Posted in TMJ Disorders

TMJ Disease Management

Diseases of temporomandibular joint


The temporomandibular joint is crucial to the everyday functioning of modern man. It is subject to all the diseases and disorders that can affect other joints, but vast majority of these problems can be dealt effectively with reversible nonsurgical methods. However, in small number of cases surgical procedure is indicated to eliminate the disease or deformity and to restore the function and anatomy. One should be aware of the basic biology of the joint, sound diagnostic knowledge and also on the efficacy of alternative treatments in managing these conditions


The disorders of temporomandibular joint can be classified into structural and functional disorders:

Structural disorders:

  1. Developmental
  2. Inflammation
  • Acute
  • Chronic
  1. Infection
  2. Degenerative
  3. Neoplasia
  4. Mobility disorders
  • Hypomobility / ankylosis
  • hypermobility
  1. Trauma

Functional disorders

Pain/ dysfunction syndrome

Congenital and growth abnormalities of the TMJ

The congenital defects and growth abnormalities of the temporomandibular joint occur less frequently than the common functional disorders of the temporomandibular joint seen in adults. The abnormalities may be unilateral or bilateral. The abnormalities seen are hypoplasia or hyperplasia of the condyle with associated facial asymmetry. The causes might be prenatal/ congenital or postnatal or acquired ones.


The causes for underdevelopment of the joint are

  1. Unilateral
  2. Prenatal growth disturbance
  • Confined to condyle
  • Widespread developmental failure e.g. Otomandibular dyostosis, hemifacial microsomia
  1. Postnatal growth disturbance
  • Trauma
  • Infection
  • Inflammation
  • Irradiation
  • Unknown causes
  1. Bilateral
  2. Prenatal growth disturbance
  • Hereditary e.g. Mandibulofacial abnormalities
  • Non-hereditary e.g. Pierre-Robin anomaly, fetal irradiation
  1. Postnatal growth disturbance
  • Endocrine defects
  • Osteodystrophy
  • Inflammation e.g. Juvenile rheumatism
  • Trauma
  • known causes

The most serious form of congenital abnormality occurs in otomandibular dyostosis. The defect is caused by rupture of the stapedial artery in the sixth week of pregnancy prior to the development of the carotid system. It has varied forms. In the severe form there is absence of the coronoid process and angle of the mandible. In less severe cases the condyle and ramus are hypoplastic.

Hemifacial microsomia is characterised by variable asymmetric defects involving the skeletal, soft tissues and neuromuscular component. The aetiology is unknown. Poswillo states that following bleeding from the developing stapedial artery results in the formation of hematoma in the area of the first and second branchial arches. The size of the hematoma determines the degree of involvement.

In cases of unilateral cases the features include

  1. Facial asymmetry with deviation of the chin to the affected side and deficient chin.
  2. There will be apparent deficiency of tissue on the normal side.
  3. There will be development of occlusal cant. This is more prominent in cases of hemifacial microsomia.

The skeletal deformity of the hemifacial deformity is classified based on the anatomy of the mandibular ramus and temporomandibular joint

Type I                    Skeletal deformity consisting of mini mandible and mini temporomandibular joint, with all structures normal in shape but small in size.

Type II                   Skeletal deformity consisting of abnormal shaped mandibular ramus with hypoplastic and medially displaced temporomandibular joint

Type II A              The degree of hypolplasia does not warrant replacement

Type II B               The hypoplasia is severe and requires reconstruction.

Type III                 There is complete absence of ramus and temporomandibular joint

In cases of bilateral cases there is facial defect of deficient chin. In Treacher Collins syndrome there is also hypoplasia of other structures of face.


The management of hypoplasia of the condyle requires extensive evaluation of photographs, lateral cephalograms, posteroanterior cephalograms, models of face, stereolithic models etc. for outlining the deformity. The management is mainly surgical with reconstruction of the temporomandibular joint and orthognathic surgical procedures.


Condylar hyperplasia is a postnatal growth problem seen common in females. This is manifested as development of mandibular asymmetry during puberty.  This is due to an abnormal, hypermetabolic growth center in the affected condyle. There are two types of growth pattern in this disorder:

  1. Vertical: In this group the mandible grows vertically. These patients are characterised by vertical long ramus and body of the affected mandible. Intra-orally there is open bite on the affected side. There is no crossbite, or deviation of chin, or midline.
  2. Rotational: This group has resemblance with patients with hemifacial microsomia in clinical appearance. Ramus is of normal length but the mandibular body is convex and the chin points to the normal side. Intra-orally there is deviation of dental occlusion and crossbite on the normal side.

Diagnosis is by clinical evaluation and from radiography. Bone scans shows the presence of actively growing condyle. All these patients require evaluation of the deformity by means of lateral and posteroanterior cephalograms, photographs, models etc.


The treatment depends on the diagnosis and whether the deformity is progressive or stable. Progressive deformity requires high condylectomy and the patient followed up with scans periodically.

In stable deformity, there is no need for joint surgery, unless there is mechanical interference. The facial asymmetry and malocclusion is corrected by means of orhtodontics and orthognathic surgical procedures.

Infections of the temporomandibular joint

Infections of the temporomandibular joint are not common. Prompt diagnosis and therapeutic intervention is required because joint distension is painful and permanent changes can occur.

Patients with joint infections usually exhibit a posterior open bite on the ipsilateral side as a result of increase in joint fluid. Patients will often maintain a posture to the contralateral side. The surface overlying the joint is usually warm and sometimes it is fluctuant.


The source of infection is spread of infection by hematogenous route. Joints with underlying arthritic disease tend to be more susceptible to distant infection. Spread of infection from dental infections of maxillary teeth and also by direct inoculation following traumatic injury is also possible.

The causative microorganisms include Nisseria gonorrhhoeae in sexually active adults and in children under 2 yrs it is usually due to Haemophilus influenzae. Other microorganisms isolated from TMJ joint infections include Staphylococci and ß haemolytic Streptococci.

Complications of infection of the temporomandibular joint infection include

  1. Fistula formation
  2. Fibrosis or bony ankylosis
  3. Temporal bone osteomyelitis
  4. Intracranial abscess formation.


History and review of systems aids in the diagnosis of acute infectious arthritis of the TMJ. Aspiration of the joint should be considered to relieve the pain and for obtaining the material for identification of the microorganisms. Arthrocentesis is usually done under sedation or general anaesthesia. The aspiration is performed using 20-gauge needle or using a heavier gauge needle under strict aseptic conditions. The aspirate is examined for direct smear and cultured for both aerobic and anaerobic bacteria.

The synovial fluid of an inflamed joint contains more than 2000 WBC/mm3 (normal is < 200 WBC/mm3). Septic joints have WBC count greater than 50,000 per mm3. The cells are predominantly polymorphonuclear cells. The synovial fluid of the joints involved with gout, pseudogout and rheumatoid arthritis often contain greater than 100,000 WBC/mm3. The cells are predominantly mononuclear cells.  In cases of fungal or mycobacterial infection of the joint the synovial fluid contains less than 20,000 WBC/ mm3, which are predominantly mononuclear cells.


This condition is managed by initiation of antibiotic therapy and followed by lavage of the joint. The best choice for initial empirical antibiotic therapy for an acute infectious TMJ arthritis is an agent that combines penicillin with a ß –lactamase inhibitor. Thus combination of ampicillin and sulbactum will cover infections from Staphylococcus, Streptococcus and Nisseria organisms. Other antibiotics that have been used for treating the septic arthritis include clindamycin 6oomg, cefotaximine, and tobramycin. The duration of treatment depends on the clinical course and the organisms isolated. Usually it requires antibiotic therapy for a period of 1 month with initial two weeks of parental antibiotics followed by oral antibiotics.

Following institution of antibiotic therapy lavage of the joint helps in removing the products of inflammation, reducing the bacterial count and relieving the joint distension. This would relieve patient’s symptoms and also may decrease the likelihood of spread of infection to temporal bone.

Following resolution of acute symptoms it is necessary to start on active physiotherapy for prevention of fibrous or bony ankylosis.


Internal derangement of the temporomandibular joint

Internal derangement of the temporomandibular joint is a localised mechanical fault in the joint, which interferes with its smooth function.

This is caused by the anteromedial displacement of the disk with associated posterosuperior displacement of the condyle in the closed jaw position and there is dysfunctional centric relation.

The existence of altered articular disk-fossa relations resulting in pain and abnormal function of the temporomandibular joint has been mentioned in the writings of Annandale since 1887. In 1814 Hey was the first to use the term “internal derangement” to describe a localised mechanical fault interfering with smooth articular function.  Other authors who have reported internal derangement in the literature include: Unlakeley (1929), Costen (1934), Burman and Senberg (1946), Bowman (1947), Ireland (1951), Kechn (1952), Christie (1953) and Silver and Simon (1956).  Despite this considerable amount of information, the dental profession for the most part choose to identify the musculature as the source of pain and dysfunction in TMJ problems.  Schwartz (1955) and later Laskin (1969) emphasised a psychological and muscular approach with very little emphasis on internal derangement or intracapsular pathology.  In the 1970s Farrar and McCarthy stimulated a renewed interest in internal derangement of the TMJ by correlating radiographs, range of motion measurements and patient history.  With the introduction of arthrogram, the validity of the concept of internal derangement became a reality. 

Internal derangement of the temporomandibular joint is progressive in nature and this can be demonstrated by changes seen in the range of movement, radiographs taken over a period of time and in other studies that are used to make a diagnosis.

The initiating factors can be classified into two groups.

  1. Sudden trauma
  2. Microtrauma over a period of time usually caused by missing posterior teeth, incisal interference, posterior deflective contacts or a deep curve of space.

This is a defect usually of gradual onset, which is caused by longstanding microtrauma (abnormal mandibular posture or excessive muscle activity). This leads to deranged functional adaptation of the articular disk resulting in stretching of the posterior ligament and stretching of the articular disk. Loosened disk will move to a medial position during activity. This produces pain and clicking of the joint during function.

Longstanding microtrauma

Stretching of posterior ligament

and loosening of articular disk

Intermittent clicking                                  Early stage feature

Continual clicking                            Intermediate

Clicking and locking                        late stage


Acute (↓ Opening, ↓ lateral excursion, ↑ deviation)

Chronic (↑ Opening, ↑ lateral excursion, ↓ deviation)

Degenerative joint disease

Signs and Symptoms:    The signs and symptoms of internal derangement are similar to those of temporomandibular patients in general.  They are headache in the retrobulbar and temporal area, earache, pain and tenderness, joint noise and limited range of motion.

Pain may be perceived by the patient as joint pain, head ache or symptoms relative of musculature. Pain will be dull aching, or sharp, gradually increasing and of long duration.

Clicking of the joint will be present in almost all patients. Joint clicks seen in internal derangement is called reciprocal clicking. In this as the condyle translates the disc remains lodged in front of the condyle until the opening click occur.  At this point, the condyle moves downwards and forward beneath the thickened posterior band of the disc, which moves backward and condylar translation proceeds normally now with the disc in a correct anatomic position.  During the closing motion the disc and condyle remain in their correct anatomic position until the condyle nears the terminus of its retrusive movement.  When the closing click occurs, the condyle is most often displaced posterio-superiorly and the disc becomes displaced anterio-medially with the posterior band slipping downward and forward.  Clinically the reciprocal click can be characterised as early, intermediate or late depending upon where the opening click occurs.  An early reciprocal click occurs at 10-29mm of opening and a late click at 40-50mm of opening.  A later grade reciprocal click usually progresses from an early grade reciprocal click as the posterior ligament is stretched and at this point the disc is probably beginning to be deformed.

The progressive variant of internal derangement is known as closed lock.  Most patients progress from intermittent locking or reciprocal clicking to the closed lock.  Some patients may be able to self reduce the lock.

Closed locks are classified into acute and chronic based on

  1. The length of time since occurrence
  2. The amount of condylar translation

            The degree of chronicity is proportional to the degree of condylar translation. 

            An acute closed lock has an average mandibular opening of 27mm with an average lateral excursion to the contralateral side of 4mm.  Deviation to the ipsilateral side is marked. 

            As the closed lock becomes more chronic, mandibular opening increases, excursion to the contralateral side increase and deviation decreases.  The joint may be basically, silent but by this time, the posterior ligament is stretched and the disk is generally deformed in a prolapsed anterior and medial position.  Following this perforations of the posterior ligament or disk can occur along with degenerative changes of both the condyle and fossa.

There is excellent clinical evidence that internal derangement is the precursor of degenerative joint disease since there is seldom radiographic evidence of degenerative joint disease without arthrographic or surgical evidence of internal derangement.


The diagnosis of internal derangement is based on the thorough history and clinical examination and diagnostic radiographs.  Arthrograms may be used where radiographs and correlated tomograms are not diagnostic.

While taking history the following information should be included.

  1. A description of the problem in the patient’s own words
  2. Location of symptoms – A typical TMJ patient complains of headache in the retro orbital and temporal areas.
  3. The length of time a patient has had symptoms and how often the symptoms occur.
  4. Whether any particular event preceded the symptoms – chewing or excessive jaw use or stressful events.
  5. Character of pain – Dull aching pain may be joint or muscle related whereas sharp lighting pain is indicative of neuralgia.
  6. The type of noises the patient perceives in the joints.
  7. Incidence of bruxism, migraine headaches and emotional stress.
  8. The type of treatment the patient has previously received and its effect.

Clinical Examination:

Clinical examination includes

–  Palpation of muscle

–  Occlusal analysis

Careful and objective range of motion of these the most important is the range of motion study.

Range of motion study:
Mandibular opening:

Normal mandibular opening is between 40 and 54mm.  Patients may have limited jaw opening because of temporomandibular joint pain, adhesions, fibrous and bony ankylosis and the closed lock variant of internal derangement.  Limitation may also be extracapsular.  A mandibular opening limited by an acute closed lock will have an opening of around 27mm.  If the opening is less than that, consideration must be given to superimposed pain, adhesions, fibrous or bony ankylosis or extracapsular problems.

Lateral excursions:

Measurement of lateral excursions is important in differentiating limited opening caused by intracapsular or extracapsular pathology.

A normal lateral excursion measured at one cm of opening is 9-13mm.  In a normal joint the ratio of maximum lateral excursion to maximum opening is around 1:4 (i.e. if the patient has a maximal opening of 40mm there should be 10mm of lateral excursions to both sides).

If the patient has a limited opening but normal lateral excursion then the limitation is extracapsular.  Limited opening and limited lateral excursions may indicate an intracapsular problem.


A patient whose jaw deviates consistently to one side could have both a joint problem and a muscular problem.  Deviation is seen in internal derangement, unilateral loss of condylar height, posterior capsulitis, fibrous adhesions, ankylosis and true muscular or neurologic problems.

Joint noises:

Not all clicking within the joint is indicative of an internal derangement.  Reciprocal clicking should be graded for a specific diagnosis and treatment planning.

The following guidelines were drawn up by William and Farrar to grade reciprocal clicking.

        The opening click is graded on a scale of 1 to 5.  An opening click occurring at 1cm of opening would receive a grade of 1.  An opening click at 40mm would be graded 3.5 and so on.

        The closing click is graded by the degree of posterior condylar displacement that occurs coincident with the closing click. Instruct the patient to close into the intercuspal position and mark the teeth.  Then have the patient open past the opening click and close in a protruded position.   Next, instruct the patient to slide the jaw backward very slowly and gradually to cause the posterior teeth to fit together.  As the mandible extrudes, there will be a point at which it will hesitate.  This hesitation occurs because the posterior band of the disc is in its normal position before the closing click occurs.  Record this point forward of the original mark.  When the patient closes into the intercuspal position the closing click can be heard or observed.  The measurement between the two marks is the grade for the closing click.

        The grade of the reciprocal click is the average of the grades of the opening and closing clicks.  The higher the grade the more severe the problem.

There are other joint noises that are mistaken for reciprocal clicking.  One type occurs at the same point in the opening and closing, which is due to presence of a ridge in the disk or a deviation in the form of the condyle or fossa. Grinding and crepitus are indicative of late stage changes and are most often heard during translation. Grinding occurs as a result of irregular bony or disk surface or a perforation of the posterior ligament or articular disk.


There is no perfect temporomandibular radiograph in the diagnosis of temporomandibular diseases.

Panaromic radiographs are excellent for screening, but not good for diagnosing internal derangement. This can demonstrate changes in condylar shape, image coronoid process and look for antegonial notching.

Transcranial radiographs is of some value in the diagnosis of internal derangement. As disk displacement occurs there is superior positioning of the condyle, which is seen in radiographs as lack of joint space.


The arthogram is the gold standard in the diagnosis of internal derangement.  This clearly demonstrates the phenomena of reciprocal clicking and locking in both acute and chronic.  Plain films may show a narrow joint space and some degree of arthritic change but the arthrogram will show the displacement.


This is helpful in diagnosing the presence and degree of disk displacement, which is seen as anteriorly positioned inflamed retrodiskal tissue with varying degrees of synovitis.


After a thorough evaluation, management of internal derangement should begin with the nonsurgical phase.

The nonsurgical modalities include

  1. The soft diet
  2. Physical therapy by means of exercise, thermal agents, ultrasound and transcutaneous electric nerve stimulation.
  3. Muscle and trigger points injections.
  4. Occlusal modification and Splint therapy
  5. Stress reduction techniques by means of biofeedback.
  6. Medical therapy with agents such as analgesics, muscle relaxants, coticosteroids, anxiolytics, antihistamines and antidepressant medication can be used.
  7. Manual reduction of displaced disk.

Surgical treatment should be considered if dysfunction and pain is not corrected to the level of patient’s satisfaction. Surgical treatment is indicated if there is

  1. Severe pain resistant to conservative therapy.
  2. Considerable limitation of opening.
  3. Radiological evidence of disk, condyle or fossa damage.

The surgical procedures recommended are

  1. Disk repositioning and Diskoplasty
  2. Disk repositioning and arthroplasty (Eminectomy)
  3. Low or high Condylectomy
  4. Condylotomy and modified condylotomy
  5. Partial or total diskectomy/ menisectomy and replacement.

Reconstruction arthroplasty with repair or replacement of the damaged meniscus is the most accepted modality of treatment. The damaged disk can be repaired by means of plication procedure or by means of reconditioning the posterior band. If the disk is severely damaged it is better removed and replaced with materials such as silastic, metallic fossa, dermis, dura, temporalis fascia, temporalis muscle, choncal cartilage.

Degenerative diseases of temporomandibular joint

Degenerative disease of the TMJ is the most common organic disease of the joint and occurs when the capacity of the joint to adapt to insults of various types is exceeded.

These diseases include

  1. Osteoarthrosis
  2. Rheumatoid arthritis
  3. Ankylosing spondylitis
  4. Psoriatic arthritis
  5. Sarcoid arthritis
  6. Reiter’s syndrome
  7. Post traumatic arthritis
  8. Condylar resorption

The articular surface of the condyle is covered by a layer of fibrocartilage. A thin layer of cartilage cells is present between the articular surface and subchondral bone. This has the capacity to respond to physical forces (stress) by either progressive or regressive remodelling. Once the ability of the subarticular tissue to adapt to stress is exceeded, degenerative changes occur.

Toller in 1974 carried out histological studies and found four stages. These include

  1. Fibrillation
  2. Perforation
  3. Erosion
  4. Repair


Osteoarthorosis is a non-inflammatory degenerative disease affecting the articular surfaces, which is accompanied by remodelling of the underlying bone.

The clinical picture of ostoarthorosis is similar to those of other temporomandibular disorders. But the clinical course in the TMJ is outstandingly different from that occurring elsewhere. Toller (1973) named it as temporomandibular arthropathy.

Toller (1974) carried out an intensive survey and made the following observation.

  1. A primary symptom of the disease is pain on movement of the jaw. This is not confined to biting or attempted wide opening of the mouth but is frequently present at any part of the range of available movement.
  2. Pain becomes more prominent as the day progresses and is most noticeable when the patient is tried. This contrasts with those affected by the TMJ pain/dysfunction syndrome who more commonly experience pain and stiffness upon awakening.
  3. Tenderness is usually present when the TMJ is palpated, especially during movement. It is very much noticeable when palpation is directed against the back of the mandibular condyle with the mouth in open position.
  4. Limitation of condylar movement on the affected side is common and result in deviation of the jaw to the affected side together with a reduced jaw gap.
  5. There are characteristic sounds within the TMJ best described as grating, grinding or crunching noises. They are audible to the patient and are very noticeable on auscultation of the joint.  Clicking, which is heard in the TMJ dysfunction syndrome is a completely different sound.
  6. Radiographic changes on the surface of the mandibular condyle are present in all established conditions but may not be observed when the disease is of recent onset, only appearing at a later stage.

The majority of those who attend complaining of TMJ pain are found on examination to be suffering from TMJ pain/dysfunction syndrome.

Radiographic Observations

According to Toller (1969) the most suitable radiograph to show the structure of the bony surface of the condyle is achieved by using the transpharyngeal technique.  With this it is usually possible to obtain a finely defined image of the articular surface with minimal distortion of the condyle and with no overlying bony shadows.

The radiographic signs noted include subchondral bony sclerosis, loss of integrity of the articular bony end-plate often at the point of articular contact on the anterior or superior aspect of the condyle, a shallow excavation in the articular surface, erosive lesion, subarticular cysts and osteophytes.

In plain radiographs the degenerative changes of the articular surfaces where the degenerative changes occur are not visualised. The changes seen in radiographs might be physiologic adaptation to mechanical stress, so it is difficult to differentiate between osteoarthrosis and remodelling by radiographic examination alone.

Much information about the status of the can be obtained from a computed tomography scan or MRI scan.


Several factors contribute to the breakdown of joint surfaces. This condition occurs when the intensity of the stress exceeds the functional capacity of the joint or when the functional capacity of the joint is reduced and normal stress causes degenerative disease.

Excessive stress is caused by trauma or by chronic repetitive trauma. The functional capacity of the joint to adapt is reduced in systemic diseases like rheumatoid arthritis.

Histological Findings

Toller (1974) carried out histological studies upon specimens obtained at high condylectomy for those patients who required surgical intervention and identified four stages of the disease, which he classified as (1) Fibrillation (2) Perforation (3) Erosion  (4) Repair.

Management of Osteoarthrosis

The primary aims of treatment are

  1. Relief of pain
  2. To restore the normal range of motion
  3. To prevent progression of disease
  4. To induce regeneration of the affected condyle.

Treatment may be categorised into three types

(1) Supportive conservative measures

(2) The use of intra articular steroids

(3) Surgical intervention in refractory cases

Conservative Measures:

It may be used either singly or in combination.

Reassuring the patients

Explaining to the patient the nature of the disease and reassure the patient.  It should be emphasised that an arthrosis affects solitary joint and mechanical overloading plays a major role in the onset of the disease.

Correction of Occlusal Abnormalities

Most patients have an inadequate posterior occlusion and this can be corrected by elimination of abnormal or premature occlussal contacts and the fabrication of partial dentures.  Extraction of over erupted teeth or correction of their occlusion by complex restorative procedures may be necessary.  Marked  tilting of the teeth may be compensated by crowning or by incorporating occlusal onlays into a partial denture.

In the edentulous patient a surprisingly rapid reduction of pain may occur when an overclosure is corrected.  Bite raising appliances fitted over the natural dentition or a deliberate slightly excessive increase in vertical height in the edentulous may provide relief of especially severe pain.  Such as increase in vertical height in the edentulous may provide relief of especially severe pain.  Such an increase should be considered as a short term measure only since further occlusal damage or pain can occur beneath full dentures after only a few week’s function with an excessive vertical dimension.


Drugs prescribed should be confined to simple analgesic preparation.  Osteoarthrosis is not an inflamatory disease and so the non steroid anti-inflamatory drugs makes no significant contribution.

Physical Therapy

Massage over the affected joint in combination with counter irritant ointment is of considerable benefit to patients.  Local heat either as infrared therapy or use of warm flannel over the affected joint provides relief.

Patients should be advised not to use the affected joint excessively simply because these conservative measures have reduced the pain.  It should be emphasised that symptomatic relief only has been provided and that the natural course of events including further destruction followed by a reparative stage will still occur.  It is helpful to follow the progress of the disease by use of serial radiographic techniques.

Intra-Articular Steroids:

The use of intra-articular steroid first gained enthusiastic support but was later the subject of severe criticism following reports of gross destruction especially in experimental animals.  Henny (1954) reported the beneficial results following injections of hydrocortisone into the MJ.  Chandler and Wright (1958) and Salters etal (1967) reported destructive changes in treated joints which could be demonstrated on radiograph.  Poswillo (1970) and Toller (1977) found a favourable responds with the use of intra-articular steroid injections.

The success of intra-articular steroid injections is in the symptomatic relief of pain.  There is no correlation between symptoms and radiographic appearance.  The greatest improvements and the earliest return to function occur in those where obvious condylar changes are seen on radiograph at the time of injection.  An extension of the original lesion may be seen on serial follow up radiograph.  Approximately 12 months after treatment a radiologically new bony articular end plate is seen.  The condyle itself is reduced in size and has an abnormal shape but function well.

Evidence is accumulating to suggest that the steroid accelerates the destructive stages of the disease and then repair takes place at an earlier date.

Technique for Injection of the TMJ

A strict aseptic technique is essential. After palpating the head of the condyle, local anaesthetic solution is injected to produce auriculotemporal nerve block.  Injection of the solution commences just after skin penetration in the preauricular crease 1cm below the glenoid fossa.  The needle is advanced slightly upwards, Inwards, and forwards to contact the upper lateral aspect of the condyle after which it is withdrawn slightly and local anaesthetic deposited over the lateral aspect of the joint capsule.

1cc of an aqueous suspension containing 25mg of methyl prednisolone acetate is used for injecting.  It is most important to inject into the lower joint compartment since this place the steroid in contact with damaged condyle.  The patient’s mouth is opened not more than 1cm by placing a suitable prop between the teeth.  The needle is advanced through the previous skin puncture angled slightly downwards and 45o inwards and forwards to contact the posterosuperior surface of the condyle.  Gentle manipulation allows the needle to penetrate into the lower joint space and 0.5cc of the suspension is injected.  Lack of resistance confirms that the needle is in the joint space.  Where the upper space is also to be injected the needle is withdrawn to just below the skin and the patient’s mouth opened widely.  The needle is then passed upwards, inwards and forwards at approximately 45o until the roof of the glenoid fossa is contacted.  After slight withdrawal 0.5cc of solution is deposited.  The needle is withdrawn and a small plaster placed over the skin puncture for a few hours.  Some increase in pain and stiffness in the injected joint may be experienced for 2 or 3 days and the patient should be warned of this and analgesics prescribed.  Discomfort should then steadily diminish.

Surgical Treatment:

There remains a small but well defined group in whom either the symptoms are severe and uncontrollable from the start or in whom severe symptom persist 3-4 months after a steroid injection and where obvious radiological abnormalities are present.  These should be considered for surgery.  Where doubt exists as to whether the joint is responsible for the symptoms, an injection of local anaesthetic may aid diagnosis since pain will be abolished temporarily when true intra-articular disease exists whereas pain persists in those patients whose symptoms stem from a functional disorder.  The appropriate surgical procedures are high condylectomy or high condylar shaving, condylotomy, artroplasty, temporomandibular joint replacement.

Rheumatoid arthritis

This is an autoimmune disease primarily affecting the smaller peripheral joints. It is a debilitating condition with intermittent activity and progressive joint involvement.

The clinical features are intermittent pain, swelling and progressive limitation of joint motion. Characteristically the joints of the hand and feet are first affected. Rarely are the distal interphalangeal joints of the fingers affected in early stages. The disease progresses centrally. Involvement of the temporomandibular joint is usually bilateral. In acute stages there is swelling and tenderness. There is limitation of mandibular movement and it may eventually progress to ankylosis. Gross destruction of the condyle may reduce its vertical height, leading to anterior open bite. Juvenile rheumatoid arthritis or Still’s disease involvement of temporomandibular joint might result in ankylosis. This interferes with mandibular growth, resulting in “bird face” deformity.

This disease has features of anaemia, fever, malaise and anorexia. There is a positive result for rheumatoid factor tests. There is also a raised erythrocyte sedimentation rate and in acute stages there is presence of C reactive protein.

The histopathologic features are similar to those found in other joints. This is characterised by inflammation of the synovial tissues with an intense infiltration of lymphocytes and plasma cells. There is exudation into the joint cavity of leukocytes and lysosomal enzymes. The granulomatous synovial tissue (pannus) grows over the joint surface into the subchondral bone and into adjacent tendons and ligaments. This destroys the joint and when it ceases, scar tissue forms and limits motion. This might progress to ankylosis.

The radiologic features are non-specific and may be observed as in other joint diseases. These include flattening, sclerosis, erosion, osteophyte formation, reduction of joint space and reduced mobility.

Management is based on the severity and stage of the condition. In the acute stages, physiotherapy and anti-inflammatory agents are helpful. Intraarticular steroids may be helpful in persistent cases. In chronic destructive cases, surgery may be indicated for the release of ankylosis, restoration of occlusion or both.


This is a metabolic disease in which the joint tissues become inflamed as a result of deposition of crystals of sodium urate due to excess uric acid.

The joint area is reddened, warm, swollen, tender and movement is painful. There is raised ESR and uric acid level.

Radiographically, punched out bony erosions are seen, like the other degenerative diseases.

Ankylosing spondilitis

This is a chronic inflammatory disease of unknown aetiology and this is associated with histocompatibility antigen HLA B27. This mainly affects the spinal articulations, sacroiliac joint and paravertebral soft tissues.

Here there is prominent ligamentous calcification and ossification, with a tendency for bony ankylosis. TMJ is involved in 4 to 32% of cases. The temporomandibular symptoms were mild and restriction in mandibular motion is the main clinical feature.

Radiologic feature is characteristic and includes blurring of subchondral bone margins, subchondral sclerosis, bony erosions, progressive narrowing of the joint space and developing ankylosis.

The main goal in management is the maintenance of functional posture, in association with suppression of pain by means of anti-inflammatory medication. Intraarticular steroids are useful in reducing the symptoms and dysfunction.

Psoriatic arthritis

This is an autoimmune disease manifested by scaly pruritic skin lesions, distinctive nail lesions and susceptibility to secondary infections. It is characterised by erosive, asymmetric polyarthritis and negative results from rheumatoid factor tests. It mainly affects the distal interphalangeal joints.

The temporomandibular involvement is asssociated with features of pain, joint tenderness, limitation of motion and swelling.

Radiographs show features similar to rheumatoid arthritis.

Management of psoriatic arthritis is based on anti-inflammatory medications, physical therapy, steroid therapy and immunotherapy with methotrexate for severe, refractory cases.

Sarcoid arthritis

This is a systemic, granulomatous disease of undetermined cause and pathogenesis. Mediastinal and peripheral lymph nodes, lungs, liver, spleen, skin, eyes, phalangeal bones and parotid gland are most often involved.

Sarcoid arthritis may be seen as an acute, transient, migratory polyarthritis at the onset of disease and most frequently involves the joints of long bones and phalanges. In advanced chronic cases, the peripheral joints are involved.

Diagnosis is established from clinical features and a positive Kveim test result.

Reiter’s syndrome

It is a triad of Uretheritis, conjunctivitis and arthritis associated with antigen HLA B27. Features include fever, oral and genital mucous membrane lesions, cutaneous keratosis and iritis. Joints of spine and sacroiliac region are commonly involved. The clinical signs of TMJ involvement are limitation in motion and pain. Radiography shows evidence of erosion.

Management is mainly by anti-inflammatory medications.

Hypomobility and hypermobility of the temporomandibular joint

Motility disorders of the temporomandibular joint emanating from either too little or too much movement of the condyle occur much less frequently than internal derangement, arthrtidies and other diseases of the synovial joints. Mobility disorders present stern challenges in the diagnosis and treatment.

Hypomobility resulting from ankylosis is an extremely disabling affliction, causing problems in mastication, digestion, speech and oral hygiene. Ankylosis occurring in childhood may grossly affect mandibular growth and result in gross facial deformity. Hypomobility occurring from either intraarticular bony or fibrous ankylosis is called true ankylosis, while those arising from extraarticular causes are called false ankylosis.

Hypermobility disorders result from hypertranslation of the mandibular condyle anterior and superior to the articular eminence. These disorders are composed of hypertranslation, subluxation and dislocation.

 Hypomobility disorders.

The treatment of hypomobility disorders is a clinical challenge. These disorders can be classified into the following as trismus and ankylosis.

Trismus is caused by stiffness of the masticatory muscles.

Kazanjian in 1938 classified the ankylosis into true and false.

–   False ankylosis / Pseudoankylosis results from pathology outside the joint, resulting in mandibular hypomobility.

  • True ankylosis is caused by fibrous or bony fusion of intraarticular joint structures.

The more severe form of hypomobility result from true bony ankylosis of the condyle to the glenoid fossa.

Aetiology of hypomobility disorders.

The cause of hypomobility is varied arising as a result of

  1. Trismus
  2. Odontogenic – myofascial pain, malocclusion.
  3. Infection – masticator space.
  4. Trauma – fracture of the mandible, muscle contusion.
  5. Tumours – nasopharyngeal tumours, tumours that invade jaw muscles.
  6. Psychological – Hysterical trismus.
  7. Pharmacological – Phenothiazines
  8. Neurologic – Tetanus.
  9. Pseudoankylosis
  10. Depressed zygomatic arch fracture
  11. Fracture dislocation of the condyle.
  12. Adhesions of the coronoid process
  13. Hypertrophy of the coronoid process
  14. Fibrosis of the temporalis muscle
  15. Scar contracture following thermal injury
  16. Tumor of the condyle and coronoid process.
  17. True ankylosis
  18. Trauma
  19. Intracapsular fracture (children).
  20. Medial displaced condylar fracture
  • Obstretic trauma
  1. Intracapsular fibrosis
  2. Infection
  3. Otitis media.
  4. Suppurative arthritis.
  5. Inflammation
  6. Rheumatoid arthritis/
  7. Still’s disease.
  • Ankylosing spondilitis.
  1. Marie-StÛmpell disease.
  2. Psoriatic arthritis.
  3. Surgical
  4. Postoperative complication of TMJ surgery & Orthognathic surgery.

The most frequent cause of hypomobility is muscular trismus. Trismus is derived from the Greek term meaning “grinding together” and may be myogenic, neurogenic or psychogenic origin.

Trismus is thought to be a protective reflex that minimises jaw movement to prevent the spread of bacteria, tumour cells, or further trauma to already injured tissue. Trismus id mediated through arthrokinetic reflex from propioceptive nerve endings in the periodontium, the muscle spindles and mechano-receptors situated in the joint capsule through the brainstem to the muscles of mastication.

The causes of trismus include: odontogenic sources like myofacscial pain, malocclusion etc.; infection around the masticator facial spaces; trauma with fracture of mandible; tumour invading the jaw muscles and contiguous structures; extrapyramidal reactions secondary to drugs such as the phenothiazines; and psychogenic and neurogenic sources such as hysterical trismus, tetanus toxins or brain tumours.

The management of trismus is directed at the causative factors.

False ankylosis

Hypomobility as a result of extraarticular causes of obstruction are called pseudoankylosis. There is confusing mention in the literature about false ankylosis and trismus. Miller et al in 1975 classified false ankylosis into six groups as:




Bone impingement

Fibrous adhesions


The factors frequently cited as the cause for the extraarticular obstruction are

  1. The depressed fracture of the zygomatic arch, which impinges on the coronoid process result obstruction of free movement of the mandible.
  2. Fracture dislocation of the condyle limits mobility, either as a result of direct trauma to the soft tissues and joint structures or because the head of the condyle obstructs movement of the mandible.
  3. Changes in and around the coronoid process – either hypertrophy or fibrosis causes hypomobility.
  4. Fibrosis of temporalis muscle results in hypomobility. This is seen in temporal shunt procedures carried out for the correction of hydrocephalus.
  5. Other causes are fibrosis of the elevator muscles of mandible as a result of burns or radiation therapy and dystrophic calcification in myositis ossificans.

The management of these cases of false ankylosis is directed towards eliminating the causative factors.

True ankylosis

The intraarticular cause for ankylosis may range from fibrous, fibro-osseous, osseous to osteocartilagenous. The aetiology and pathogenesis are

  1. The most frequent cause for bony ankylosis is trauma to the joint. In the child the most likely mechanism of ankylosis is following a blow to the chin or following obstetric trauma. Rich anastamosis of capillaries penetrate the articular layer of condylar cartilage and found lying just under the thin cortex in the young individuals. The condylar neck is broader in the children. There is crushing injury to the articular surfaces following trivial injury. Trauma causes extravasation of blood resulting in haemarthrosis or intraarticular comminuted fracture with fragmentation and haemarthrosis. Subsequent ossification of this fibroosseous mass ultimately results in ankylosis. Obstetric trauma is also an etiologic factor in the development of ankylosis. In the adult ankylosis results either from a medial displaced fracture of condyle and bony fusion of the neck of condyle to the zygomatic arch or from fibrous ankylosis.
  2. Intraarticular infection is the second leading cause for true ankylosis. Before the use of antibiotics, the incidence of ankylosis resulting from infection exceeded that caused by trauma. Infection to the temporomandibular joint can produce prolonged limitation of motion, disturbance and destruction of articular surfaces and alteration of normal physiological process of temporomandibular joint. Destruction of articular surfaces along with limitation of motion will lead to ankylosis.
  3. Ankylosis as a result of inflammatory arthritidies occurs in less than 7 % of cases. Rheumatoid arthritis, Still’s disease (juvenile rheumatoid arthritis), Marie- StÛmpell disease, psoriatic arthritis and osteoarthritis comprise this group of disease.
  4. Fibrous and bony ankylosis can occur following TMJ arthroplasty and mandibular orhognathic procedures. Adhesions can form between the disk and the articular eminence following disk repair procedures. Bony ankylosis can occur after diskectomy procedures without proper postoperative physiotherapy or after multiple surgical procedures on TMJ.
  5. Rarely, ankylosis may result from neoplasia- either a tumor of the condyle, a metastatic lesion, or chondromatosis of the TMJ.

Diagnosis of ankylosis

The ankylosis of the temporomandibular joint has distinct clinical and radiological features.

Clinical examination

The findings depend on the time of onset, severity, duration and whether the ankylosis is unilateral or bilateral. The features seen in the ankylosis occurring at an early age before the completion of the growth of mandible are.

  1. Restriction of mandibular motion. In severe cases the mouth opening will be less than 5 mm. In false and fibrous ankylosis there will be varying degree of jaw motion, usually less than 15-mm. Unilateral ankylosis will produce deviation of the mandible to the ankylosed side on opening. This is due to the hypermobility of the condyle on the normal side and an absence of translation on the ankylosed side.
  2. Mandibular deficiency if the ankylosis has produced severe damage to the joint at an early age. There will be decreased ramal height, micrognathia and bird face appearance in cases of bilateral ankylosis. There is prominent antigonial notch due to pull of the muscles attached to the mandible. The facial deformity of the ankylosis is the combined result of loss of epiphyseal growth and absence of stimulation from the functional matrix.
  3. Facial asymmetry if the ankylosis is unilateral and occurs at an early age. There will be micrognathia with chin deviated to ankylosed side and apparent deficiency of the body of the mandible region on the normal side. This is due to normal growth of the mandible on the normal side when compared to the ankylosed side. These cases will have associated feature of canting of occlusion.
  4. Besides these there will be varying degree of malocclusion, caries tooth, poor oral hygiene, halitosis and hypertrophic suprahyoid musculature.

In case of adults the history is usually of limited jaw opening and altered mandibular function developing over a period of time. Facial morphological characteristics are normal because the alterations started after completion of growth.

When ankylosis is suspected it should be confirmed radiologically.

Radiological examination

Plain film radiographs is of little value. They help in visualising joint morphologic characteristics as narrowing of the joint in inflammatory joint disease

Arthrography may be occasionally useful in demonstrating fibrous ankylosis but it is contraindicated in bony ankylosis.

MRI imaging is of little value in the diagnosis of TMJ ankylosis.

The panoramic radiographic view is adequate for initial screening.

TMJ tomography taken in coronal and sagittal sections gives more information. They are helpful in localising and quantifying the bony ankylosis. Tomographic sections through the entire joint provide information about condyle and fossa morphologic conditions, joint space integrity and location of osseous union. They may also reveal large extraarticular mass of bone attached to the zygomatic arch laterally and to the base of the skull medially.

If ankylosis is suspected but not confirmed by tomography, then computed tomography (CT) imaging is helpful because of its greater delineation of osseous details and its ability to show spicules of bone that bridge the joint space. This is the best for visualising the medial extension of the ankylotic mass.

The more recent advance in imaging is the three dimensional CT scans with reconstruction of the joint, which can accurately reproduce the pathologic features on the medial and posterior aspects. This helps in better perception of the joint in all views. This information is important for precise surgical treatment planning because adequate resection is necessary to reduce the incidence of recurrence and postoperative failure.

Based on CT findings Sashi Aggarwal, Manorama Berry et al 1990 classified bony ankylosis of TMJ into two types

Type I        Medially angulated condyle with deformed articular fossa and a mild to moderate amount of new bone formation. Condyle could be identified – flattened irregular sclerosed or partially resorbed. The articular fossa has corresponding irregular, shallow or deep and usually sclerosed, the sclerosis extending to the adjacent areas of the temporal bone. Mild to moderate new bone formation which extends from the neck of the condyle or lateral superior aspect of the ramus to the squamous temporal bone and or zygomatic arch, frequently encroaching on the lateral aspect of the articular fossa.                                            Aetiology specific – trauma associated.

Type II      Joint architecture completely disrupted with no recognisable condyle or articular fossa. There are large masses of new bone, funnel shaped, extending from the thickened ramus to the grossly sclerosed and irregular base of the skull.                                                          Squealae of both trauma & non trauma cases.


The management of this condition is by surgical means. This is by gap arthroplasty after resection of the ankylotic mass or inferiorly to the ankylotic mass. The main disadvantage with gap arthroplasty is reoccurrence of the ankylosis. To prevent reankylosis interpositonal arthroplasty with various materials have been used.

The objectives of treatment for ankylosis are

  1. To improve joint movement and function, which requires meticulous and radical removal of the ankylosed bone or creation of pseudo joint.
  2. To prevent recurrence of the ankylosis. This is by means of active postoperative physiotherapy, interpostional substances to prevent reankylosis, using radiation postoperatively to prevent reankylosis.
  3. To restore occlusion.
  4. To correct and restore the secondary facial deformity.

The actual surgical treatment varies, depending on several factors:

  1. The extent and type of ankylosis.
  2. The age of the patient at onset
  3. The age of the patient at the time of surgery.
  4. Whether the ankylosis is unilateral or bilateral.

The clinical and radiographic examinations will usually provide enough information to accurately determine the nature and extent of ankylosis. A surgical plan has to be developed, determining the location and extent of bone resection and the type of reconstruction that will be employed.

Raveh et al 1989 classifies temporomandibular ankylosis based on the extent of involvement of the articular fossa, median structures and skull base as

Class I             Ankylotic bone tissue limited to the condylar process and articular fossa.

Class II           The bone extends out of the fossa involving the medial aspect of the skull base up to the carotid- jugular vessel.

Class III          Extension and penetration into the middle cranial fossa.

Class IV          Combination of class II and III.

The authors advocates radical exposure and extensive resection of the ankylotic mass to avoid recurrence, particularly if the bony ankylosis extends beyond the fossa up to jugular-carotid vessels. If penetration into the middle cranial fossa is evident, removal of the ankylotic tissue may cause dural tear and result in CSF leak. This requires duraplasty by adapting the temporal fascia with glue and the resulting defect in the roof of the articular fossa is bridged with a thick layer of lyophilised cartilage. The authors advocate the use of interpositional substances as the lyophilised costochondral cartilage and aloplastic materials such as silastic.

Sawhney in 1986 described four types of ankylosis of the TMJ joint and discussed the selection of appropriate surgical treatment.

Type I              Condylar head is flattened or deformed in close approximation to the upper joint space. Dense fibrous adhesion is present within. Restricted motion is due to fibrosis in and around the joint.

Type II            Flattened condyle in close approximation to the glenoid fossa, bony fusion of the outer (lateral) aspect of the articular surface either anteriorly or posteriorly and limited to a small area.

Type III           Ankylosis usually results from a medially displaced fracture dislocation of the condyle with bone bridging the ramus of the mandible to the zygomatic arch. The atrophic condylar head is either free or fused to the medial aspect of the superior portion of the ramus.

Type IV           A wider bony block bridges the mandibular ramus and zygomatic arch, extending and obliterating the upper joint space and completely replacing the architecture of the joint.

The surgical procedures advocated by Sawhney et al are:

Type I and II ankylosis are amenable to lysis of either the fibrous or bony ankylosis. Recountouring of the condyle can be done with high condylar shave. When the disk is found, it is mobilised and sutured over the condylar stump. If the disk is not amenable, then dermis or temporalis fascia is suitable substitute.

Type III and IV ankylosis usually requires sufficient removal of bone to create a gap between the ramus and the superior joint structures. It is recommended to place an interpostional substance to reduce the incidence of recurrence of ankylosis and to minimise the loss of the posterior vertical dimension of the ramus.

Nitzan et al in 1998 advocated the preservation of the condylar stump and the disk in case type III ankylosis. He advocated the contouring of the remnant of the condyle would fulfil for the mandibular growth and function. There is no need for interpositional substance in these type of cases.

Kaban et al in 1990 laid down a protocol for management of temporomandibular joint ankylosis. These include

  1. Aggressive resection of the ankylotic segment with special attention for the medial aspect to ensure total resection.
  2. Ipsilateral coronoidectomy along with dissection and stripping of the temporalis, masseter and medial pterygoid to be done. This results in loss of one third of the ramus height.
  3. Contralateral coronoidectomy to be performed when the interincisal mouth opening was less than 35mm. This could be done through the intraoral approach.
  4. Lining the joint with temporalis or cartilage. If an intact disk is present it could be used to line the joint. In other cases, TMJ to be lined with temporalis fascia flap rotated over the arch pedicled inferiorly to the deep temporal vessels.
  5. Reconstruction of the ramus with a 6-cm long costochondral graft with 5mm thick costal cartilage contoured to the shape of the condyle.
  6. Rigid fixation of the graft and
  7. Early mobilisation and aggressive physical therapy.

With this protocol the authors advocate that there is minimised chance for reankylosis with adequate restoration of function.

Salins in 2000 gave a new perspective in the management of the ankylosis by performing an osteotomy inferior to the ankylotic mass(subankylotic approach) and producing a pseudoarthrosis. The author advocates use of temporalis muscle flap and interpostional substance of 7 to 8 mm thick to prevent reankylosis. Three major problems exist when conventional approach of resecting the ankylotic mass is carried out.

  1. The volume and extent of the ankylotic bony mass in relation to the cranial base is highly variable and so radical excision may prove to be a considerable risk.
  2. The scar tissue that surrounds the ankylotic mass often impedes mandibular movement even when the bony mass has been excised. Hence the management of reankylosis is difficult as the scar tissue increases with each successive surgical intervention.
  3. Radical removal of bone leaves large opposing surfaces of healing bone, which is likely to be bridged by dense scar tissue. The scar tissue thus formed can result in restriction of mandibular movements and give rise to reankylosis.

This technique differ form conventional technique in the following aspect

  1. The ankylotic mass is not resected / manipulated.
  2. Bone is not removed to create a gap as in the case of gap arthroplasty.
  3. A functional pseudoarthrosis is created between normal bone surfaces.

The advantages of this technique include

  1. A pseudoarthrosis is encouraged to form in normal bone below the base of the ankylotic mass.
  2. Since thin ridges of normal bone border the gap created with this technique, scar tissue formed is minimal and an effective interposition arthroplasty is made possible.
  3. There is no bone sacrifice to create a gap, therefore no reduction in ramal length.

Whatever the technique used in the release of ankylosis, the postoperative physiotherapy is vital in acquiring a normal jaw function and preventing re-ankylosis. Physiotherapy should be started at the earliest, possibly on the first postoperative day. Physiotherapy consists of active and passive jaw motion exercises.

The heterotropic ossification can be prevented by medical therapy and radiotherapy. The medial therapy is by means of antiresorptive agents like biphosphonates (sodium etidronate, pamidronate and allendronate). Radiation of up to 5oooGcy has been advocated to prevent osteoblasts from depositing osteoid.

Surgical treatment in children

Children who develop ankylosis before 5 yrs of age are more susceptible to deformities of the face as a result of interference from the ankylosis. The objectives for surgical treatment of ankylosis in children includes

  1. To improve mandibular function
  2. To maintain normal mandibular growth and development of the face.

The surgical option is same as in the management of the ankylosis in the adult, except in severe cases accompanied by growth disturbances where the destroyed condyle is to be reconstructed with grafts capable of growth. This is achieved by costochondral rib graft, which has growth potential that can restore facial skeletal harmony and also allows for improved function.

The surgical procedure requires both preauricular and submandibular approach. It involves lysis of ankylosis / creation of a gap and insertion of costochondral graft. In cases of unilateral ankylosis with facial asymmetry it might require a ramus osteotomy on the contralateral side to correct the deformity. This requires prior evaluation of the deformity by means of posteroanterior cephalograms, photographs and models to quantify the degree of facial skeletal deformity (asymmetry, vertical dysplasia & retrognathia).

Hypermobility disorders.

Hypermobility disorders mean excessive mobility, when applied to temporomandibular joint it means hypertranslation. In 1832, Sir Astley Cooper proposed the principles for diagnosis and treatment of dislocation of the lower jaw. He introduced the terms complete dislocation (luxation) and imperfect dislocation (subluxation).

Hypermobility can be divided into three interrelated clinical entities:

Hypertranslation / hypermobility

Subluxation and


Hypertranslation refers to the excessive anterior movement of the condyle during opening. Normally the condyle translates to the inferior aspect of the articular eminence on full opening. It may be predisposing factor to subluxation, dislocation or internal derangement. Treatment is seldom required for hypertranslation.

Subluxation is defined as the displacement of the condyle out of glenoid fossa and anterosuperior to the articular eminence, which can be reduced by the patient (self-reduced). Patient might usually complaint of temporary inability to close the jaw completely. Subluxation can occur along with internal derangement, here it occurs when the condyle translates over the posterior surface of the disk and comes to rest anterior to it. Treatment is not indicated in the absence of pain.

Dislocation is similar displacement of the condyle, which cannot be self-reduced. Dislocation might be acute or may be recurrent or habitual. The highest incidence of recurrent dislocation is among females.


The dislocation is caused by

  1. Dysfunction of TMJ
  2. Abnormal Glenoid fossa
  3. Abnormal Condylar head
  4. Relaxation of ligaments
  5. Relaxation of capsule
  6. Dysfunction of muscles of mastication

Acute dislocation is caused by

  1. Trauma
  2. Sudden movement as in singing or yawning or as a result of excessive downward pressure during extraction of teeth.

Factors precipitating dislocation can be grouped into extrinsic and intrinsic factors

Intrinsic factors:

Overextension injury



Wide biting

Seizure disorders

Extrinsic factors:


Blow to the chin when mouth is wide open

Manipulation of the jaw during

  • Intubation
  • Endoscopy
  • Tooth extractions

Miscellaneous causes

Internal derrangement

Occlusal discrepencies

Factors modifying dislocation:

Connective tissue diseases

Ehlers-Danlos syndrome

Marfan syndrome


Habitual dislocation

Parkinson’s disease

Tardive orofacial dyskenesia

Drug induced



The laxity of the ligaments and joint capsule predisposes the joint to dislocate. Looseness of the capsule and ligaments can result from inadequate healing from injury, as well as from long standing degenerative joint diseases. Occlusal abnormality and loss of vertical dimension can contribute to laxity.

Spontaneous dislocation is due to a break in the timing of muscular action in the first phase of closing. Dislocation can occur when the protractors fail to relax at the appropriate time and the elevators contract to dislocate the mandible in to the infra temporal fossa.

Once the condyle is out of fossa, anterior to the eminence, there will be excessive stretching of masseter.  This will cause involuntary reflex contraction of masseter. There is also a reflex initiated by proprioreceptors in the TMJ, ligaments and lateral pterygoid muscle. These contractions produce excessive dislocation of the condyle and form a vicious cycle.

Signs and symptoms of acute and chronic dislocation are the same and include

1.Inability to close the mouth.

  1. Preauricular depression of the skin
  2. Prominence of the condylar head anterior to the articular eminence.
  3. Elongated face.
  4. Excessive salivation
  5. Tense, spasmodic muscles of mastication and
  6. Severe pain of the TMJ.

Acute dislocation will produce damage to the disk, ligament and capsule. There is an inflammatory oedema characterised by swelling, tenderness and increased temperature.

In chronic dislocation pain will be minimum and there won’t be any swelling.

Radiologic examination is essential to rule out associated condylar fracture prior to reduction.


Treatment of mandibular dislocation depends on time elapsed between occurrence and treatment. The longer elapsed period indicates a difficult reduction. In acute cases immediate reduction should be done and most often it will be adequate. In chronic and longstanding cases other forms of surgical treatment are to be considered.

Manual reduction will be complicated with difficulties because of

  1. Anxiety, apprehension of the patient
  2. Severe spasm of masseter.

Therefore before attempting reduction the following measures are to be taken

  1. Reassure the patient.
  2. Asking the patient to open the mouth
  3. Mild sedatives like Diazepam
  4. Tranquillisers
  5. Massage over the coronoid and masseter
  6. Injection of local anaesthetic to the joint, for disruption of reflex contraction reflex.
Manual reduction

This is done by standing in front of the patient. Patient is firmly seated and head supported. Thumbs wrapped with gauze and placed over the occlusal surface of mandibular molar teeth or alveolar ridge. The lower aspect of chin is grasped with fingers. Patient is encouraged to relax and open in the direction of dislocation. The condyle is depressed by pressing down in the mandibular molar region and simultaneously elevation of the anterior region with fingers will rotate the condyle over the articular eminence into the fossa.

After a successful reduction, immobilisation with follow up care is necessary for the soft tissue of the joint to heal. In chronic cases jaw immobilisation will not be helpful because the damaged ligaments will be highly laxed and by repeated dislocation this may not be relieved. In these cases jaw exercises to improve muscle tension are to be advocated.

Reduction of dislocation of several days duration are complicated by severe muscle spasm. Injecting local anaesthetic into the joint can facilitate reduction by blocking the sensory reflex mechanism of the joint, which reduces the spasm of muscles. Alternatively diazepam 10mg may be given 1-hour prior to sedate and reduce the muscle spasm before reduction.

The difficulty encountered with treating mandibular dislocation increases with the duration of dislocation. In long standing cases the dislocated condyle would have undergone fibrous adhesions to the disk and articular eminence. The jaw muscles would also have undergone fibrotic changes. These prevent nonsurgical methods of reduction. In such cases the modalities of management include:

  1. Manual reduction under general anaesthesia and muscle relaxant.
  2. Using functional appliance
  3. Using class III elastics.
  4. Surgical methods
  5. Open technique. Here wires are hooked around the sigmoid notch and the condyle is distracted inferiorly and condyle is repositioned into the fossa.
  6. In case of fibrotic temporalis coronoidectomy aids in repositioning of the condyle.
  7. Condylectomy
  8. Eminectomy
  9. Sagittal split osteotomy.
Management of chronic recurrent dislocation

Management of cases with chronic persistent dislocation is troublesome. These are ideally managed by surgical methods. Before initiating surgical intervention, all reversible etiologic causes should be investigated and possible psychological factors evaluated. Many procedures have been devised to manage this problem

Surgical procedures for correction recurrent dislocation can be divided into three types:

  1. Those that removing the blocking factor in the path of the condyles
  2. Those that limit the range of motion
  3. Those that alter muscle balance.

Blocking factors are removed by procedures such as eminectomy, diskectomy, condylectomy and high condylar shave.

Motion limitation can be achieved by directly restraining the condyle or by tightening of the joint capsule and ligaments or by creating mechanical barrier to the dislocation of condyle. The procedures include tethering of the mandible to another stable structure, capsular plication, arthroscopic sclerosis of the oblique protuberance and procedures that create an obstruction in the path of condylar translation by augmenting the eminence or repositioning of the disk is done.

Muscle balancing is accomplished by reducing the influence of the lateral pterygoid muscle. Procedures include lateral pterygoid myotomy, myotomy combined with diskectomy or arthroplasty and condylotomy.

All these surgical procedures create a scar around the TMJ which limits the motion of the condyle.



Chondromalacia means softening of the articular cartilage. TMJ chondromalacia is caused by stress-related microtrauma of chronic masticatory muscle hyperactivity (bruxism) overloading of the joint’s articular cartilage. This condition is more common in women.

The pathogenesis is following chronic microtrauma results in release of collagenases, which causes splitting of proteoglycans and softening of cartilage.

Stress Bruxism

Chronic microtrauma

Compression and shearing

Chondrocyte damage – Cathepsin release and other collagenases

Splitting of proteoglycan chain and water loss

Loss of cartilage resilience – Water reabsorption


Grade I        Softening of articular cartilage – Collagenases causes degradation of proteoglycans in fibrocartilage.

Grade II       Rupture of deep fibrils attached to the subchondral bone – Loss of proteoglycans & Ability to withstand compressive & shearing forces.

Grade III      Rupture of parallel articular fibres of fibrocartilage producing fibrillated and frayed cartilage strands and resulting in increased frictional surface.

Grade IV      Degeneration of fibrocartilage with exposure of subchondral bone.

The treatment of chondromalacia is not clinically necessary until grade III or grade IV is reached. Treatment is necessary when obvious fibrillation is present. The treatment consists of motorised shaving of the fibrillation. In grade IV chondromalacia abrasion arthroplasty can be done with motorised arthroscopic unit.


Synovial chondromatosi is a benign monoarticular lesion that most frequently affects the larger articular joints. Involvement of temporomandibular joint is very rare. It is of unknown etiology. Trauma has been implicated as an etiological factor.

Synovial chondromatosis is characterised by the development of metaplastic, highly cellular cartilagenous foci in the synovial membrane. It is belived to be cartilagenous metaplasia with primitive skeletogenic mesenchymal tissue remanants in it.

It has been classified by Milgram et al in 1977 into three developmental stages.

  • Metaplasia is found in the synovial membrane without presence of detached particles.
  • Metaplasia is found in the synovial membrane with the presence of detached particles in the joint that are nourished by diffusion of synovial fluid..
  • Only detached particles are found in the joint.

Synovial chondromatosis has been described in primary and secondary form. Secondary form chondromatosis is associated with degenerative, inflammatory or non-inflammatory diseases. Primary form is aggressive and may erode bone.

Radiographic feature is presence of loose bodies in the joint space. Calcification or ossification of these loose bodies are required to demonstrate it by radiographs. CT and MRI can detect these masses.

The treatment of synovial chondromatosis of the temporomandibular joint is surgical exploration of the joint or arthroscopical removal of the mass together with the loose bodies and the affected synovium. Condylectomy and meniscectomy is indicated in case of extensive damage to them.


Tumours affecting the temporomandibular joint area are exceedingly rare. The tissues from which neoplasm may arise include the synovium, bone, cartilage and associated musculature.

The benign tumours include osteomas, chondromas, synovial chondromatosis and other tumours. The features include deforming swelling associated with pain. Synovial chondromatosis is metaplasia of the synovial membrane, which is characterised by the formation of cartilage particles in the synovial membrane. These migrate into the joint compartments. Treatment of benign tumours includes condylar head resection with or without reconstruction. For synovial chondromatosis the treatment is by surgical removal of the freely mobile particles in the joint space.

The malignant tumours reported in temporomandibular joint include chondrosarcoma, synovial fibrosarcoma, osteosarcoma and malignant fibrous histiocytoma and other metastatic tumours. Primary malignancies of the Temporomandibular joint require aggressive therapy to prevent intracranial extension. Radiation therapy can be used for palliation in disseminated disease to control pain.



The temporomandibular joint is crucial to the everyday functioning of modern man.  It is subject to all the diseases and disorders that can affect other joints, but the vast majority of these problems can be dealt effectively by non-surgical methods.  However, in a small number of patients surgery is indicated to eliminate disease or deformity and to restore function and anatomy.  Before such decision can be made the clinician needs to be aware of the basic biology of the joint, the diagnosis must be secure and the efficacy of alternative treatments assessed.




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  5. Diseases of the Temporomandibular joint. The Temporomandibular joint pain / Dysfunction syndrome. P S Rothwell. Surgery of the mouth and jaws. J R Moore. 588 – 599. Blackwell Scientific Publications.
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  7. Surgery of the temporomandibular joint. David Alexander Keith. Blackwell Scientific Publications.
  8. The role temporalis fascia and muscle flap in temporomandibular surgery. M A Pogrel & L A Kaban. J. Oral Maxillofac Surg. 1990: 48 : 14 – 19.
  9. Bony ankylosis of the temporomandibular joint: A computed tomography study. Shashi Aggrarwal, Sima Mukhopadhyay, Manorama Berry & Sneh Bhargava. Oral Surg Oral Med Oral Pathol 1990: 69: 128 – 132.
  10. The arthroscopic appearance of acute temporomandibular joint trauma. Alastair N Goss & Arthur G Bosanquet. J. Oral Maxillofac Surg. 1990: 48: 780 – 783.
  11. Arthroscopic lavage and lysis of the temporomandibular joint: A change in perceptive. Dorrit W Nitzan, M Franklin Dolwick & Marc W Heft. J. Oral Maxillofac Surg. 1990: 48: 798 – 801.
  12. Bony ankylosis of the temporomandibular joint; Case report of a child treated with Derlin Condylar Implants. Andres H Westermark, Steen Sindet Pedersen & Philip J Boyne. J. Oral Maxillofac Surg. 1990: 48: 861 – 865.
  13. A protocol for management of temporomandibular joint ankylosis. Leonard B Kaban, David H Perrott & Keith Fischer. J. Oral Maxillofac Surg. 1990: 48: 1145 — 1151.
  14. The role of physical therapy in recovery after temporomandibular joint surgery. Blaine D Austin & Stephen M Shupe. J. Oral Maxillofac Surg. 1993: 50 : 495 – 498.
  15. Anatomy and pathology of the Temporomandibular joint. Joseph F. Piecuch, Stuart E Lieblich. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 1857 – 1872. Lippincott – Raven Publishers.
  16. Evaluation of the patient with facial pain. Myron R Tucker. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 1873 – 1904. Lippincott – Raven Publishers.
  17. Non surgical management of Temporomandibular disorders. Steven B Syrop. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 1905 – 1932. Lippincott – Raven Publishers.
  18. Surgery for internal derangements of the temporomandibular joint. Leslie B Heffez. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 1997. 1933 – 1968. Lippincott – Raven Publishers.
  19. Surgical management of the degenerative temporomandibular disease. David A Keith. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 1969 – 1988. Lippincott – Raven Publishers.
  20. Management of Hypomobility and Hypermobility of the temporomandibular joint. Kenneth S Rotskoff. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 1997. 1989 – 2014. Lippincott – Raven Publishers.
  21. Arthroscopy of the mandibular joint. Howard A Israel. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 2015 – 2042. Lippincott – Raven Publishers.
  22. Management of the failed surgical patient. Steven M Roser, A Thomas Indresano, Bruce Sanders, Ralph Merrill, Ralph D Buoncristiani. Principles of Oral & Maxillofacial surgery. Vol. III. Larry J Peterson, A Thomas Indresano, Robert D Marciani, Steven M Roser. 2043 – 2051. Lippincott – Raven Publishers.
  23. Surgical management of temporomandibular joint ankylosis type II by retaining the displaced condyle and disc. Dorrit W Nitzan, Jacob Bar Ziv & Arie Shteyer. J. Oral Maxillofac Surg. 1998: 56: 1133 — 1138.
  24. Temporomandibular Disorders. Robert A Bays & Peter D Quinn. Oral & Maxillofacial surgery. Vol. IV. Raymond J Fonseca. 2001. W B Saunders Company.
  25. New perceptives in the management of cranio-mandibular ankylosis. Paul C Salins. Int J. Oral Maxillofac Surg. 2000: 29: 337 – 340.
  26. Dislocation of the temporomandibular joint. Christoper W Shorey & John H Campbell. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000: 89: 662 – 668.







I am a practicing maxillofacial surgeon working in India.

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