Wheeler. The codyles with their menisci are returned to rest position. Each internal pterygoid muscle exerts a medial pull on the mandible. the right and left condyles do not follow similar paths. this prevent further depression of the mandible during the protrusive movement. just the reverse of the protrusive movement(Wheeler. the posterior fibers principally. During this movement the condyles are pulled forward with their menisci. Movement of the condyles distally is resisted by the posterior wall of the glenoid cavity. If it is the purpose of this movement to bring the teeth back into centric occlusion. teh mandible returns along the same path it traveled in the protrusive movement. since it does not operate on a line with the forward or joint to move independently of the .1984).temporal pull upward with a counter action on the coronoid processes. The lateral of the Mandible The lateral movement (right and left) of the mandible are asymmetrical movements. but their forward movement is quite limited (Wheeler. Retraction of the Mandible In retraction. 4.1984).1984). This movement is nonfuctional and consequently very limited. including elongation. by a slight depressive movement of the mandible. tearing. capsule. the right internal pterygoid and other muscles relaxing. In the return movement. This action results in the rotation of the mandible about the pivontal point in the right condyle. the right condyle turning on the pivontal point. synovitis. The mandible is returned to rest position. The activity of the left internal pterygoid pulls the left condyle forward and inward in a circular path which rotates about a point in the right condyle. therefore. Disc Displacement .1984) 2. adhesion. or articular surfaces of the condyle or eminentia. The right internal pterygoid muscle contract an dcauses the movement of the mandible to the left. which action depresses the mandible and moves both condyles forward. the condyles retrace their path.1984). The right lateral movement of the mandible is affected.protrusive movement of the jaw.1984). both external pterygoid operating. The left lateral movement of the mandible is affected in the same manner.6 Temporomandibular Joint Disorder Internal derangement is a biomechanical interferences with smooth gliding movements of temporomandibular joint resulting from disturbance of the disk. In this instance the right condyle is pulled forward and inward while the left condyle pivots. or the teeth into centric occlusion. moving the mandible to the right. and so forth. Its action pulls the condyle inward as well as forward(Wheeler. through the activity of the left temporal muscle (mainly posterior fibers). The right temporal is the muscle mainly operative which affects the return of the mandible to centric relation with the assistance of the other mucles in balance with it(Wheeler. other muscles of mastication of both sides joining forces as the teeth approach central occlusion with final masticatory thrust(Wheeler. At this point the left internal pterygoid contracts indepently. noise. general anesthesia. or chronic. These dislocations are classified as acute. and soft tissue imaging showing nonreducing disk. and inferior retrodiscal lamina and discal copllateral ligaments elongate. In the cronic state. dental extraction. 2009) Disc Dislocation The mandible can dislocate in the anterior. The disc move to anteriorly to articular surface of the condyle.Disc displacement occurs because of posterior of disc becomes thinner.(Mangi. posterior. marked limited jaw opening. deviation of mandible to affected side on opening. The masseter and temporalis muscles elevate the mandible before the lateral pterygoid muscle relaxes resulting in . vomiting. but they are usually a result of extreme mouth opening such as with yawning. This deviation cause joint sound during mouth opening and closing. there is generally no pain. 2004) Anterior dislocations are the most common and result in displacement of the condyle anterior to the articular eminence of the temporal bone. 2004) • Anterior dislocations are usually secondary to an interruption in the normal sequence of muscle action when the mouth closes from extreme opening. or superior position. limited laterotrusion to contralateral side. lateral. Diagnostic criteria for the acute state include pain precipitated by function. chronic recurrent. Description of the dislocation is based on the location of the condyle in comparison to the temporal articular groove. On the basis of including imaging as part of the criteria there is the implication that imaging is necessary to make the diagnosis to acute or chronic (Wright. • Acute dislocations can be seen after trauma or dystonic reactions. Anterior dislocations after endoscopic procedures have been reported. or seizures. there is a past history of joint noise or limitation of the jaw opening there maybe slightly limited mandibular opening and laterotrusion to contralateral side and soft tissue imaging reveals displaced disk without reduction.(Haddon. leakage of cerebrospinal fluid. Stone.(Haddon.(Harstall. Ohura. and damage to the eighth cranial nerve resulting in deafness. temporalis. loss of joint capsule from previous mandible dislocations. Injury to the external auditory canal from the condylar head may occur from this type of injury. 2005) Lateral dislocations are usually associated with mandible fractures.the mandibular condyle being pulled anterior to the bony eminence and out of the temporal fossa. and pterygoid muscles causes trismus and keeps the condyle from returning into the temporal fossa. to intracranial hematomas. This can result in fracture of the glenoid fossa with mandibular condyle dislocation into the middle skull base. 1998) Structural Incompatibility of the articular surfaces 1. 2006) The condylar head migrates laterally and superiorly and can often be palpated in the temporal space. 2004. Further injuries from this type of dislocation can range from facial nerve injury. (Schwab. (Undt. • Chronic dislocations result from untreated TMJ dislocations and the condyle remains displaced for an extended time period. 1998. Adhesion . also referred to as central dislocations. 1997) • Acute chronic dislocations result from a similar mechanism in patients with risk factors such as congenitally shallow mandibular fossa. 2004. cerebral contusion. The mandibular condyle is pushed posteriorly toward the mastoid. (Undt. The angle of the mandible in this position predisposes upward migration of the condylar head. 2008) Superior dislocations. Open reduction is often required. or hypermobility syndromes. Hoard. Spasm of the masseter. Ozcelik. 1997. 2008) Posterior dislocations typically occur secondary to a direct blow to the chin. can occur from a direct blow to a partially opened mouth. These dislocations can be both unilateral and bilateral. (Haddon. It can be cause the abridgment dimension on the fracture region and also cause the other sides doesn’t contact. The patient can be still opening their mouth 2. disturbance of TMJ functions. The sign of this deviation is a single click when patient attempts to move the mandible. Effusion or haemathrosis: occurs when there is a bleeding in the joint because of bump which can be blocked the occlusion. Pseudo-prognathism. fossa and disc resulting in impairment of smooth sliding movement. and mandibular grown disturbance There are four kind of fracture of condyle: 1. Condyle Dislocation Occurs when the condyle on one ar both sides are displaced anteriorly over the articular tubercle and locked in place by the spasm of elevator muscles. The clinical sign of this deviation is clicking or deviation of the mandibular opening pathway. ankylosis of the TMJ. Superior joint space adhesion Limit the translation of the condyle disc complex it can be cause to limiting joint movement to only rotation. Clinically limit joint movement to only 25 – 30 mm Inferior joint space adhesion Restrict rotation of the disc on the condyle but allow translation of the condyle disc complex. Alteration Alteration in the shape of articular surface of condyle. Characteristic sign is the patient unable to close their mouth.Sticking of the erticular surface. may be found in superior or inferior joint spaces. and complain of pain in TMJ region Fracture of Condyle May cause malocclusion (open bite). Unilateral Fratcture Duslocation: condyle’s neck has been fracture on the one side. The result of prolonged static position is clicking voice during sleeping. click only accurs once and cannot be repeated without another prolonged period of static loading. 2. . that can be cause the abridgment dimensi ramus on the both side. It can be cause the posterior region is contact but in the anterior region doesn’t contact.3. Excision of a completely ankylosed shoulder or elbow may restore free mobility and usefulness to the limb. When inflammation has caused the jointends of the bones to be fused together the ankylosis is termed osseous or complete. 2007) Symptoms present as bony ankylosis. which may be the result of injury or disease. "Ankylosis" is also used as an anatomical term. 4. bones being said to ankylose (or anchylose) when. Bilateral Dislocation: Patient’s mouth cannot be closed because of disc islocation Anchylosis Anchylosis is a stiffness of a joint due to abnormal adhesion and rigidity of the bones of the joint. impairing the ability to speak and eat. in which the disease is within the joint. 1. they coalesce. or surgery. Bilateral Fracture Dislocation: leher condyle fracture on the both side. Fibrous ankylosis: Fibrous ankylosis is a fibrous connective tissue process which results in decreased range of motion. in which osseous tissue fuses two bones together reducing mobility. or become so joined together that no motion can take place between them. the term "false" ankylosis has been used in contradistinction to "true" ankylosis. Pathology may be the result of trauma. (Chabner. 1999) When the structures outside the joint are affected. (Deeb. . chronic inflammation. which is why fibrous ankylosis is also known as false ankylosis. Noma—a gangrenous disease still widespread among malnourished children living on the borders of the Sahara desert—can cause ankylosis of the maxilla and mandible. disease. from being originally distinct. The rigidity may be complete or partial and may be due to inflammation of the tendinous or muscular structures outside the joint or of the tissues of the joint itself. The size of the oral orifice. and the resting length of the elevator muscles are the determinants of a “normal” opening for an individual. Abnormality in this regard is an individual matter. That’s why someone with bony ankylosis on one side will occur fibrous ankylosis on the other side. (Bell. Bony ankylosis: fusion between head of condyle and glenoid fossa There are several characteristics in a person with temporomandibular joint disorder: • Restricted Range of Jaw Motion 2. inability to open the mouth adequately. (Bell.1 The Characteristics of Temporomandibular Joint Disorder The mandibular of motion should be sufficient to meet the normal requirements for talking and masticating foods. such measurements may not apply to the individual. The main cause of fibrous ankylosis in this case is the TMJ that is not used or no movement in the TMJ (Ikeno. For a particular individual. or . Arbitrary range of motion without proper consideration of functional compability shold be avoided. Restrictions of movement are displayed as inability to close the mouth.Some research suggests fibrous ankylosis may precede the development of bony ankylosis because someone with bony ankylosis usually doesn’t use their TMJ. Although is may be quite true on average.6.1990) Restricted range of motion can result from a variety of extra-articular causes. or inability to protrusive or contralateral excursions. 2006) 2. This may be accompanied by deflection of the opening or the protrusive path. restriction of mandibular movement is symptomatic of masticatory activity. the amount of overbite of the teeth. including a shortened elevator muscle. 1990) The lower limit of normal for individuals of average height of interincisal opening is about 50 for men mm and 45 mm for women. symptoms.from fibrotic contraction of the capsule. Constrictions in these nerves and vessels would presumably have negative effects on the inner ear structures they service. A third theory involves two tiny muscles. the tensor veli palantini and the tensor tympani. intracapsular adhesions. The tensor veli palatini constricts and dilates the eustachian tube which in turn is responsible for equalizing the air pressure on either side of the tympanic membrane (the eardrum). 3. which function in the middle ear. including inflammation. Both vertigo and tinnitus are associated with structures The first theory involves inflammation of the joint capsule which spreads to adjoining areas in the skull. (Bell. Disease processes affecting the cochlea. would cause hearing loss and tinnitus. or discal obstruction. The nerves that supply these . 2. This would include the vestibular organ which contains the semicircular canals. but allows the damaged joint itself to place pressure on nerves and blood vessels that supply the structures in the inner ear.1990) 1. A second theory posits that pressure on the temporomandibular joint not only injures the joint. 1990) • Vertigo (dizziness) and Tinnitus (ringing in the ears) can be may cause these associated with severe cases of TMD. including the structures in the inner ear. There are a number of competing theories explaining why TMD in the inner ear. and provides the sense of balance. (Bell. Fluid movement in these canals responds to movements of the head. The second major organ in the inner ear is the cochlea which is responsible for converting the vibrations in the air to nerve impulses that can be perceived by the brain. This is the muscle that functions when you "pop" your ears. The tensor tympani attaches directly to the eardrum and helps to protect the inner ear by dampening vibrations within it. Disease processes in this organ would cause vertigo (dizziness). although the reasons for this are not exactly clear. 2010) Tinnitus. headaches. (Anonymous. A fourth theory. 4. along with headaches and neck aches. It has also been shown that when subjects clench their teeth. It is hypothesized that chronic tension in this muscle triggers periodic episodes of vertigo. It has been shown that pressure on certain trigger points in the SCM can trigger vertigo. These are chewing muscles and are highly active when the patient is bruxing (grinding) the teeth. clicking joints. involves the reflexive contraction of the sternocleidomastoid muscles (SCM) when patients clench their teeth. especially chronic jaw soreness. the more obvious symptoms of TMD precede the vertigo. People who have learned to live with all the other symptoms of TMD may finally seek treatment for the tinnitus. is a common disorder and is frequently associated with severe TMD.muscles are closely associated with the nerves that supply the medial and lateral pterygoid muscles. not realizing that the other . neck aches. and the one that most experts are leaning toward right now . but in a majority of cases. Some evidence exists that the vertigo may occur in the absence of these symptoms. the SCM will also contract. Vertigo associated with TMD is a fairly rare symptom. on the other hand. you need to ask yourself if you have at least some of the symptoms listed above. This theory seems unlikely since both muscles function on structures in the middle ear and do not impinge directly on the inner ear where the organs responsible for balance and hearing actually reside. If you have a problem with chronic dizziness and think it may be due to temporomandibular dysfunction. chronic jaw dislocation and/or an inability to open the Jaws wide. The theory is that spasm in the chewing muscles due to TMD causes spasm of these two tiny "ear muscles" which in turn affects the semicircular canals and the cochlea causing dizziness and tinnitus. ear aches. 1990) Grating sounds is sliver or swipe sound that occurs during movement of the mandible. (Ogus H. (Anonymous. (Anonymous. near the ear or around the area of the wisdom teeth. The majority of pain is. or at night when there was a motion to open the mouth. (Ogus H.A. This pain may radiate to the ear. and its etiology is the overextertion of the muscles either by continual contractions in normal physiologic state or. This situation can occur in the morning. muscular in origin. Refer to the image above for areas most affected by TMJ dysfunction.A.1990) Although the conditions necessary to initiate pain have . at midnight. clicking can also occur during the motion to close the mouth as in the motion to open the mouth. if in a stretch pathologic length.2010) The pain in the jaw is usually at the back of the jaw.craniomandibular symptoms are part of the same syndrome. especially the movement from one side to another. also referred to as popping jaw or TMJ (temporomandibular joint) syndrome/dysfunction is a symptom associated with inflammation of the temporomandibular joint or uncoordinated action of the facial muscles. Toller P. 2010) • movement Clicking jaw.D. a combination of contractions and stretch reflexrelaxation reactions.D. The sound can often be better known under the palpability than hearing. however. Sound examination can also be done by using a stethoscope. (Bell. 1990) • Pain Clicking/Popping or grating sounds in jaw TMJ dysfunctions result in pain of the joint and related musculator. Toller P. temples of the head or neck. it should be investigated if other possible causes could be the source of pain in this region. Before diagnosing any jaw pain as TMJ dysfunction. but generally feasible if the discussion about the physiological or acute pain and two pathological conditions: inflammatory pain and neuropathic pain. Unexplained headaches is a common symptom of a TMJ problem.2008) Inflammatory Pain After experiencing an injury that is not mild. (Luther.2 Pain Pain is the main characteristic shown in temporomandibular disorder. namely that the pain gives warning that something is wrong. which can persist for hours (immediate pain). pain precedes the other signals.been explained. Pain in the shoulders and back due to muscle contraction. central nosiseptor pathways through facilitation and reorganization. related to teeth clenching and TMJ. Postexertion muscular pain can be divided into the following two types: pain during and immediately after exercise.2007) The immediate pain experienced with muscular overextertion can be largerly atributted to diffusible end-products of cellular metabolism acting upon pain receptors within the muscular tissues. persistent inflammatory pain arise until the injury healed. Generally speaking. The delayed type pain is usually referred to as myositis. and the pain associated with unpleasant feelings. and a more localized soreness that does not appear for 24 to 28 hours (delayed pain). (Luther.6. There is still much to be learned.(Ganong. Stimulation in areas of injury that under normal circumstances usually causes only mild pain cause excessive responses (hiperalgesia). and are usually . overexertion of muscles will produce pain. the mechanism through which continual contraction actually produces pain must now be developed. Usually a TMJ-caused headache is located in the temples or in the back of the head.2007) 2. Pain sensation is different from others. Pain is a sensation that was very complicated because if the prolonged pain and tissue damage. Reflex sympathetic dystrophy are also common. Research on Animals showed that nerve injury causes excessive growth of nerve fibers into the sympathetic noradrenergic nerve ganglion sensory dorsal roots of the injured area. However.2008) Neuropathic Pain Neuropathic pain can occur if the injured nerve fibers. neuropathic pain found in various forms. Surgery being undertaken to overcome severe pain. Pain is usually severe and difficult to overcome. In humans. the effect of this action only for a moment if the network has undergone peripheral? 'Short-circuiting' by the sympathetic nerves or other central jaras jaras-experiencing reorganization. One of them is a pain (in addition to other sensation) at the limb that has been amputated. This is what causes hiperalgesia and alodinia. In kausalgia. inhibition of alpha adrenergic-type kausalgia will relieve pain. Many of these substances work to improve the perception and sensation in the regional distribution of the skin and in the dorsal cornua. Pain is often accompanied by hiperalgesia and alodinia. . In these circumstances.harmless stimuli such as touch leading to pain (alodinia). the skin in affected areas will be thinned and polished. All types of inflammation causes the release of various cytokines and growth factors ("dough inflammation") in areas experiencing inflammation. ie cutting jaras spinotalamikus done carefully. (Ganong. among others. In humans. burning spontaneously arise after the injury seems minor. and an increase in hair growth. although the reasons are not clear-adrenergic inhibitor is more effective than α1-α2 adrenergic inhibitors. is the termination of the nerve from injury or kordotomi anterolateral spot. Simpntis discharge then trigger pain. it seems to happen 'short-circuiting' and respective fibers are stimulated by norepinephrine at the level of the dorsal roots ganglia. Therefore. Pain can often be treated with analgesic drugs given in adequate doses. (Ganong. referred to as "physical complementary aspects of protective reflexes absolute. These fibers deliver the slow speed of 0. (Ganong. One nosiseptor system formed from fibers small A ∂ bermielin 2-5μm diameter. in addition.2 μm. Pain impulses delivered to the central nervous system by two fibers. Receptors And Pathways Sensory organs for pain are free nerve endings which at many places on almost all body tissues. Sinap transmitter which in secretion by afferents which delivers mild pain quickly is glutamate. (Ganong. The most effective drugs for this is morphine. including lateral spinotalamikus tract. where pain impulses can be modified. Because it is also known as the dorsal cornua of the gate / door. Another system that consists of no myelins C fibers with a diameter from 0. While the fiber ends in C radik dorsalis neurons in lamina I and II. the other half into the ventrolateral systems. and from here to kortes cerebral.2008) . fibers over A ∂ neurons mainly in lamina I and V.although not always to be delivered. which is a specific sensory relay nucleus in the thalamus. This latter fibers found in the dorsal lateral roots and is often called the dorsal roots C fibers. Some fibers ascending projection to form the nucleus ventralis posterior. among the various sensations." Pain stimulus triggers a response generally withdraw or avoid strong.5 to 2 m / sec. by Sherrington.2008) Some axons of neurons ending in the dorsal cornua of the spinal cord and brain stem. pain is unique is that the pain has "innate" as unpleasant effects.4 to 1. both groups of fiber ends in the dorsal cornua.2008) Links nosiseptor peripheral synapse between fibers and cells in the dorsal cornua of the spinal cord is the part that is very plastic.2008) Pain. (Ganong. Some increase in the dorsal spinal cord. and the transmitter delivers the latest severe pain is substance P. If the blood supply has been restored. pain. although the distribution is much less when compared with that found in somatic structures. these chemicals can be cleaned or metabolized. viscera often spread or transferred to the autonomic nervous lain. The identity of the P factor is still unconfirmed. pain arising substernum if myocardial ischemia during exercise experience (angina pectoris) is a classic example of the P factor accumulation in muscles. such as somatic. However. (Ganong. There were no proprioseptor in an instrument in. Receptors for pain and other sensory modalities contained in the viscera contained similar to the skin.Sistem areas. integration centers in the central. the contraction will cause pain immediately. After the contractions stopped. will not usually painful. Intermittent claudication.(Ganong. Angina disappeared with the rest because it lowered the needs of 02 myocardial blood flow and allows the cleaning of these factors. and effector lines. and associated with nausea and autonomic symptoms. and only rarely found the temperature and touch receptors. pain arising in the calf muscles padaorang who suffer from vascular occlusion. Pain receptors can be found. pain persists until the blood flow restored. These observations are difficult to interpret unless the release of chemicals ("P factor" Lewis) during contraction. but the blood supply remains adequate.Muscle Pain When the muscle to contract rhythmically. Sefcara clinical. if the blood supply to the muscle is blocked. has afferent components.2008) Viscera Pain Besides not having a good localization.2008) . is another example. The pain usually occurs when patients walk and disappeared when he stopped. which causes pain when its local concentration is high enough. but probably was K+. but there are notable differences Emitter distribution. causing an unpleasant feeling. Another dramatic example is at the top of the shoulder pain caused by irritation at the center of the diaphragm and the pain in the testes caused by stretching of the ureter. and cortex area of the recipient for Visceral sensation mixed with the recipient cortical areas of somatic sensation. (Ganong.Visceral afferents reach the CNS from the structure through the sympathetic and parasympathetic. (Ganong. there is in the viscera afferent facial nerve. (Ganong. . It should be noted that at least there is some substance Pcontaining afferent makes relationships through collateral to pascaganglion sympathetic neurons.2008) In the CNS.2008) Reffered Pain Irritation of the internal organs often causes pain that is felt not in the organs but in some somatic structures that may be located quite a distance. and roots in the sacrum. This relationship may play a role in reflex control of viscera that does not depend on the CNS. There is also an eye afferents in the viscera of the trigeminal nerve. Another example is found in many areas of medicine. in torakal and lumbar dorsal roots above. knowledge about pain control and often become the place where the transfer of pain for each and every organ in the very important for the doctor. However. and dental. Visceral sensation sepanjamg run on the same line with somatic sensation in the tract spinotalamikus and radiatio thalami. Fiber cell bodies are located in the dorsal roots and cranial nerve ganglia are homologous. but the pain is not superficial. and the vagus. Perhaps the best example is the transfer of pain to the side of the heart in the left arm. Pain like this is said to be transferred (Referred) to the somatic structure. glosofaringeus. and there is often a place of pain rather unusual. Specifically. as in the inferior ganglion mesenterikus. surgical.2008) Clearly. Visceral pain is local if and diverted. In somatic pain can also be transferred. sometimes it looks like the spread of pain (radiation) from local to distant places. where pain control is not always the same. Peripheral neurons and viscera together in laminae I-VI ipsilateral dorsal cornua. but if the viscera prolonged stimulation. stress and malocclusion.2008) Cause of the Pain The main cause of pain rather seems to be plasticity in the CNS are accompanied by the convergence of peripheral pain fibers and viscera on the second level of the same neurons that berproyeksi to the brain.3 Factors that Can Cause Temporomandibular Joint Disorder 1. rubbing of the teeth.Cardiac pain. can be felt only in the abdomen. bruxism. gnashing. The causes of bruxism are unknown The word "bruxism" comes from the Greek "brychein" meaning to grind or gnash the opposing rows of upper and lower molar teeth. (Ganong. TMJ and stress is an injury to the jaw due to incorrect positions during the day but especially at night. there will be facilitation of peripheral nerve endings. because the real cause of malaocclusion. chafing.6. but neurons in lamina VII receive afferent from both sides of the body-terms if convergence will be used to explain the place of transfer to the side opposite the side of the source of pain. This is not true. (Gnatologia it Galiffa's Mandibular Decubitus Syndrome). But may be read in any cases that bruxism has two main causes. Bruxism Bruxism is the medical term for the grinding. Pain control can be triggered experimentally by stimulating the cut nerve splanknikus. Bruxism is the violent and noisy . and of course the brain can not distinguish whether the stimulation comes from the viscera or of pain over the area.2008) 2. (Ganong. clenching of the jaw. Stimulating the peripheral fibers are now the second level neurons. Peripheral pain fibers normally do not trigger the second level neurons. or can be diverted to the right arm or even to the neck. for example. especially during deep sleep. as they weigh heavily with static load on their jaws (health and sleeping position). The muscles of the jaw and face spasm and attempt to move the jaw to a more comfortable position. on their stomach or on their hips. It is hard to blame teeth-grinding on stress in a young child. we know there is a link between bruxism and the body's survival mechanism to keep the airway open. This is particularly apparent in people suffering from sleep-disordered breathing.rubbing of the lower teeth against the upper teeth lasting a few seconds Bruxism is one of the most common sleep disorder Bruxism occurs predominantly during sleep. (Galiffa. the teeth slide back and . Enlarged tonsils and adenoids are a common cause for airway obstruction in children and even contribute to obstructive sleep apnea. (Slabach. the most severe cases being obstructive sleep apnea. Adults with compromised airways also brux to keep the airway open. In adults the cause is usually not enlarged tonsils and adults. but a collapsible windpipe that contributes to the sleep apnea. From some of the research done on children. the first causative factor to look for is an obstructed airway. always and only in those people who sleep lying face downwards on the bed. If a child is grinding his or her teeth at night. 2010) When the jaw is in the wrong position. the body attempts to correct it by bruxism. Bruxism triggers a muscle in the back of the throat to spasm and keep the airway open. Most children do not have the level of emotional stress that adults do. As these muscles spasm. 2007) Causes of Bruxism The dental and medical community a like have blamed stress for the gnawing and gnashing of teeth at night. Our fastpaced society does indeed pose a considerable level of physical and emotional stress and we do know that bruxism increases with additional stressors. . a properly trained dentist in the Tanner methods can make you comfortable. However. face. jaw and neck pain . Nature sends us messages via dreams. Clenching Sleep clenching. etc. The lower jaw fits in to a socket of the upper jaw and is protected by a cartilage disc. a signaling method. which occurs while dreaming is an unconscious act. something we fail to acknowledge. but it 'ain't' that easy to figure out.Displacement of the cartilage disc. yet. It is an unconscious act. It could be a gift from Nature. popping or grating noises upon opening and closing of the jaw . to let us know that Nature is trying to tell us something. there is probably a conflict between the conscious and unconscious mind. indicating a dislocation of the joint and resulting in clicking. that is.forth in response to that muscle activity . squeezing teeth together while sleeping is not always dysfunctional. Effects of Bruxism After even a short period of grinding.Further compromise of the airway. a couple of things can occur: . cognitions. the lower jaw can recede backward causing a jaw joint disorder or TMJ disorder. making obstructive sleep apnea even more possible 2. which can cause headaches. This can occur particularly in a person whose facial and jaw muscles are shortened-a muscle cramp in the jaw. The teeth grind to relieve the spasms much like stretching the relieves a cramp in the calf muscles.Compression of the nerves and blood vessels in the back of the jaw joint. it is needed . In other words. If the lower jaw is allowed to retrude to the back of the socket. that is. Most people need help from a qualified Jungian trained psychiatrist or physchologist. intuitions. The second deals with damage to teeth and their supporting structures. Chewing on one side. if one continues to clench. The Clenching Syndrome (also called the TMJ Syndrome) is a cycle. It has a beginning. which is always the same. A slight (subtle) looseness of the teeth is the first sign of sleep clenching--something you can detect yourself. It forced one side’s muscles to do more activities so it can cause hyperactivities and hypercontraction. which is advanced periodontal disease (teeth that may have to be removed). We all know that TMJ are placed on both right and left side of the face that’s why if a person do this bad habit. The first is concerned with irritation of the muscles of the head and neck with irritation to the TM joints and ear apparatus. Nevertheless. Sleep clenching is only However. Bad sleeping position that uses one side of the body to prop the whole body. the cycle will continue reaching the final stage.for the eruption process of teeth. 4. Researchers generally agree that the conditions fall into three main categories: . 2. The final stage. which is always the same.4 Types of Temporomandibular Joint Disorder Temporomandibular joint disorder is disorder of the jaw joint and chewing muscles. There are two parts of the clenching syndrome: occlusomuscular problems and occlusodentition problems. is not experienced in every person.6. if it progresses to its end. and a final stage. their TMJ is forced to prop a big mass so it is forced and can cause pain and will become a disorder. Usually one side of the face will prop the whole mass of the body. 3. many of us have an episode of clenching that occurs and will continue until we modify our consciousness to Nature’s import. Often. clinical examination. limitation of jaw motion. with reduction or without reduction. and there may be intermittent locking of the disk. with opening and translational movement. patients have no pain with this condition. and MRI scan in the open.1. This situation may worsen. and limitation of motion. face. Internal derangement of the joint involves a displaced disc. temporomandibular disorder resulting from displacement of the TMJ disk from its normal position or from deformation of the disk. The vast majority of patients present with facial pain. 2. The mandible deviates to the affected side on opening until the click occurs and then returns to the midline. Reduction implies that to some extent the disk is gliding normally. This may lead to synovitis. Myofascial pain Myofascial pain disorder of the masticatory muscle system is the most common of all temporomandibular disorders. Internal derangements may include anterior displacement of the disk. Anterior displacement with reduction is defined as disk displacement in the closed-mouth position that reduces (with a click) to the normal relationship at some time during opening. along with any number of associated symptoms in the head. and neck region. Intermittent locking may progress over time to anterior disk . if necessary. Diagnostic or therapeutic arthroscopy may also be helpful in confirming the diagnosis and providing minimally invasive surgical manipulation. or injury to the condyle. The diagnosis is confirmed by history. pain. Imaging studies of the TMJ usually show no evidence of anatomic pathology. muscle tenderness and stiffness. In these circumstances. the patient reports a click with a variable amount of pain on opening. The derangement disorder is defined as a dislocated jaw.and closed-mouth positions. There may be acute tenderness to palpation of the joint. or limitation of motion in the TMJ. Osteoarthritis Osteoarthritis of the TMJ may result from trauma (acute or chronic). symptoms may develop in the TMJ . These patients have a marked decrease in mandibular opening on the affected side and a variable amount of pain. Maximal opening may be limited to 20 to 25 mm (the normal range of maximal interincisal opening ranges from 35 to 55 mm. infection. The patient reports pain on moving the mandible. It feels to them as if there is a mechanical obstruction to opening in the joint. and a loss of joint space. 50% present with pain. Imaging studies typically reveal degenerative changes. In such cases. metabolic disturbances. Joint sounds are described as grating. Rheumatoid Arthritis There may be involvement of the TMJ in adults and children with rheumatoid arthritis. There may also be a history of clicking with intermittent locking. but not as clicking or popping. In adults with longstanding rheumatoid arthritis. limited motion. grinding. and deviation of the jaw to the affected side. Arthritis refers to a group of degenerative/inflammatory joint disorders that can affect the temporomandibular joint. and previous joint surgery. with a mean of 40 to 43 mm). the signs and symptoms of degenerative joint disease may also be present. remodeling. There may be associated growth restriction of the jaw resulting in micrognathia and ankylosis.displacement without reduction (closed lock). with restricted movement to the contralateral side. swelling. Among children with juvenile idiopathic arthritis (also known as juvenile rheumatoid arthritis). or crunching. This implies that the dislocated disk acts as a mechanical obstruction to the opening and translation of the condyle. 3. MRI shows a displaced disk without reduction on opening (closed lock) and may also reveal degenerative changes in the condyle. Disc displacement with reduction There is a clicking sound or temporal sticking motion when opening and closing the mouth Type IIIb. Imaging of the TMJ varies depending on the stage of the disease. Type IV. a trismus or a joint sound. with shortening of the mandibular ramus–condyle unit and potential reduction of joint space and hypomobility. Disc displacement without reduction There is trismus and jaw opening pain or clenching pain after the disappearance of clicking. but ultimately there is resorption of the condyle. Capsule-ligament disorder There is movement pain in the TMJ with palpation tenderness. Scrivani et all. Masticatory muscle disorder There is jaw movement pain in the muscle whose region can be identified. Cases not included type I-IV (Yasuyuki Shibuya et all. Disc disorder Type IIIa.late in the course of the disease. and these patients may report discomfort only when they have marked limitation of jaw motion. 2007) . (Steven J. Other signs of rheumatoid arthritis will be evident. Type II. A picture image reveals marginal proliferation (osteophyte). erosion or a deformity of the mandibular condyle. A protrusive slide of the mandibular condyle is usually disturbed on the problem side. osteoarthritis. joint capsule or ligament) Type III. osteoarthrosis There is at least one of joint pain. Type V. (This category includes chronic and traumatic diseases of either the retrodiscal tissue. 2008) Here is the classification (subtype) of TMJ disorder from Japanese Society for the Temporomandibular Joint in 2001: Type I. Degenerative joint diseases. 2007) LEAST ONE OF THE QUESTIONS TYPE III NO Is there jaw movement pain in the muscle whose region can be identified? YES NO TYPE I Is there movement pain in the TMJ with palpation tenderness? YES TYPE II TYPE V NO . The second type of TMJ disorder is caused by the damaged capsule and ligaments. and other muscles in the face. complicated with a protrusive sliding disorder of the mandibular condyle on the problem side? Is a disc TMJ disorder type determination is performed with analysis of displacement revealed by magnetic resonance imaging (MRI)? YES. The third type of TMJ disorder is caused by the abnormality of disc’s position. In type IIIA.The first type of TMJ disorder is caused by pain on mastication muscles around the TMJ which region can not be identified. With the existence of such defects. also the trauma in retrodiscal tissue. the whole head. when opening and closing the mouth? Are there a trismus and a jaw opening pain or as found in type Patients only feel the pain without any indication clenching　pain after the disappearance of clicking which are usually I-IV. Is there at least one of joint pain. There can be clicking sounds because it is possible that the NO condylus head changed place (not on the central zone pf the disc). It happens because TMJ pain can not be centralized and can even affect other parts that are all around TMJ area such as ears. Is there a clicking sound or a temporal sticking motion TYPE IV The fifth type of TMJ disorder is uncharacterized well. the patient will feel pain when he opens his jaws. ATsome of the following questions: (Yasuyuki Shibuya et all. head condylus can back into place after the movement. That situation resulted in a click when the head moves translational condylus through the disc. erosion or by inflammation The fourth type of TMJ disorder is caused deformity of mandibular condyle? of the joints or degenerative joint disease. Given this disparity. whereas in type IIIB condylus head can not go back into place. the condylus head placed not on the central zone of the disc because of depletion and elevation of the disc. Pain is felt in at least one YES joint. a trismus or a joint sound with imaging findings of marginal proliferation (osteophyte). Pada masa ini pula terjadi penurunan jumlah cairan synovial serta elastisitas ligamen. Pada masa ini. Kebiasaan ini dapat menyebabkan hiperaktivitas dan hiperkontraksi otot. Impaksi atau gigi yang tertanam lama dapat menyebabkan kaku otot yang mengakibatkan TMD. Hormon progesteron yang merupakan antidepresan alami juga menurun sehingga pasien tersebut menjadi stress hingga sering mengkonsumsi obat antidepresan. Kedua hal tersebut dapat menyebabkan gangguan saat pergerakan sendi hingga menyebabkan TMD. Kebiasaan buruk tersebut juga dapat mengakibatkan disc displacement . Hal ini menyebabkan spasme otot yang menyebabkan kaku dan dull pada otot serta menyebabkan TMD. Dengan stress ini. pasien menjadi sering gelisah hingga dapat menimbulkan kebiasaan buruk burxism dan clenching. Kemungkinan kedua karena ia telah memasuki masa menopause atau pra menopause. hormon estrogen dan progesteron akan menurun. Maloklusi menyebabkan ketidaknyamanan pada pasien sehingga menimbulkan kebiasaan buruk bruxism dan clenching yang akan dijelaskan pada tahap berikutnya. Pertama karena impaksi yang bisa menyebabkan kaku otot dan maloklusi.Isi Ibu 46 tahun terkena TMJ disorder karena 2 kemungkinan. That movement is called bruxism. she has been feeling stiffness. it can produce a sudden sensitivity when consuming hot or cold foods.bila telah menjadi amat parah. At this stage. Disc displacement dapat menimbulkan clicking sound saat membuka dan menutup mulut. women who are at the age of 40 years experienced a period of transition to menopause. At this stage there is a change in a woman. If left untreated it can cause headaches. Someone who experienced bruxism is caused by anxiety that clearly. for example. sleep disorder in which sufferers of bruxism sliver teeth during sleep. Anxiety is seen as a trigger . It also can cause loss of teeth or broken fillings from teeth. So the anatomical form of the teeth of someone who experienced bruxism will be changed because of abrasion. was awakened from sleep. as a result during sleep the muscles around the jaw depressed to do work. Stress can cause the jaw to tense. dull. resulting in errors in occlussion. whereas there is no dental cavities CHAPTER 4 DISCUSSION In general. a woman tends to be a serious thinker and a highly-sensitive person to other people so that women are particularly vulnerable to stress at the time. the sensitivity of brain chemicals (neurotransmitters such as dopamine and serotonin). jaw pain and can decrease tooth enamel of teeth and if it is done consequently. women tend to become unstable emotions and thoughts expenses increased. so that during sleep there is movement of the jaw or grinding. changes in mood. CHAPTER 3 CASE REPORT 46 year old female patient came to the dentist with a complaint that this 1 year. clicking sound as well as pain in the left and right cheek area when she opens her mouth. bruxism is caused by a condition known as sleep apnea and stress. especially on mornings when she wakes up. At this time a woman's emotions become overwhelming. Hal ini menjadi salah satu tanda seseorang menderita TMD. It can cause joint and muscles problems. Depression can happen to anyone of any age. which is a significant change in mood for an extended period of time associated with loss of interest in usual activities. An increase of aches and pains throughout the body muscles associated with soreness and stiffness in muscles. Menopause can also cause stiffness of the muscles because of the reducing endorphine. which are unrelated to trauma or exercise. Serotonin Reuptake Antidepressants such as selective inhibitors or SSRIs (eg Prozac. But if such feelings persist or impair your daily life. Menopause can cause TMJ disorder because in it’s symptom. 2002). or irritability. there’s reducing of estrogen and progesteron hormone.or exacerbating factors. Severity. Paxil. Depression is a feeling of sadness can be normal. and up to one in five American women will suffer from clinical depression at some point in her life. Or you may feel blue or unhappy for short periods of time without reason or warning. 2002). In the past. She consumes antidepresan because she feels stress that is one of menopause’s symptoms. It is thought that more than half of all postmenopausal women experience varying degrees of joint pain. but may be related to immune system effects mostly caused by fluctuating hormone levels. 2002). It afflicts almost 19 million Americans each year. duration and the presence of other symptoms are the factors that distinguish ordinary sadness from a depressive disorder. Zoloft) known to worsen the grinding. Aching Joints and muscle problems is one of the most common symptoms of menopause. malocclusion is viewed as a major factor in bruxism. It is not wise to ignore these aches and pains (Nanette. appropriate and even necessary during life's setbacks or losses. This is called: Depression. which also is normal and ordinary. Many women first experience symptoms of depression during their 20s and 30s (Nanette. and withdrawal from family and friends (Nanette. sleep and eating disorders. We can say that the patient is in depression because she is in menopause age. Joint pain is basically an unexplained soreness in muscles and joints. Women are two to three times more likely than men to suffer from depression. you may have a depressive disorder. Women whose general health . has pledged to oppose the thrust of the weight that lies heavily on the jaw This is the real reason for the bruxism is especially active during sleep. so it may help improve moods and has been found to significantly reduce many physical and psychological PMS symptoms. teeth are not in contact. in the rest position and in the absence of disease. Normally. It results from a physiological and highly functional activity: Spontaneous Deglutition or Spontaneous Swallowing. balanced and suspended under the skull while muscles are relaxed. (maximum Intercuspidation occlusion). Throughout the night the Neuromuscular component. condyles are symmetrical in their position in articular cavities. grinding teeth between them. 2002). In order to swallowing. in anatomical and functional harmony with the other chewing elements. can also . periodontium and TMJ . masticatory muscles must activate themselves to centre the jaw and then they must bring the teeth from forced lateral malocclusion to centred occlusion (maximum Intercuspidation occlusion). gum. months. Malocclusion. This precious gift of nature and health can only occur whether the jaw is free to move and make contact with the teeth in the right position. In wrong sleeping position ( sleep stomach. their movement generates a bad occlusion. try to run it off (Nanette. years move sideways. the body's natural painkillers. in which the upper and lower teeth occlude in a disharmonic way. therefore obstructing blood circulation and moving the teeth to a lateral bad occlusion position(TMJD). and enjoy the Benefits of inactivity . rubbing .and resistance are good are apt to have less premenstrual tension than those women suffering from poor nutrition and lack of physical exercise. through premature contact of back tooth the relationship disharmony between the teeth and the imbalance of the jaw. There are some things you can do to try to keep symptoms to a minimum: Exercise helps boost endorphins. the jaw is centred. instead of being relaxed. periodontium and TMJ disfunction. face down) the weight of the head pushes the mandibula to lateral occlusion and exerts non-stop compression ( for many hours) on the teeth. balanced and tonic. this is the cause of nocturnal bruxism and negative trophic action on the gum . The teeth are pushed sideways for hours. Next time you have a build-up of tension or anxiety. Stress can cause a bad habit called bruxism and clenching. hum. buzzing and crackling. teeth grinding and dysfunction of the jaw joint. hypercontraction. face and mandibular joints. pyorrhoea. The rubbing causes tooth facet wear but also mobility and parodontal disease pyorrhoea . clicks. hence they deform. it can cause disc rupture or inflammation that causes pain. tinnitus. clicking sound. 2010) It is explained before that bruxism and clenching activity causes pain. migraine. (Galiffa. (Kopp. and even can change the position of the disc in TMJ. In the nerve sensation of pain caused due to local iskhemia as a result of strong muscle contractions and continuous or inadequate microcirculation as a result of the sympathetic system in which disregulation with the excessive activation of the sympathetic nervous system will lead to nutritional . Compression lasting all night on the teeth. The joints . headache. This explains why bruxism is often associated to limitations. which might ensue cause suffering to all the anatomical components of chewing. are subject to structural and functional damage . etc. persistent face pimples. in particular in support of the teeth (periodontium). gingivitis. In the muscle occurs as a reaction from hiperfungsi hipertonus musculoskeletal system. It happens because that activities force the muscles and joints to work hard while it is time for the muscles to be relaxed. cervical and lumbar pain from postural problems. TMJ. prevents the circulation of blood in all components. teeth chafing. if it continues. gnashing of teeth. pain.cause bruxism during the day in an attempt to reposition the teeth. So that habits cause hyperactivity. The ischemia and dystrophy. Articular disc displacement can occur which increases the activity so that the discus experienced over use causes decreased flexibility in the discus. which can cause hipertonus / muscle spasm or hipotonus which can cause muscle weakness and inflammation that can cause pain. which are under pressure all night . periodontitis. Stress and psychological problems are not the cause but pro-factors.2003) Ligaments associated with the TMJ will also experience stiffness as a result emphases of muscle contractions that cause the flexibility of these ligaments will decrease or decreases can cause stiffness hipomobile contractures that resulted occurred and caused laxity resulting hipermobile occur and can lead to rupture pain. 1990) Cerebral cortex can inhibit the activity of afferent sensory pathways which bring painful stimuli. hydrotherapy. lowered monoamine activity (serotonin. Endorphin are proyein molecules composed of chains of amino acids (peptide). γ-aminobutyric acid (GABA). and substance P. If central nociceptive neuron’s stimulability is increased. vibration. This forms the basis of various treatment modalities such as massage. The development of transcutaneous electrical nerve simulation (so-called TENS units) for the symptomatic relief of pain is based on inhibitory effects of cutaneous stimulation. including the enkephalins. electroacupunture. noradrenalin. Brain stem with monoamine cores has the most significant role in pain modulation. a known morphine antagonist. it will be painful. Thus.microcirculation resulting in reduced network resulting in ischemic tissue. Anxious and depressive patients have lowered levels of painful stimuli. They are secreted by brain tissues into cerebrospinal fluid (CSF) and by the pituitary gland into the bloodstream. thermal applications. opioid peptide β-endorphin – “endogen morphine”) decreases the . glycine. betaendorphin. the activity of afferent sensory paths is greater. and counterirritation. Its effects decreases with the duration of the pain. The mechanism of pain is modulated are extremely complex and only partially understood. Endorphin (endogenous morphine) exerts a definite analgesic effect that is reversible by naloxone. (Bell. analgesic balms. 1990) The brain stem descending inhibitory mechanism obtunds pain by way of serotonin released into the CSF when the serotoninergic neurons in the periaqueductal gray (PAG) and the nucleus raphe magnus (NRM) are activated by nonpainful stimulation of thick cutaneous neurons. dynorphin. vapoocolants. This endogenous antinociceptive system is activated by intermittent painful stimuli as well as by acupuncture. serotonin. an important element pain chronicity. Many neurochemicals that take part have been identified. (Bell. TMJ disorder will be followed by pain. The discovery of endrigenous opioids that act as inhibitory neuromodulator in nociceptive pathways opened a door to pain behavior at a molecular level. and electroanalgesia. mild stimulation of cutaneous sensory nerves exerts an inhibitory influence of pain. The areas of the higher center receiving input from the TMJ also receive input from facial skin and intraoral sites. endogen opioid. the lowered activity of noradrenaline system. has also a role in the development of painful symptoms. vagus and hypoglossal cranial nerves and the upper cervical nerves.possibility of modulating the activities of afferent sensory pathways and control of pain stimuli entrance from the peripheral part to the central nervous system (Gate control theory). However. glossopharyngeal. biochemically and physically sensitive individuals react to stress by releasing ACTH that antagonizes the analgesic effects of β-endorphin . 2010) Endorphin. as well as converging input from the facial. A precise way of antidepressants’ activity is unknown but can be the result of an increased concentration of monoamines in midbrain whose role is to modulate the pain. (Buljan. emotionally. (Buljan. alleviating pain with tryciclic antidepressants is as successful as in non-depressed. Theoretically speaking. 2010) There is extensive convergence of sensory nerves that serves the orofacial region. (Wright. Hypothetically. It has been shown that at least one-half of the pain-carrying neurons that normally are activated by the trigeminal nerve can be activated by electrical stimulation outside their normal receptive field. (Wright. It has been observed that 80 percent of the neurons from the TMJ and masseter muscle converge in the trigeminal subnucleus caudalis. 2010) Serotonin is probably the most important transmitter in descendent inhibitory pathways and a lowered activity of serotonergic system is considered responsible for painful symptoms in depressive or anxious patients. Biochemical basis of chronic pain is confirmed by its connection with depression and efficacy of tryciclic antidepressants in the treatment. 2000) . 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