TEMPOROMANDIBULAR JOINT DISORDERS

TEMPOROMANDIBULAR JOINT DISORDERS

Development of TMJ takes place mostly between the 7th and 20th week of intrauterine life and a particularly sensitive period is morphogenesis between the 7th and 11th week.

Three stages in TMJ development:

  • Blastemic stage (7th-8th week) – Development of the condyles, articular fossa, articular disk and capsule.
  • Cavitation stage (9th-11th week) – Beginning of lower joint space development and condylar chondrogenesis
  • Maturation stage – After the 12th week

TMJ is the articulation of the condyle of the mandible, and the inter-articular disc with the mandibular fossa (glenoid fossa) of the temporal bone.

TMJ is a ginglymosdiarthroidal joint.

  • Ginglymos means hinge type movement.
  • Arthroidal means gliding movement.

Compound joint requires the presence of at least three bones.

TMJ is made up of two bones. Functionally, the articular disc serves as a third non ossified bone permitting the complex movements of the joint. Thus TMJ is also known as compound joint.

The joint cavity is filled with the synovial fluid (filterate of plasma with added mucin and proteins) which is mainly composed of hyaluronic acid which decreases the friction during joint compression and motions.

  • It is a fibrocartilagenous plate that divides the joint cavity into an upper and a lower compartment and contains collagen fibers, elastic fibers, proteoglycans and cartilaginous cells.
  • The disc provides an interface for the condyle as it glides across the temporal bone.
Ligaments do not enter actively into the joint function but act as a passive restraining device to limit and restrict the border movements. The ligaments include:
  1. Functional ligaments :
    • Collateral (discal) ligaments.
    • Capsular ligament.
    • Temporomandibular ligament.
  2. Accessory ligaments:
    • Sphenomandibular ligament.
    • Stylomandibular ligament.

They are two in number:

  • Medial collateral ligament – attaches the medial border of the articular disc to the medial pole of the condyle.
  • Lateral collateral ligament– attaches the lateral border of the articular disc to the lateral pole of the condyle.

These ligaments divide the joint mediolaterally into the superior and inferior joint cavities.

The articular surfaces are covered with a white fibrocartilage in which collagen fibers predominate with a few cartilaginous cells called as fibrous capsule.

  • Capsular ligament acts to resist any medial, lateral or inferior forces that tend to separate or dislocate the articular surfaces.
  • Capsular ligament encompass the joint thus retaining the synovial fluid.

The lateral aspect of the capsular ligament is reinforced by strong tight fibers that form the lateral or temporomandibular ligament.

It is the main ligament that strengthens the capsule laterally.

This ligament is made of:

  • Outer oblique portion.
  • Inner horizontal portion.
  • It is an accessory ligament.
  • It is attached superiorly to the spine of the sphenoid bone and inferiorly to the lingula of mandibular foramen.
  • It is also an accessory ligament.
  • It is attached superiorly to the lateral surface of the styloid process and inferiorly to the angle and posterior border of ramus of the mandible.
  • It limits the excessive protrusive movements of the mandible.

Muscle is a band or bundle of fibrous tissue in a human or animal body that has the ability to contract, producing movement in or maintaining the position of parts of the body.

Muscles are classified by three different methods, based on different factors:

  1. Depending upon the presence or absence of striations.
  2. Depending upon the control.
  3. Depending upon the situation.
  • Striated muscle
  • Non-striated muscle.
  • Striated muscle is the muscle which has a large number of cross-striations (transverse lines).
  • Skeletal muscle and cardiac muscle belong to this category.
  • Muscle which does not have cross-striations is called non-striated muscle.
  • It is also called plain muscle or smooth muscle.
  • It is found in the wall of the visceral organs.
  • Voluntary muscle
  • Involuntary muscle.
  • Voluntary muscle is the muscle that is controlled by the will.
  • Skeletal muscles are the voluntary muscles.
  • These muscles are innervated by somatic nerves.
  • Muscle that cannot be controlled by the will is called involuntary muscle. Cardiac muscle and smooth muscle are involuntary muscles.
  • These muscles are innervated by autonomic nerves.
  1. Skeletal muscle
  2. Cardiac muscle
  3. Smooth muscle.
  • Skeletal muscle is situated in association with bones forming the skeletal system.
  • The skeletal muscles form 40% to 50% of body mass and are voluntary and striated.
  • These muscles are supplied by somatic nerves.
  • Cardiac muscle forms the musculature of the heart.
  • These muscles are striated and involuntary.
  • Cardiac muscles are supplied by autonomic nerve fibers.
  • Smooth muscle is situated in association with viscera.
  • It is also called visceral muscle.
  • It is different from skeletal and cardiac muscles because of the absence of cross striations, hence the name smooth muscle.
  • Smooth muscle is supplied by autonomic nerve fibers.

There are four pairs:

  • Masseter
  • Temporalis
  • Medial pterygoid.
  • Lateral pterygoid.

Accessory muscle of mastication:

  • Buccinator (prevent the accumulation of food in vestibule).

Muscles of mastication are striated muscle.

The temporalis, masseter and medial pterygoid muscles supply the power for pulling the mandible against the maxilla (elevating and closing the mandible).

Digastrics, geniohyoid and mylohyoid muscles help when mouth is opened wide.

Protrusion occurs by lateral and medial pterygoid muscles.

Retraction produced by posterior fibres of temporalis. It may be resisted by middle and deep fibers of masseter, digastrics and geniohyoid muscles.

Turning the chin to left side is produced by left lateral pterygoid and right medial pterygoid and vice versa.

On Denture Border

  • An active masseter muscle will create a concavity in the outline of the distobuccal border and a less active muscle may result in a convex border.
  • In this area the buccal flange must converge medially to avoid displacement due to contraction of the masseter muscle because the muscle fibers in that area are vertical and oblique.

On the distobuccal border

  • Moderate activity will create a straight line.
  • An active muscle will create a concavity.
  • An inactive muscle will create a convexity.
  • Most commonly involved muscle in MPDS.
  • Unilateral failure of lateral pterygoid muscle to contract results in deviation of the mandible toward the affected side on opening.
  • Bilateral failure results in limited opening, loss of protrusion and loss of full lateral deviation.
  • Most commonly involved in MPDS.
  • Trismus following inferior alveolar nerve block is mostly due to involvement of medial pterygoid muscle.
  • The medial pterygoid muscle is not usually involved in gnathic dysfunctions but when they are hypertonic, the patient is usually conscious of a feeling of fullness in the throat and an occasionally pain on swallowing
  1. Derived from external carotid artery.
  2. Within the substance of the parotid gland, it gives two branches:
  • Facial artery.
  • Lingual artery.

 At the level of condylar neck, the external carotid artery bifurcates into:

  • Superficial temporal artery.
  • Internal maxillary artery.

These two arteries supply the muscles of mastication and the TMJ.

  • Temporomandibular Joint is innervated by the same nerve (trigeminal nerve) that provides motor and sensory innervation to the muscles that control it.
  • Innervation is provided by auriculotemporal nerve as it leaves mandibular nerve behind the joint. Ascends laterally and superiorly to wrap around the posterior region of the joint.
  • Deep temporal and masseteric nerves provide additional innervation.
  • Analogous to knee jerk.
  • When a downward tap is applied to the chin, there is a reflex contraction of the jaw closing muscles.
  • This reflex relates to the fine control of the jaw movements to take into account the different consistencies of food.
  • When the mechanoreceptors within the mouth or nociceptors from the mouth are stimulated, the jaw opening reflex is triggered.
  • This reflex results in an inhibition of the activity of jaw closing muscles.
  • This reflex is thought to help prevent injury when biting or chewing something that may cause damage.

The most valuable aspects of diagnostic assessment are:

  • Thorough history taking.
  • Physical / Clinical examination.
  • Diagnostic imaging (of value only in selected cases – for detection of internal derangements & abnormalities of articular bones).

To start evaluating the patient for TMJ dysfunctions, the following questions should be asked:

  • History of pain- Pain in the face, in front of the ear and temple areas.
  • Headache, earaches, neck ache, or cheek pain.
  • Pain when using the jaw.
  • Pain in the teeth.
  • Time of worsening of pain (morning / evening.)
  • Does the joint click – when normal relation between meniscus and condyle is disturbed, giving rise to a click on opening the mouth
  • Is movement limited, either in range or by locking?
  • Inability to open suggests meniscus displacement, which is usually unilateral, and in which at least 1 cm of mouth opening is always retained.
  • If closing is impossible, a luxation of the mandibular condyle is most likely.
  • Excessive limitation coming on rapidly may be the result of hysteria or of tetanus.
  • Is there crepitus – Crepitus is the result of movement across an irregular surface
  • Does the patient suffer from pain on clenching or grinding – This occurs mainly at night in stressed people
  • Is there tinnitus, vertigo or a hearing problem– Vertigo may result from differences in vestibular impulses as a result of TMJ problems.
  • Has there been a change in sensibility– In atypical facial neuralgia, severe diminished facial sensibility is often found. Trigeminal neuritis is seldom accompanied by disturbed sensibility.

The physical/clinical examination that is directed towards diagnosing temporomandibular dysfunction should include the following steps:

Inspection:

  • Facial asymmetry.
  • Swelling
  • Hypertrophy of masseter & temporalis muscle.
  • Opening pattern
  • Limitations during opening.
  • Symmetry of the face- Mild to moderate asymmetry is common, but gross asymmetry may reflect a growth disorder.
  • Patients who during childhood had experienced trauma to the chin that resulted in TMJ ankylosis and abnormal facial bone growth.

A. Normal mouth opening without pain:

  • 8 mm for males (38.7mm to67.2mm).
  • 3 mm for females (36.7mm to 60.4mm).
  • 9 mm for children (32mm to 64mm).
  • Maximum opening should be measured without pain, as wide as possible even with pain, and after opening with clinician assistance.
  • Assisting the jaw during mouth opening is accomplished by applying mild to moderate pressure against the upper and lower incisors with the thumb and index finger.
  • Assisted mouth opening if more than 5 mm with a soft end feel indicates muscular problems but if less than 5mm with a hard end feel indicates joint disorders (acute non reducing disk displacement)

B. Lateral movements

  • Maximum normal lateral movement is more than 7mm.
  • Measurement made with teeth slightly separated and measuring the displacement of the lower mid line from upper mid line and adding or subtracting lower mid line displacement if any at the start of movement.

C. Protrusive movements

  • Maximal normal protrusive movement is more than 7mm.
  • It is measured by adding the horizontal distance between the upper and lower central incisors and adding the distance the lower incisors travel beyond the upper incisors.

RDC / TMD (Research Diagnostic Criteria for Temporomandibular Disorders) have recommended a maximum pressure of 2 lb for palpating the    masticatory muscles.

A. Temporalis

  • The anterior region is palpated above the zygomatic arch and anterior to the TMJ.
  • The middle region is palpated directly above the TMJ and superior to the zygomatic arch.
  • The posterior region is palpated above and behind the ear.
  • The tendon of the temporalis is palpated intraorally by running the index finger along the anterior border of the ramus up to the coronoid process where the tendon is inserted.

Masseter Muscle:

B. Extra oral approach

  • Palpated bilaterally at its superior & inferior attachments.
  • First the index & middle fingers are placed on each zygomatic arch and are

then dropped down slightly to the portion of the masseter attached to the zygomatic arch just anterior to the joint (deep masseter). The fingers are then dropped to the inferior border of the ramus. The area of palpation is just above the attachment of the body of the masseter (superficial masseter).

Bimanual palpation

The masseter muscle is most effectively examined by simultaneously pressing from inside & outside the mouth in the process of bimanual palpation.

Lateral pterygoid

The lateral pterygoid is palpated by inserting a finger intraorally each behind the maxillary tuberosity.

Medial pterygoid

The medial pterygoid is palpated by running a finger intra orally in an antero-posterior direction along the medial aspect of the mandible in the floor of the mouth.

Enumerate the palpation of TMJ?

RDC / TMD has recommended a maximum pressure of 1 lb for palpating the joint. Palpation reveals:

  • Pain
  • Irregularities during condylar movements like clicking & crepitus.

Palpation of the TMJ is done by two approaches:

  • Extra auricular
  • Intra auricular

A. Extra auricular approach:

  • Lateral pole of the condyle is the most accessible for palpation.
  • Pain on palpation just anterior & posterior to the lateral pole is related to the TMJ capsular ligaments.
  • On palpation, the condyle that does not translate may not be palpable during mouth opening and closing.

B. Palpation of pretragus area:

Ask patient to slowly open and close the mouth while the practitioner bilaterally palpates the pretragus depression with the index fingers.

Intra auricular approach:

  • Performed by inserting the little finger into the ear canal and pressed anteriorly to explore the anterior wall of external wall of the meatus for pain and tenderness that are usually associated with arthritic changes and capsulitis.
  • Check whether the condyles are moving symmetrically with rotation or not and whether the translation phase is evident or not.
  • When unilateral problems exist, the mandible will always deviate to the side with limited condylar movement.

Cervical muscles:

Palpation of the cervical muscles reveals:

  • Mobility of the neck.
  • Pain & limitation of movements of the neck.
  • Origin of pain (whether muscular or related to vertebral column).

When the patient with limited range of movement can passively be stretched to a greater range, the problem is muscular. Patient with vertebral problem cannot be stretched to a greater range.   

Among the various cervical muscles, the muscles of clinical significance are:

  • Sternocleidomastoid
  • Trapezius

Sternocleidomastoid

Palpation is done bilaterally near its insertion on the outer surface of mastoid fossa, behind the ear. The entire length of the muscle is palpated, down to its origin near the clavicle. Response of the patient is noted. Trigger points, if any are also noted.

Trapezius

  • Extremely large muscle of the back, shoulder and the neck.
  • The main purpose of its palpation is to search for trigger points that may be producing referred pain to the face.
  • The upper part is palpated from behind the sternocleidomastoid, inferolaterally to the shoulder and trigger points if any age recorded.
  • Helps to confirm a diagnosis.
  • Helps to differentiate the pain arising from joints or muscles.
  • If the pain subsides after giving the injection in the joint, the pain is of joint origin.
  • Similarly, injecting trigger points or tender areas in the muscle should eliminate pain from that site indicating the problem of muscular origin rather than of joint origin.
  • Lidocaine 2% without a vasoconstrictor is used.
  • The site of injection is anterior to the tragus to minimize the chances of intravascular injection of ECA (external carotid artery) or the accompanying vein.
  • The injections which are given from the lateral aspect does not anesthetize the joint completely because the auriculotemporal nerve enters the capsule from the medial aspect.

(Approved by American Society of Temporomandibular Joint Surgeons)

I. INTRA-ARTICULAR (INTRACAPSULAR) PATHOLOGY:

A. ARTICULAR CAPSULE

  • Displacement
  • Deformity
  • Adhesions
  • Degeneration
  • Injury
  • Perforation
  • Anomalous development.

B. DISC ATTACHMENTS

  • Inflammation
  • Injury (laceration, hematoma, contusion).
  • Perforation
  • Fibrosis
  • Adhesions

C. SYNOVIUM

  • Inflammation / effusion.
  • Injury
  • Adhesions
  • Synovial hypertrophy / hyperplasia.
  • Granulomatous inflammation.
  • Infection
  • Arthritides (rheumatoid, degenerative).
  • Synovial chondromatosis.
  • Neoplasia

D. ARTICULAR FIBROCARTILAGE

  1. Hypertrophy / hyperplasia
  2. Degeneration(Chondromalacia)
  • Fissuring
  • Fibrillation
  • Blistering
  • Erosion

E. MANDIBULAR CONDYLE AND GLENOID FOSSA

  • Osteoarthritis (osteoarthrosis, degenerative joint disease).
  • Avascular necrosis (osteonecrosis).
  • Resorption
  • Hypertrophy
  • Fibrous and bony ankylosis.
  • Implant arthropathy.
  • Fracture / dislocations.

II. EXTRA ARTICULAR (EXTRACAPSULAR) PATHOLOGY:

A.MUSCULOSKELETAL

  1. BONE
  • Anomalous development (hypoplasia, hypertrophy, malformation, ankylosis.
  • Fracture
  • Metabolic disease.
  • Systemic inflammatory disease (connective tissue/ arthritides).
  • Infection
  • Dysplasia
  • Neoplasia
  1. MASTICATORY MUSCLES AND TENDONS
  • Anomalous development.
  • Injury
  • Inflammation
  • Hypertrophy
  • Atrophy
  • Fibrosis, contracture.
  • Metabolic disease.
  • Infection
  • Dysplasias
  • Neoplasia
  • Fibromyalgia

B. CENTRAL NERVOUS SYSTEM / PERIPHERAL NERVOUS SYSTEM

  • Reflex sympathetic dystrophy.
  • Recent trauma.
  • Sensory or motor abnormalities.
  • Severe restrictions in mandibular motion.
  • Acute alterations of the occlusion.
  • Degenerative changes of the bone
  • Disc displacements.
  • Pain, headache, and muscle spasms.
  • Clicking, snapping, popping, grating noises in the TMJ.
  • Dizziness and possible nausea.
  • Ear-ache, ringing in the ears (tinnitus), a fullness or pressure backlog in ear.
  • Pain or burning sensation of tongue.
  • Partial or complete inability to open the mouth.
  • Limited range of function of the mandible in one or more directions, with or without pain.
  • Tender areas on face and head where palpation elicits painful response either in the area palpated or to a referred pain area.
  • Neck aches and backaches.

Etiological factors include:

  • Occlusal abnormalities.
  • Orthodontic treatment.
  • Bruxism and orthopedic instability.
  • Macrotrauma and microtrauma.
  • Joint laxity.
  • Exogenous estrogen.
  • Stress
  • Mental tension.
  • Anxiety or depression.

Microtrauma is internal, such as grinding the teeth (bruxism) and clenching (jaw tightening). This continual hammering on the temporomandibular joint can change the alignment of the teeth. 

Macro trauma is any sudden force to the joint that causes structural alterations.

  • Posterior cross-bite.
  • Overjet/overbite greater than 5 mm.
  • Centric Relation/ Maximum intercuspal sliding greater than 2 mm.
  • Edge-to-edge bite.
  • Sagittal relation Class III.
  • Anterior open bite.
  • Five or more missing teeth.
  • Plain film radiography.
  • Xeroradiography
  • Dental panoramic tomography.
  • Computerized tomography (CT).
  • Cone beam CT.
  • Magnetic resonance imaging.
  • Arthrography
  • Arthroscopy
  • Single photon emission computed tomography.
  • Radioisotope scanning.
  • Electromyography

HARD TISSUE IMAGING:

  • Transcranial Projection.
  • Transpharyngeal Projection.
  • Transorbital Projection.
  • Submentovertex Projection.
  • Reverse Towne’s Projection.
  • Dental panoramic tomogram.
  • Conventional tomography.
  • Computed tomography.

SOFT TISSUE IMAGING:

  • Arthrography
  • Arthroscopy
  • Magnetic resonance imaging.

Activities of the masticatory system can be divided into two types:

  • Functional – Which includes chewing, speaking.
  • Parafunctional– Which includes clenching or grinding of the teeth (referred to as bruxism).
  • Also known as muscle splinting.
  • It is the first response of the masticatory muscles to injury or threat of injury.
  • It is a CNS response to injury.
  • The activity of the appropriate muscle seems to be altered so as to protect the injured part from further damage.

All muscles are maintained in a mildly contracted state known as tonus which persists without fatigue because if the alternating contractions and relaxations of the muscle fibers which keeps the overall muscle length unchanged and resist any sudden elongation. When protective co – contraction occurs, the CNS increases the activity of antagonist muscle during contraction of the agonistic muscle.

A. Altered sensory or proprioceptive input:

  • Poorly fitting crowns.
  • Opening the mouth too wide.
  • Long dental appointments.
  • Dental injections.

B. Constant deep pain input.

C. Increased emotional stress.

  • Myalgia (not common complaint).
  • Structural dysfunction.
  • No pain at rest.
  • Slight pain with function.
  • Feeling of muscle weakness.
  • Remove the cause, example restorations and crowns to be contoured properly.
  • Source of deep pain if any to be removed.
  • Stress to be managed by physical self management techniques.
  • Also known as non inflammatory myalgia.
  • It is the first response of the muscle tissues to continue protective co–contraction. Although, co-contraction is a CNS induced muscle response, local muscle response represents a change in the local environment of the muscle tissues.
  • Protracted protective co – contraction.
  • Constant source of deep pain.
  • Local tissue trauma or unaccustomed use of the muscle.
  • Increased levels of emotional stress.
  • Structural dysfunction: marked decrease in the velocity and range of mandibular movement.
  • Minimum pain at rest.
  • Increased pain to function.
  • Actual weakness of muscle.
  • Local tenderness of involved muscles on palpation
  • Altered sensory or proprioceptive input to be eliminated.
  • Source of deep pain to be eliminated.
  • Stress to be managed with physical self regulation (PSR) techniques.
  • Known as tonic contraction myalgia.
  • Involuntary CNS induced tonic muscle contraction associated with local metabolic conditions within the muscle tissues.
  • Continued deep pain input.
  • Fatiguity of the muscle.
  • Overuse of the muscles.
  • Change in local electrolyte balance.
  • Structural dysfunction: marked restrictions in the range of mandibular movements.
  • Pain at rest.
  • Pain increased with function.
  • Affected muscle is firm and painful to palpation.
  • Generalized feeling of muscle tightness.
  • Reducing the pain and then passively stretching the muscle.
  • Reduction of the pain can be achieved by: Manual massage.
  • Vapocoolant spray or the ice.
  • Injection of a local anesthetic agent into the muscle.
  • Sources of deep pain if present should also be removed to lessen the likelihood of recurrent myospasm.
  • It is a chronic, continuous muscle pain disorder originating predominantly from the CNS that is felt peripherally in the muscle tissues.
  • It is referred to as myositis because it presents clinically with symptoms similar to inflammation but the classical signs of the inflammation are absent.
  • Protracted local muscle soreness.
  • Protracted myofascial pain.
  • Structural dysfunction: decrease in velocity and range of mandibular
  • Pain at rest.
  • Increased pain with function.
  • Local muscle tenderness.
  • Feeling of muscle tightness.
  • Muscle contractures.
  • Presence of constant aching myogenous pain.
  • The most common clinical feature is the extended duration of the symptoms.
  • Mandibular use should be restricted within painless limits.
  • Exercises and injections to be avoided.
  • Teeth to be disengaged.
  • Anti-inflammatory drugs eg: Ibuprofen 600mg qid for two weeks so that blood levels are sufficiently elevated to achieve a clinical effect.

Hypertrophy refers to an enlargement caused by an increase in the size but not in the number of cells.

  • Masticatory muscle hypertrophy can affect all the muscles of mastication, several muscles or just one muscle.
  • In 1880, Legg reported a case of bilateral hypertrophy of the masseter and temporal muscle in a 10-year-old girl.
  • It can occur either bilaterally or unilaterally, and most commonly the masseter muscles alone are affected.

Occasionally occur as a congenital form but mostly it presents as an acquired condition.

Etiological factors:

  • Bruxism
  • Clenching
  • Unilateral chewing.
  • TMJ disorders.
  • Malocclusion
  • Psychological factors.
  • Masseter muscle hypertrophy (MMH) may present as unilateral or bilateral, benign increase in size of masseter muscle.
  • Mostly seen in late adolescence and early adulthood.
  • Affects both males and females but has slight male predominance.
  • Attrition, periodontal breakdown or temperomandibular joint problem.
  • Unaesthetic appearance due to facial asymmetry or ‘square’ face appearance. Pain, headache, muscle stress, trismus and intermittent masticatory claudication.
  • The radiographic findings: Bone spurs at the angle of mandible or flaring of mandibular angle and hyperostosis of mandibular ramus (anteroposterior skull radiograph)
  • CT and MRI scans provide useful diagnostic information regarding this condition.
  • Reactive masticatory muscle hypertrophy (RMMH) was coined by Harriman in 1996.
  • Isolated unilateral temporalis muscle hypertrophy, also known as reactive masticatory muscle hypertrophy (RMMH).
  • It is a rare cause of a painful soft tissue swelling of the temple.
  • Bilateral temporalis and masseter muscles are hypertrophic resulting in “pseudomasses”.
  • Management of muscle hypertrophy is multifaceted.
  • Para functional habits must be corrected.
  • Dental restorations and occlusal adjustments to correct premature contacts are important.
  • Non-surgical modalities of treatment include reassurance, tranquilisers or muscle relaxants, injection of Botulinum toxin type A 40–60 IU per muscle administered by intramuscular route.
  • Surgical modality includes cosmetic surgery to reduce the bone prominence from mandibular angle.

It is a regional myogenous pain condition characterized by local areas of firm, hypersensitive bands of muscle tissue known as trigger points. This condition is also referred as myofascial trigger point pain. Myofascial trigger point pain was first described by Travell and Rinzler in 1952.

  • Central nervous system plays significant role.
  • Protracted local muscle soreness.
  • Local factors: Para functional habits, poor posture and chilling.
  • Systemic factors – Fatigue, poor physical condition, hypovitaminosis and viral infections.
  • Increased levels of emotional stress.
  • Continued source of deep pain input.
  • Occlusal interferences.
  • Presence of sleep disorder.
  • Idiopathic trigger point mechanism.
  • Females more affected than males with ratio of 4:1.
  • Affects primarily young women (age 20 to 40 years).
  • Presence of trigger points which present as local areas of firm, hypersensitive, bands of muscle tissue.

There are four cardinal sign and symptoms:

  • Unilateral dull pain in the ear or preauricular region that commonly worsens on awakening.
  • Muscle tenderness. Tenderness of one or more muscles of mastication on palpation.
  • Clicking or popping noise in TMJ.
  • Limitation of jaw movement, limitation or deviation of the mandible on opening.

Trigger points are discrete, focal, hyperirritable spots located in a taut band of skeletal muscle. The spots are painful on compression and can produce referred pain, referred tenderness, motor dysfunction, and autonomic phenomena.

Trigger points are classified as:

  • Active trigger point.
  • Latent trigger point.
  • An active trigger point causes pain at rest.
  • It is tender to palpation with a referred pain pattern that is similar to the patient’s pain complaint.
  • This referred pain is felt not at the site of the trigger-point origin, but remote from it.
  • The pain is often described as spreading or radiating.
  • Referred pain is an important characteristic of a trigger point.
  • A latent trigger point does not cause spontaneous pain, but may restrict movement or cause muscle weakness.
  • The patient presenting with muscle restrictions or weakness may become aware of pain originating from a latent trigger point only when pressure is applied directly over the point.

Diagnosis is made on the basis of clinical findings.

  • Presence of trigger points Trigger points are small in head and neck region i.e. about to 2 to 10 mm and larger in shoulder region 10 to 20 mm.
  • Examination of muscle of mastication Muscles should be examined for tenderness using digital pal­pation. Muscles that should be included in examination are medial and lateral pterygoid, masseter, temporalis, sterno­cleidomastoid, and trapezius.
  • Measurement of stress A useful tool is Symptom check list 90(SCL-90). This evalu­ation provides an assessment of nine psychologic states.

Treatment of MPDS is divided in to three categories by Weinberg. These categories are:

  • Palliative therapy.
  • Causative therapy.
  • Adjunctive therapy.
  • Definitive therapy.

This therapy includes procedures such as occlusal splint, medications, home remedies (ice, moist heat application, ex­ercises and soft diet).

Drug therapy should be used on fixed dose schedule rather than as needed for pain. Following drugs can be used for treatment of MPDS:

Muscle Relaxants

Most common muscle relaxants are metaxalone 400 to 800 mg every six hours or chlorzoxazone 500 mg every six hours. Other muscle relaxants are casrisoprodol (250-350mg three times daily), methocar­bamol (500-1500mg 4-6 hourly), orphenadrine (50mg three times daily)and cyclobenzaprine(5 mg three times/day).

Nonsteroidal anti-inflammatory drugs

  • Ibuprofen should be used in doses of 400mg four times daily.
  • The cyclo-oxygenase inhibitors rofecoxib (25-50 mg/day) and celecoxib (100-200mg/day).

Benzodiazepenes

  • Diazepam(2.5 to 5mg at bed time) and clonazepam (0.25mg 2 times/day, maintenance dose 1mg/day).

Tricyclic Antidepressant

  • Drug like amitryptylline is effective.
  • It can be started with dose as low as 10mg at night and dosage can be increased to 75 to 100mg depending upon patient tol­erance.

Capsaicin

Capsaicin cream (0.025% or 0.075%) can be used for pain relief. It releases substance –P and pain related neuropep­tides to reduce pain perception and inflammation and must be applied multiple times per day for at least 2 weeks.

Passive stretching i.e. keeping the muscle fibers relaxed while slowly stretching the muscle, preventing it from tightening via the stretch reflex in conjunction with moist heat(followed by application of ice) is beneficial for de­creasing muscle and joint pain and for improving ranges of movement.

There are two methods for reducing muscular pain:

1. Repetitive action on trigger point with a mode of coun­ter stimulation.

2. Muscle rehabilitation through active and passive stretch­ing and postural exercises to restore the muscle to nor­mal length, posture and range of motion.

Spray And Stretch Non-invasive technique for counter stimulation. It involves cooling the skin with fluoromethane, ethyl chloride, spray and then gently stretching the involve muscle to perform spray and stretch therapy.

Pressure and Massage

Increased pressure applied to the trigger point can also relieve pain. Pressure is increased to about 20 pounds and is main­tained to 30 to 60 seconds

Trigger Point Injections

Procaine diluted to 0.5% with saline has been recommended because of its low toxicity to the muscle, but lidocaine (2% without vasoconstrictor) is also used.

Injections are often given to muscle group in series of weekly treatments for 3 to 5 weeks;

Consist of treatment modalities that augment and assist de­finitive or causative type of treatment for TMD. It includes:

  • Physiotherapy

It is combination of physical therapy, massage therapy and electro modalities. Both passive and active treatments are commonly included as part of therapy. Posture therapy is also useful to avoid forward head positions that are thought to adversely affect mandibular posture and masticatory mus­cle.

  • Electrotherapy

Is a part of adjunctive therapy; modalities includes electro ­galvanic stimulation, ultrasound, low level laser and infra red.

  • Electrogalvanic stimulation

It utilizes negative polarity over a painful, swollen area. The negative charge produces alkaline effect within the tissues, denaturing proteins and produces vasodilatation of the cap­illaries;

  • Transcutaneous Electrical Nerve Stimulation (Tens)

 

TENS supposedly blocks pain signals being carried over the small, unmyeli­nated C fibers by forcing the large myelinated A fibers to carry a light touch sensation. It may provide pain relief by physiologic effects of rhythmic muscle movement.

  • Ultrasound

It is a method of producing deep heat more effectively that the patient could achieve by using surface warming. These mechanical vibrations produce heat and vasodilatation by increasing the tissue temperature

  • Iontophoresis

Is a process in which ions in solutions are driven through intact skin by using a direct current between two electrodes. It uses ultrasonic energy to drive a medication deep into the tissue.

  • Low level laser

Laser therapy includes nitric oxide synthesis, which causes the endothelial linings of capillaries to dilate, improving cir­culation in the area.

  • Infra red radiation

It produces vasodilatation of capillary bed by initiating the synthesis of nitric oxide, improving circulation and decreas­ing swelling.

  • Acupuncture (dry needling) and Percutaneous electrical nerve stimulation (electro-acupuncture or PENS)

Integrating behavioural therapy and relaxation techniques in chronic pain management in MPDS are effective.

Trigger points

Tender points

Local tenderness, taut band, local twitch response, jump sign

Local tenderness

Singular or multiple

Multiple

May occur in any skeletal muscle.

Occur in specific locations that aresymmetrically located

May cause a specific referred pain pattern

Do not cause referred pain, but often cause a total body increase in pain sensitivity

  • The term ‘la bruxomanie’ was first introduced by Marie Pietkiewicz in 1907.
  • It was latter adopted as ‘bruxism’ to describe gnashing and grinding of the teeth occurring without a functional purpose.
  • According to American academy of orofacial pain; Bruxism is defined as “diurnal or nocturnal parafunctional activity including clenching, bracing, gnashing, and grinding of the teeth.”
  • According to American sleep disorders association; Bruxism is defined as “tooth grinding or clenching during sleep plus one of the following: Tooth wear, sounds or jaw muscle discomfort in the absence of medical disorder.”
  • Zarb and Carlsson defined bruxism as “nocturnal clenching and grinding of teeth.”
  • Awake bruxism or Diurnal Bruxism (DB) – Is usually seen as a jaw clenching habit that appears in response to stress and anxiety states.
  • Sleep bruxism – SB is an oromandibular behavior that is defined as a stereotyped movement disorder occurring during sleep and characterized by tooth grinding and/or clenching.

Both awake and sleep bruxism are sub classified into either primary, not related to any other medical condition, or secondary, associated to neurological disorders or considered an adverse effect of drugs.

  • The etiology is unknown.
  • It may be due to the rhythmic contractions between the temporalis muscle and the lateral pterygoid muscle.

Predisposing factors:

  • Emotional stress.
  • CNS disturbances.
  • Genetic predisposition.
  • Certain medications.
  • Dental wear.
  • Jaw muscle pain and fatigue.
  • Temporal headaches.
  • Severe forms can compromise oral functions such as chewing, speaking, and swallowing.
  • Hypertrophy of muscles of mastication.
  • Thickening of periodontal ligament space on radiographs.
  • Occlusal splints worn during sleep.
  • Injection of botulinum toxin in the masseter muscle.

Botulinum works by exerting a paralytic effect on the muscle by inhibiting the release of acetylcholine at the neuromuscular junction.

Intracapsular disorders are:

  1. Derangements of the condyle disc complex i.e. (Articular Disc Disorders).
  2. Structural incompatibilities of articular surfaces.
  3. Inflammatory disorders of the joint (Arthritis).

The articular disc disorder is an abnormal relationship between the condyle, disc, and the articular eminence resulting from stretching and tearing of attachment of the disc to the condyle and glenoid fossa.

  1. Direct injury to the joint from a blow on the mandible.
  2. Indirect trauma from:
  • Cervical flexion extension injuries.
  • Malocclusion
  1. Chronic low grade microtrauma due to bruxism or clenching of the teeth.
  2. Generalized laxity of the joints.
  • Abnormal joint sounds.
  • Limitations in the mandibular range of movements.
  • Pain during mandibular movements.
  1. Anterior disc displacement.
  • Disc displacement with reduction (clicking joint)
  • Disc displacement with reduction and intermittent locking
  • Disc displacement without reduction (closed lock)
  1. Posterior disc displacement (open lock)
  • Caused by loosening of articular disk due to elongation or tearing of restraining ligaments and has moved from its normal position on the top of the condyle.
  • In disc displacement with reduction, the articular disc is displaced anterior to the condylar head.
  • It may also be displaced medially or laterally. The posterior most border of the disc is anterior to the 11:30 position of the condylar head. The disc remains in this position as long as the mouth is closed.
  • When the mouth is opened, the disc is re‑situated on the condylar head. The movement of the disc onto and off the condylar head may result in a clicking, snapping, and/or popping sound.
  • Pain during mandibular opening especially at the time of click.
  • Reciprocal click revealed on palpation and auscultation.
  • The sound characterized by a click that occurs at a different point during opening and closing.
  • Deflection of the mandible prior to the click with correction towards the midline after the click.
  • Tenderness if capsulitis or synovitis is present.
  • TMJ effusion on T2 weighted MRI scan.
  • The treatment goal of definitive therapy for disc displacements with reduction is to reduce intra capsular pain.
  • Flat plane stabilization splints.
  • Anterior positioning appliance (provides an occlusal relationship that requires the mandible to be maintained in a forward position).
  • The position selected for the appliance is the one that positions the mandible in the least protruded position that will re-establish the normal condyle disc relationship.

This condition is identical to anterior disc displacement with reduction, with the additional feature of intermittent limited mandibular opening on the occasions that the disc does not reduce.

  • Management depends on how often locking occurs.
  • If locking is rare, and not a significant bother to the patient.
  • If the lock is frequent, increased lubrication of the articular surfaces, in an effort to decrease the frequency of locking.
  • This can be done by moving the mandible fully through all directions of movement (open, protrusive, retrusive, and laterotrusive) after capturing the disc. Usually, the disc can initially be reduced with lateral movements.
  • Ask to perform these mobilization exercises without allowing the disc to re‑displace. Rolling a tube between the teeth during these movements can provide such control.

In this condition recapturing of the disc becomes more difficult due to loss of elasticity of the superior retrodiscal lamina. When the disc is not reduced, the forward translation of the condyle merely forces the disc in front of the condyle.

Thus, limited mandibular opening occurs when the disc interferes with the normal translation of the condyle along the glenoid fossa.

  • Occurs after trauma (macro)
  • Severe long standing nocturnal bruxism (micro trauma).
  • Patients with already clicking joints that progressed to intermittent locking and then the permanent locking.
  • Pain over the joints during mandibular opening.
  • Mandible deviates to the side of displacement with a hard end feel during maximum opening (25 to 30mm).
  • Normal eccentric movements to the ipsilateral side but restricted to the contra lateral side.
  • Palpation reveals decreased translocation of the condyle of the affected side.

Reduce or recapture the disc by manual manipulation (in acute condition).

Clinician places his thumb intraorally over the mandibular 2nd molars on the affected side.   The fingers are placed on the inferior border of the mandible anterior to the thumb position.    Firm, but controlled downward force is then exerted on the molar at the same time that upward force is placed by the fingers.  The opposite hand helps stabilize the cranium above the joint that has been distracted.

While, the joint has been distracted, the condyle is brought downwards and forward which translates it out of the fossa. After constant distraction force of 20 to 30 seconds, the procedure is stopped and the fingers removed. It is also helpful to bring the mandible to the contra lateral side during distraction (as the disc is dislocated anteromedially) which moves the condyle into it better.

 Once, the full range of laterotrusive movements have been reached, the patient is asked to relax. An anterior positioning appliance is immediately placed to prevent clenching on the posterior teeth which would likely dislocate the disc again. If, the disc has not been reduced, second and third attempt can be taken. Failure to dislocate indicates dysfunctional superior retrodiscal lamina and may require surgical interference.

In patients with severe problems:

  • Intraarticular corticosteroids.
  • Sodium hyaluronate.
  • Arthrocentesis
  • Arthroscopic lyses and lavage.
  • Arthrotomy

When the condyle slips over the anterior rim of the disc during opening and the disc gets caught and is brought backwards in an abnormal relationship with the condyle when the mouth is closed. Actually, the disc gets folded into the dorsal part of the joint space preventing full mouth closure.

Westesson et al. described three different presentations:

  • A thin disc spans from the superior portion of the condylar head to posterior to the condylar head.
  • A centrally‑perforated disc is present, with a small portion anterior to the condylar head, and a larger portion posterior to the condylar head.
  • The entire disc is posterior to the condylar head.
  • Sudden inability to bring the upper and lower teeth together in maximal occlusion.
  • Pain in the affected joint when the teeth are brought together.
  • Forward displacement of the mandible on the affected side.
  • Restricted lateral movements to the affected side.
  • No restriction in opening the mouth.
  • There is no consensus concerning treatment for posterior disc displacement.
  • Conservative treatment can be prescribed in cases with functional impairment.
  • First line invasive techniques should be avoided.

Structural incompatibilities of the articular surfaces can originate from any problem that disrupts the normal joint functioning. There are four forms of structural incompatibilities:

  • Deviation in form.
  • Adhesions
  • Subluxation
  • Spontaneous dislocation.

Changes in the smooth articular surfaces of the joint and the disc due to:

  • Macro trauma. eg: sudden blow (closed mouth).
  • Micro trauma which loads the joints.
  • Repeated alteration in the pathway of opening and closing.
  • Clicking, if any always occur at the same position of opening and closing.
  • Deviations may or may not be painful.
  1. Bony incompatibilities are smoothened and rounded surgically.
  2. Discoplasty to repair the disc.
  3. Supportive therapy which includes:
  • Educate patient for opening and chewing that avoids or minimizes the dysfunctions.
  • In bruxism, flat stabilization splints should be used.
 

Adherence

Adhesion

1

Temporary sticking of articular surfaces during normal joint movements

More permanent and caused by a fibrosis attachment of the articular surfaces.

2

Caused by:

·         Prolonged static loading of the joint  structures.(nocturnal bruxism & clenching)

·         Closed mouth trauma.

Caused by:

·         Persistence of adherence

·         Hemarthrosis caused by macro trauma and surgery

3

Adherences represent a temporary sticking of articular surfaces during normal joint movements

Adhesion produces a more permanent limitation.

If the adhesion affects only one joint  the   opening movement will deflect to the ipsilateral side

These may occur between the disc and the condyle & between the disc and the fossa.

  • Decrease the loading of the joints.
  • Flat plane stabilizing appliances (decrease the muscle hypertrophy).
  • If, the adhesions are recent, passive stretching, ultrasound and distraction of joint.
  • If, the adhesions are permanent, arthroscopic surgery is indicated.
  • Also known as hypermobility.
  • Characterized by movement of condyle anterior to the articular eminence.

Steep short posterior slope of the articular eminence.

During the final stage of maximal mouth opening, the condyle can be seen to suddenly jump forwards with a “thud”.

  • Surgical alteration of the joint.
  • Eminectomy is done which reduces the steepness of the articular eminence and thereby decreases amount of posterior rotation of the disc on condyle during full translation.
  • Commonly refers to as an open lock.
  • Can occur after wide open mouth procedures.
  • Refers to a spontaneous dislocation of both the condyle and the disc.
  • The condyle becomes trapped in front of the eminence, resulting in patient’s inability to close the mouth.
  • Patient remains in a wide open mouth condition with inability to close the mouth.
  • Pain present secondary to the patients attempt to close the mouth.
  • Deep depression in pre tragus area (as the condyle has been positioned anterior to the articulating tubercle.)
  • Definite treatment is directed towards increasing the disc space, which allows the superior retrodiscal lamina to retract the disc.
  • When, the spontaneous dislocation becomes chronic or recurrent, eminectomy is considered (because dislocation generally occurs after subluxation).

These disorders are characterized by continuous joint area pain, often accentuated by function.

  • Synovitis
  • Capsulitis
  • Retrodiscitis
  • Arthritides
  • In synovitis there is inflammation of the TMJ synovial lining and in capsulitis there is inflammation of the capsular ligament.
  • It is not possible to differentiate the two conditions clinically except through arthroscopy or arthrotomy.
  • Trauma
  • Infection
  • Secondary to macro or micro trauma.
  • Any movement accentuates the pain.
  • Site of pain is in front of the ear.
  • Lateral aspect of condyle tender on palpation.
  • Remove the etiology.
  • Decrease adverse loading.
  • Restore normal function.
  • Resumption of activities of daily living.
  • Nonsteroidal anti-inflammatory medication.
  • Thermotherapy (application of moist heat).
  • Soft diet.
  • Instructions to limit mandibular movement.
  • Stabilization appliance tends to disengage the condyle from the inflamed posterior attachment. 

It is an inflammatory condition of retrodiscal tissues.

Trauma:

  • Extrinsic: sudden movement of condyle into retrodiscal tissue.
  • Intrinsic: anterior displacement or dislocation of disc.
  • Constant preauricular pain accentuated with jaw movement.
  • Clenching teeth increase the pain.
  • Loss of posterior occlusal contact on ipsilateral side.
  1. From extrinsic trauma:
  • Analgesics
  • Ultrasound and thermotherapy.
  • Intracapsular corticosteroid.
  • Re-establishment of mandibular movement.
  • Stabilization appliances.
  1. From intrinsic trauma:
  • Eliminate the traumatic condition.
  • Anterior positioning appliance.

Arthritis means inflammation of the articular surfaces of the joint.

What are the various types of arthritis can affect the TMJ?

  1. Osteoarthritis
  2. Osteoarthrosis
  3. Polyarthritis
    • Traumatic arthritis
    • Septic / infectious arthritis
    • Rheumatoid arthritis
    • Psoriatic arthritis
  • Also known as degenerative joint disease characterized by chronic degeneration of the various hard and soft tissues around the joint
  • It is a disorder of the articular cartilage and subchondral bone with inflammation of the synovial membrane.
  • When the bony changes are active, the condition is painful and referred to as osteoarthritis.
  1. Overloading of the articular structures of the joint.
  • Continuous abrasion of the articular surfaces with advancing age.
  • Chronic para functional activities.
  1. Disc displacements without reduction
  1. Early Phase:
  • This may take on average 2.5–4 years.
  • Associated with clicking sounds and intermittent locking.
  1. Intermediate Phase:
  • Associated with TMJ destruction.
  • Lasts on average 6 months to a year.
  • Spontaneous joint pain at rest or with function.
  • Limitation in opening, and grating sounds.
  1. Late Phase:
  • No degenerative activity,
  • Joints are said to be stable or in the “burnout phase”.
  • It lasts about 6 months, and it will eventually stabilize with time.
  • Unilateral pain over the condyle, gets aggravated by mandibular movements.
  • Pain is usually constant but often worsens in late afternoon or evening.
  • Limited mandibular opening.
  • Soft end feel is common unless it is associated with an anteriorly dislocated disc.
  • Lateral palpation and manual loading increases the pain.
  • Deviation of the mandible to the affected side.
  • Crepitations can be felt.
  • Narrowing of the joint space.
  • Irregular joint space.
  • Flattening of the articular surfaces.
  • Osteophytic formation.
  • Anterior lipping of the condyle.
  • Presence of Ely’s cysts
  • Joint effusion better detected in T2 weighed MRI images.
  • Decrease the joint load.
  • Anterior positioning appliance (correct condyle disc relation).
  • Flat plane stabilizing appliance (in muscle hyperactivity).
  • Attempt to be made to avoid the para-functional habits.

Supportive therapy:

  • NSAID
  • Soft diet.
  • Rest (movement restricted within the painless limits).
  • Thermotherapy
  • Passive muscle exercises.
  • Arthroplasty commonly performed.
  • Artificial TMJ reserved for the patients with advanced degenerative changes in TMJ.
  • Also k/a articular chondrosis and synovial chondrosis.
  • SC was originally described by Ambroise Pare in 1558 and the involvement of the TMJ was described in 1933 by Auhausen.
  • It is an uncommon articular disorder characterised by synovial metaplasia with intra-articular proliferation of cartilaginous nodules originating from the synovial membrane.
  • This disorder usually affects large joints and is rarely observed in the temporomandibular joint (TMJ).

SC can also be divided into two forms according to the cause:

  1. Primary: In the primary form, metaplastic changes develop in the synovium and cause cartilaginous foci to develop within the synovial membrane. These foci enlarge, detach and ossify in the synovial cavity.
  • Primary form is more aggressive and tends to recur.
  1. Secondary: Secondary form occurs following trauma or other arthropathies. Fragments of cartilaginous or bony tissue dislodge and are nourished by the synovial fluid.
  • Secondary form is usually slow and has a chronic presentation.
  • In secondary form, the loose bodies are more uniform and show less cellular atypia than that observed in the primary form.

The pathogenesis of SC is unknown. Fibroblast growth factor 2 and fibroblast growth factor receptor 1 play important roles in the pathogenesis of SC.

Contributing factors:

  • Previous trauma.
  • Parafunctions
  • Degeneration
  • Inflammatory disease.
  • Infections
  • Slow progressive swelling in the pretragus region.
  • Pain and limitation of mandibular movement.
  • TMJ clicking, locking, crepitus and occlusal changes.
  • Intracranial extension may lead to neurologic deficits such as facial nerve paralysis.

Imaging tools for diagnosis:

  • Conventional radiography, CT, MRI, Arthroscopy.
  • Features of SC in the TMJ are widening of the joint space, soft tissue swelling, irregular surfaces of joints and multiple calcified loose bodies. 
  • Coronal CT images detect loose bodies in the joint spaces.
  • MRI findings, depend on the degree of mineralization, although the most common pattern reveals low- to-intermediate signal intensity with T1-weighting and very high signal intensity with T2-weighting with hypointense calcifications.

On the basis of histopathological findings, SC can be divided into the following three stages:

  1. Initial stage: in this stage, the lesions include metaplasia of the synovial membrane with proliferation of undifferentiated cells. Detached loose bodies are not observed at this stage.
  2. Transitional stage: This stage shows the presence of progressive metaplasia in the synovial membrane along with formation of loose bodies that contain active chondrocytes partially covered by the synovial membrane.
  3. Advanced stage: No intrasynovial metaplastic activity is detected in this stage; only detached loose bodies are observed.
  • The treatment options for SC are surgery and arthroscopy.
  • Arthroscopy is a less invasive technique, but it is difficult to retrieve the intra-articular loose bodies using arthroscopy.
  • In some cases, the lesion may show extracapsular and intracranial extension and SC of the TMJ has the potential to undergo malignant transformation. Therefore, the treatment of choice is surgical exploration.

Osteoarthrosis (OA) of temporomandibular joint (TMJ) is a progressive degenerative disease, gradually affecting cartilage, synovial membrane and bone structures.

  • Due to imbalance between reparative and degenerative processes of the joint.
  • When bony changes are active, condition is known as osteoarthritis. As remodeling occurs condition becomes stable yet bony morphology remains altered. This condition is known as, osteoarthrosis.
  • History may reveal a time when symptoms were present (osteoarthritis).
  • Sound phenomena associated with jaw movements.
  • With the progression, degenerative changes occur.
  • Pain and restriction of mouth opening.
  • Height of the condylar process may be shortened.
  • Development of anterior open bite and Angle’s  Class II.

Structural changes in the sub-articular bone.

  • As it is an adaptive process, no treatment is indicated.
  • However, if the bony changes in the condyle are significant enough to alter the occlusal condition, treatment should be carried out.
  • The infection of TMJ is usually blood borne bacterial infections or by the extension of the infections from middle ear, maxillary molars or parotid glands or may be due to the direct trauma (punctured wound).
  • In the previously normal joints, gonococcus is responsible.
  • In the previously arthritic joints, staphylococcus is responsible.

However, streptococcal, pneumococcal and viral infections (measles & influenza) also have been reported to involve the joint.

  • Pre-existing joint diseases.
  • Diabetes
  • Immunosuppressive drugs.
  • Long term corticosteroids.

Clinical features:

  • Severe pain.
  • Trismus
  • Redness & swelling over the infected joint.
  • Cervical lymphadenopathy.
  • Deviation of the mandible to the affected side.
  • Inability to occlude the teeth.
  • Osteomyelitis of the temporal bone
  • Ankylosis
  • Facial asymmetry in children
  • Brain abscess
  • Surgical drainage.
  • Joint irrigation.
  • Appropriate antibiotics for 4 to 6 weeks.
  • Before starting the antibiotics, the affected joint should be aspirated and the fluid obtained should be cultured.

Psoriatic arthritis (PsA) is a chronic seronegative, inflammatory arthritis, usually preceded by psoriasis and can directly affect the hard tissues, such as the temporomandibular joint.

  • It is an erosive polyarthritic disease, affects about 6% of the patients with psoriasis.
  • It is generally unilateral.
  • History of chronic psoriatic skin lesions.

The diagnosis is based on the presence of the triad of:

  • Psoriasis
  • Erosive polyarthritis.
  • Negative serological test for rheumatoid factor.

Radiographic findings show erosion of the condyle and glenoid fossa rather than proliferation.

  1. No definite treatment.
  2. Supportive therapy includes:

A. NSAID

B. Physiotherapy

  • Gentle massages.
  • Thermotherapy
  • Ultrasound therapy.

C. Immunosuppressive drugs (methotrexate

3. Surgery (for intractable pains & severe functional impairments)

4. Arthroplasty

5. Condylectomy

Rheumatoid arthritis is systemic inflammatory disease manifesting the synovial membrane of diarthroidal joints.

Rheumatoid arthritis of the TMJ begins with vasculitis of the synovial membrane (synovitis) that leads to the destruction of the articular surfaces and the sub articular bones.

There is no known etiology;

Predisposing factors are:

  • Combination of infection
  • Autoimmunity
  • Genetic factors.

 Rare:

  • Acute injury
  • Surgeries
  • Trauma
  • Pain
  • Swelling
  • Movement impairment.
  • Crepitation
  • Malocclusion of the teeth and anterior open bite (advanced stages).
  • Preauricular pain.
  • Sensitivity during joint movement.
  • Joints are tender upon pressure.
  • Morning stiffness usually lasting more than 30 min and decreased masticatory force.

In children:

  • Disturbance in mandibular growth,
  • Facial deformity
  • Ankylosis
  • Abnormal blood antibodies like “RF” and “ANA”.
  • Raised ESR values.
  • Flattening of the mandibular head.
  • Cortical erosion.
  • Gradual decrease in joint space due to granulation.
  • Deossification
  • Pencil head or spiked deformity of the condylar head
  • Sub cortical cysts.
  • Destructive lesions of the condyle and glenoid fossa under T2 weighed CT    

Radiographic changes is graded according to Larsen’s classification into following grades (0–V):

0: Normal.

I: Slight abnormality, joint space is slightly narrow.

II: Early abnormality, joint space is slightly narrow, with erosion.

III-moderate destruction, joint space is narrow and eroded.

IV-severe destruction, joint space is narrow, with erosions and bone deformity.

V-mutilating abnormality, disappearance of joint space, with erosion and bone deformity

  • No definite treatment as the cause is unknown.
  • Refer patient to rheumatologist
  • Supportive treatment consists of ;
    1. Pain reduction by NSAID.
    2. Soft diet during acute exacerbations.
    3. Physiotherapy
    4. Intra-articular steroids if pain is severe.
    5. Prosthetic joints for the patients with severe functional impairment and intractable pain not successfully managed by other means.

It is an arthritic condition, in which due to the elevated levels of serum uric acid, monosodium urate monohydrate crystals get deposited in the joints triggering an inflammatory response.

  • Males commonly involved.
  • Distal extremities are most commonly involved with great toe being involved mostly.
  • Acute pain in a single joint (monoarticular arthritis) is the characteristic feature.
  • TMJ involvement is very rare.
  • Presence of monosodium urate monohydrate crystals from the aspirated synovial fluid by polarized light microscopy.
  • High serum uric acid.
  • Colchicine
  • NSAID’s
  • Intra-articular corticosteroids
  • Uricosuric drugs (allopurinol)

Traumatic disorders of TMJ include:

  • Fractures
  • Dislocations
  • Ankylosis
  • Pain and oedema over the joints involved.
  • Limitations of the mandibular opening.
  • Deviation of the mandible during opening towards the side involved
  • Bilateral fracture shows anterior open bite.
  • Fracture is always confirmed by radiographs.
  • Intracapsular and undisplaced fracture treated simply by immobilization.
  • Prolonged immobilization not recommended to prevent bony or fibrous ankylosis.
  • Displaced fractures require surgical intervention.
  • In dislocations, the condyle is positioned anterior to the articular eminence and cannot return to its original position without assistance.
  • Dislocation can be unilateral or bilateral.
  • Muscular incordination in wide openings.
  • Trauma (less commonly)
  • Inability to close the jaws.
  • Pain due to muscle spasm.
  • In acute dislocation, pain in the pre auricular region is present, but chronic recurrent dislocation is rarely associated with it.
  • Usually bilateral.
  • Unilateral dislocation may lead to deviation of the chin to the contra-lateral side.
  • Palpation over the preauricular region may suggest emptiness in the joint space.

On the basis of the clinico‑radiological evaluation, Akinbami classified TMJ dislocation into:

Type I ‑ the head of the condyle is directly below the tip of the eminence.

Type II ‑ the head of the condyle is in front of the tip of the eminence.

Type III ‑ the head of the condyle is high‑up in front of the base of the eminence.

  • Condyle to be repositioned (which is generally done without the use of muscle relaxants or general anesthesia).
  • But, if the muscular spasms are very severe, reduction is very difficult, so, diazepam 10mg IV will be beneficial.
  • Manipulation or reduction of TMJ
  • Botulinum toxin A (BTX‑A) in recurrent TMJ dislocation.

Manual reduction is performed by first pressing the mandible downward, then backward, and finally upward as described by Hippocrates.

Lewis modified it in his way by stating that the patient should be made to sit down and the clinician should stand in front of him/her or at 11o’ clock position. Then, the thumb should be pressed down on the occlusal surface of the lower molar teeth. At the same time, the chin should be elevated with the fingers and the entire mandible should be pushed posteriorly.

It acts by causing temporary weakening of the skeletal muscle by blocking the Ca2+‑mediated release of acetylcholine from the nerve endings of the neuromuscular junction.

Ankylosis of the temporomandibular joint (TMJ) is an intra-capsular union of the disc‑condyle complex to the temporal articular surface that restricts mandibular movements, including the fibrous adhesions or bony fusion between condyle, disc, glenoid fossa, and eminence.

  • Macro trauma (hemarthrosis).
  • Infections
  • Progression of joint adhesions.
  • Prolonged immobilization following condylar fractures.
  • Chronic inflammation.

Ankylosis is of two types:

  • True ankylosis– In this condylar movement is limited by mechanical problem in joint.
  • False/pseudo ankylosis – in this mechanical cause is not related to joint components.

True ankylosis is of two types:

  • Fibrous ankylosis
  • Bony ankylosis

Fibrous ankylosis is common and occurs between condyle and the disc or between the disc and the fossa.

  • Bony ankylosis is rare, occurs between the condyle and the fossa.
  • Children are more prone due to greater osteogenic potentially and an incompletely formed disc.

Unilateral ankylosis:

  • Unilateral hypoplasia of the mandible
  • Deviation of the chin to the affected side.

Bilateral ankylosis:

  • Severe retrognathia.
  • Mandibular alveolar protrusion.
  • Open‑bite deformity.
  • Bird‑face appearance.
  • Hypertrophic and thick coronoid process.
  • Night snoring.
  • Obstructive sleep apnea

In long standing cases:

  • Chronic isometric contractions of the masticatory muscles gives rise to shortening of the mandibular ramus/rami (pterygomassetric muscle sling) recession of the chin and its elongation in a cephalocaudal direction.
  • Development of the antegonial notch owing to the antagonistic actions of the pterygomassetric sling and the depressor muscles.
  • Marked anti-gonial notch.
  • Enlarged coronoid process.
  • Reduced vertical ramus height on the affected side.
  • The ankylosed mandibular condyle can be hyperplastic with irregular contours and absent joint spaces.

Treatment options for TMJ ankylosis include:

  • Gap arthroplasty
  • Interpositional arthroplasty
  • Joint reconstruction with autogenous or alloplastic materials.

These result in anomalies in the size and shape of the condyle.

 These include:

  • Agenesis (no growth).
  • Hypoplasia (insufficient growth).
  • Hyperplasia (too much growth).
  • Bifid condyle.

Hypoplasia or aplasia of the mandibular condyle indicates underdevelopment or non development associated mainly with various craniofacial abnormalities.

It may be either congenital or acquired

Characterized by unilateral or bilateral underdevelopment of the mandibular condyle and usually occurs as a part of some systemic condition originating in the first and second branchial arches such as:

  • Mandibulofacial dysostosis (Treacher Collins syndrome).
  • Hemifacial microsomia (first and second branchial arch syndrome).
  • Oculoauriculovertebral syndrome (Goldenhar syndrome).
  • Oculomandibulodyscephaly (Hallermann- Streiff syndrome).
  • Hurler’s syndrome.
  • Proteus syndrome.
  • Morquio syndrome.
  • Auriculocondylar syndrome.

It takes place if the condyle is injured during active growth, because of which development may be arrested.

Mechanical injury:

  • Trauma (before the age of 2).
  • Infection of the joint itself or the middle ear.
  • Childhood rheumatoid arthritis.
  • Radiotherapy
  • Parathyroid hormone-related protein deficiency which affect bone formation and chondrocyte differentiation.

Deviation of the mandible towards the affected side.

Facial deformity:

  • Short & wide ramus.
  • Shortening of the body of the mandible.
  • Antegonial notch on the affected side with elongation of the mandibular body and flatness of face on the normal side.
  • Asymmetric shift of the midline with associated malocclusion.

Costochondral graft transplant, preferably before the growth spurt, orthognathic surgery at the end of the growth period, or both.

Condylar hyperplasia (CH) is a rare disorder characterized by excessive bone growth that usually presents unilaterally, resulting in facial asymmetry.

Its etiology is unknown.

Predisposing factors:

  • Post-trauma mandibular condyle hyper-remodeling.
  • Joint infection.
  • Hormonal disorders.
  • Mandibular condyle hypervascularization.
  • Intrauterine changes and genetic factors.

Obwegeser and Makek classification:

 

Type

Clinical findings

1

Type 1 (Hemimandibular Elongation)

Chin deviation towards contralateral side, Midline shift to contralateral side, Lingual deviation of contralateral mandibular molars, Possible posterior crossbite

2

Type II (Hemimandibular Hyperplasia)

Sloping rima oris with minimal chin deviation, Supra-eruption of maxillary molars on affected side, Possible open bite,  No midline shift

3

Type III (Combination of Type I and Type II)

Chin deviation towards contralateral side with a sloping rima oris, Midline shift, Possible open bite and/or cross bite.

  • Mandibular ramus osteotomy of affected condyles.
  • Combining the osteotomies with Le Fort I is effective in restoring occlusal discrepancies.
  • Condylectomy and orthognathic surgery.

The term ‘bifid’ is derived from the Latin word ‘bifidus’ which means cleft into two separate parts. The BMC or double-headed condyle is considered to be a rare pathology of the TMJ characterised by the duplicity of the head of the mandibular condyle.

  • Although the exact aetiology is not known.
  • A developmental abnormality or secondary to trauma.
  • Obstructed blood supply.
  • The articulating surfaces of the bifid condyle are divided by a groove and can be oriented mediolaterally or anteroposteriorly.
  • May occur on both sides but is frequently unilateral.
  • The condylar splitting ranges from a shallow groove to two distinct condyles with a separate neck.
  • Usually conservative.
  • Analgesics
  • Anti-inflammatory agents.
  • Muscle relaxants.
  • Physiotherapy
  • Splint

Surgical treatment is described in TMJ anklyosis that used to appear in BMC secondary to trauma

Condition

Location

Pain characteristics

        Caries

Affected tooth

Intermittent to continuous dull pain

Cracked tooth

Affected tooth

Intermittent dull or sharp pain

        Dry socket

Affected tooth

Continuous, deep, sharp pain

Giant cell arteritis

Temporal region

Sudden onset of continuous dull pain

Migraine headache

Temporal region, behind the eye, cutaneous allodynia

Acute throbbing, occasionally with aura

Glossopharyngeal neuralgia

Most often ear, occasionally neck or tongue

Paroxysmal attacks of electrical or sharp pain

Postherpetic neuralgia

Site of dermatomal nerve and its distribution

Continuous, burning, sharp pain

Trigeminal neuralgia

Unilateral trigeminal nerve

Paroxysmal attacks of sharp pain

Sinusitis

Maxillary sinus, intraoral upper quadrant

Continuous dull ache

  • Patients with suspected early disk displacement, synovitis, and arthritis benefit from early treatment with NSAIDs.
  • Muscle relaxants can be prescribed with NSAIDs if there is evidence of a muscular component to TMD.
  • Tricyclic antidepressants—most commonly amitriptyline, desipramine (Norpramin), doxepin, and nortriptyline (Pamelor)—are used for the man­agement of chronic TMD pain.
  • Benzodiazepines are also used, but are generally limited to two to four weeks in the initial phase of treatment. Longer-acting agents with anticonvulsant properties (i.e., diazepam [Valium], clonazepam [Klonopin], gabapentin [Neu­rontin]) may provide more benefit than shorter-acting agents.

Medication

Dosage

Anticonvulsant: gabapentin (Neurontin)

300 mg per day, increased by 300 mg incrementally

Clonazepam (Benzodiazepines)

0.25 mg every night, increased by 0.25 mg each week to a maximum of 1 mg per day

Diazepam (Benzodiazepines)

2.5 mg four times per day for one week, then 5 mg four times per day for three weeks

Triazolam (Benzodiazepines)

0.125 mg every night

Intra-articular injection of corticosteroids (e.g., triamcinolone, methylprednisolone)

Injection of 0.5 mL local anesthetic and 5 to 20 mg steroid using 23- to 27-gauge 0.5- to 1-inch needle

Systemic corticosteroid

Short course (five to seven days), with or without tapering

Hyaluronate

Single-dose vial, with second injection in two weeks

Cyclobenzaprine ( Muscle relaxant )

10 mg every night

Celecoxib (NSAID)

100 mg two times per day

Diclofenac (NSAID)

50 mg three times per day

Ibuprofen (NSAID)

600 mg four times per day

Naproxen (NSAID)

500 mg two times per day

Piroxicam (NSAID)

                       20 mg per day

Amitriptyline

(Tricyclic antidepressant)

25 mg per day

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