THE TEMPOROMANDIBULAR JOINT

Introduction:

The mandibular condyle articulates at the base of the cranium with

the squamous portion of the temporal bone. This portion of the temporal
bone is made up of a concave mandibular fossa or articular or glenoid
fossa, in which the condyle is situated.

The area where cranio mandibular articulation occurs is called the

temporo-mandibular joint (TMJ). It is by far the most complex joint in
the body. It provides for hinging movement in one plane and therefore
considered as gingilymoid joint. At the same time it also provides for
gliding movements which classifies it as an arthroidal joint. Hence called
as gingly moarthroidal joint.

The articular eminence forms the anterior part of the articular

fossa. The condyle and fossa or temporal bone from direct articulation.
TMJ is a compound joint. (By definition compound joint requires the
presence of at least 3 bones, yet TMJ has only 2 bones). Functionally
articular disc serves as a nonossified bone that permits the complex
movements of the joint. Since the articular disc acts as a 3 rd bone this
joint is considered a compound joint.

The mandibular condyle is 8 to 10mm wide and 15 to 20 mm long

and articulates with the cranium through its antero superior surface. It is
strongly convex anterior posteriorly.

The articular disc is composed of dense fibrous conncective tissue

devoid of any blood vessels or nerve fibres. In a sagittal plane it can be
divided into 3 regions according to thickness. The central area is the

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thinnest and is called the intermediate zone. Both anterior and posterior to
the intermediate zone the disc becomes considerably thicker. The
posterior border is generally slightly thicker than the anterior border. In
the normal joint the articular surface of the condyle is located on the
intermediate zone of the disc.

Ligaments:

The ligaments of the joint are made up of collagenous connective

tissues, which do not stretch. They do not enter actively in joint function
but instead act as passive restraining devices to limit and restrict joint
movement.

Functional Ligament:

1) Collateral (Discal) ligament

2) Capsular ligament

3) Temporo mandibular ligament.

Accessory ligament:

1) Sphenomandibular ligament

2) Stylomandibular ligament.

Masticatory Muscles:

There are 4 pairs of muscles making up a group called muscles of

mastication. They are as following.

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Masseter:

From zygomatic arch to the lateral aspect of lower border of ramus

of mandible. It has got three layers.

a) Superficial layer:

It is arise the anterior 2/3rd of the lower border of the zygomatic

arch and from the zygomatic process of the maxilla the fibers pass down
at an angle of 450 and insert in to the lower part of the lateral surface of
the ramus.

b) Middle layer:

Arises from the anterior 2/3rd of the deep surface and posterior 1/3rd
of the lower border of the zygomatic arch. The fibers pass vertically
down and are inserted in to the middle part of the ramus.

c) Deep layer:

Arises from the deep surface of the zygomatic arch and are inserted
into the upper part of the ramus and the coronoid process.

Nerve supply:

Massectric nerve, a branch of the division of the mandibular nerve.

Blood supply:

Maxillary artery – a branch of the external carotid artery.

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Action:

The main function of this muscle is, mandibular elevation

(Closure) and is adductive of the mandible and is also somewhat active
during protraction probably because of the oblique course of the fibers.

Temporalis:

This is a fan shaped muscle which arises from the temporal fossa
(Excluding the zygomatic bone) and from the temporal fascia. Its fibers
coverage and pass through the gap deep to the zygomatic arch and are
inserted into the margins and deep surface of the coronoid process and the
anterior border of ramus of the mandible.

Nerve supply:

By deep temporal branches of the anterior division of the

mandibular nerve.

Action:

Elevates mandible and the posterior fibers retract the protruded

mandible.

According to studies conducted by vitti and Basmajcon (1977) the

temporal was found to be more active in forced elevation but less active
in slow elevation. It also takes part in lateral movement of the mandible.

Lateral pterygoid:

This is a short conical and thick muscle. It comprises of 2 head one

upper and one lower. The upper head is small and arises from the
infratemporal surface and crest of the greater wing of the sphenoid bone.
Lower head from lateral surface of lateral pterygoid plate to pterygoid

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fovea an anterior surface on neck of mandible and anterior margin of
articular disc and capsule of TMJ.

Function:

Depresses the mandible to open the mouth acting along with the
suprohyoid muscles.

 Protrudes mandible along with medial pterygoid

 lateral movements along with medial pterygoid.

Medial pterygoid (Internal):

This is a quadrilateral muscle which has a small superficial head

and a large deep head which forms the major part of the muscle.

Superficial Head:

Arises from the tuberosity of the maxilla and the adjoining bone
and the deep head arises from the medial surface of the lateral pterygoid
plate and the adjoining part of the palatine bone.

The fibers run down and back ward and lateral to be inserted into
the roughened area on the medial surface of the angle and the adjoining
part of the ramus of the mandible, below and behind the mandibular
foramen and the myohyoid groove.

Nerve supply:

Branch of the main trunk of the mandibular nerve.

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Actions:

Take part in elevation of the mandible and also to protude the

mandible and to produce side to side movements contracting alternately
with the lateral pterygoid.

The Temporomandibular joint:

The TMJ is a condylar joint between the articular tubercle and the
anterior portion of the mandibular fossa of the temporal bone above and
the head of the mandible below. An articular disc divides the joint into
upper and lower cavities.

The fibrous capsule is attached, above the articular tubercle in

front, to the lips of the squamotympanic fissure behind, below to the neck
of the mandible. The ‘Synovial” membrane lines the fibrous capsule.

TMJ is synovial joint and synovial fluid serves 2 purposes.

1) Provides metabolic requirements to avascular articular surface.

2) Lubrication and there by reduces friction.

Lubricating mechanism:

a) Boundary lubrication

b) Weeping lubrication.

In the normal resting position of mandible the elevators and their

antagonistic depressor muscles are in a resting state of postural
contraction. The mandible is balanced in between when the condyle disc
assembly moves down the eminence, the vacated space above and behind
the condyle must be filled rapidly, since the closed system could not

6
tolerate a vacuum. The area must be emptied just as rapidly when the
condyle returns. To accomplish this, a glomus cell arteriovenous shunting
system shunts blood in and out. This is called “Vascular knee”

Normal mandibular function results form harmonious inter

relationship of all the muscle that move the jaw. Muscles becomes
fatigued if not allowed to rest. Muscles should not be forced into
prolonged activity with no chance to rest.

During elevation of mandible, the absence of any deviating

interferences, the closing until it is stopped by bone at the medial pole. If
tooth inclines interfere with this position. The LPM is forced into
positioning the mandible to accommodate to the teeth. Till the
interference are removed, the muscle cannot relax. Even though it
overrides the normal tendency of the muscle to rest when it becomes
fatigued.

The pattern of deviation is reinforced every time. Contact is made,

and it is retained in the brain memory bank. So that muscular closure into
the deviated jaw relationship becomes automatic. The most important fact
of proprioceptive memory, however, is that it fades rapidly if continual
reinforcement of the pattern ceases. Eliminating interference almost
immediately restores normal muscle function.

Williamson (1983 JPD) demonstrated the effect of occlusal

interferences on muscle coordination and normal muscle activity using
EMG procedure. He showed that interfering contact on posterior teeth in
any eccentric poison caused hyperactivity of the elevatory muscle. But if
the anterior guidance was allowed to disclude all posterior teeth from
contact other than centric relation, the elevator muscle either stopped

7
active contraction or reduced noticeably the movement posterior teeth
were discluded.

TMJ is regarded as the most stable component of the masticatory

system, but remodeling can change the shape of the disc or the condyles.
The teeth are the usual site of structural alterations because of its
venerability to wear, become loose or move. Mongini (1983 DCNA)
showed a direct relationship between the shape of the condyle after
remodeling and the abrasion patterns on the teeth.

Healing is part of the body’s adaptive response but only in a

friendly environment of balance. Mongini showed that the condyle
regained its shape or normal contour after all the interference were
eliminated.

Cartilage of the mandible condyle:

Two schools of thought exists

According to I school:

The mandible is comparable to the long bones and that its condylar
cartilage is identical in structure and function to the growth plate of the
long bone.

Brodie (1941)

Showed that the predominant course of growth at the condyle was

actually posteriorly and claimed that the resulting forward projection of
the jaw was a direct consequence of this condylar movement. Massler and
Schour (1944) concluded with the use of alizarin red, that the condylar
cartilage was a major growth site. Wienmann (1946), Moore (1949),
Syman (1951-52), Gorlin (1951), Jarabak (1953), Crawen (1956), Sarnat

8
(1957), Scichor (1960), Jolly (1961), Blackwood (1958,65). Baunc
(1969,70) all were of similar opinion.

According to II School:

Moss proposed that condylar growth is merely a response to the

functional requirements of the oral viscera or to stimuli conditioned by
the orofacial musculature . Accordingly the primary function of the
condylar cartilage is to provide enough growth to enable the condyle to
remain in contact with the articular fossa. While the mandible is carried
down as the result of forces exerted by the surrounding soft tissues so
condylar cartilage acts as a growth center.

Researchers who back this concept are Keith (1922), Morant

(1936), Cleaver (1937), Collins (1946), Beeks (1948), Rushton (1948),
Scott (1953), Moss (1959, 60,62), Bjork (1963), Gianelly and Mooress
(1965) (who studied on condylectomized rats and suggested that condylar
growth was an adaptive response). Beresford (1971), Durkin (1972).

It is also apart from the recent literature that mandibular cartilage is

definitely not the same as seen in growth plate cartilages.

Developmental stages of condylar cartilage:

a. Intra uterine stage (Embryonic form

Human mandible is the second bone of the body to exhibit an

ossification center.

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6 weeks in Utero:

Mandible developing from mandibular process of 1 st branchial arch

appears as a thin plate of bone close to the outer side of the anterior
region of Mekel’s cartilage.

TMJ aries from two different blastemata

1) Glenoid blastema

2) Condylar bastema.

10th and 12th week, morphological changes in condylar process of

developing condylar blastema is seen. These changes are a direct result of
formation of condylar cartilage.

b. Immature stage (Hypertrophic form)

Characteristic features:

i. Cellular organization : haphazard

ii. Matrix formation :Scanty amount relative to cell population.

iii. Calcification pattern: pericellular, circumscribing the lower

hypertrophicchondrocytes.

iv. Mechanism of erosion: chondroelastic resorption of mineralized

matrix.

v. Capillary patterns: tree like branches with bulbar type of terminal

type of terminal ends passively adapting to resorbed areas.

vi. Bone forming process : not involved in ordinary endochondral

bone formation, but rather intravenous nonexistent.

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vii. Growth mechanism: response is adaptive in nature.

C. Mature form (non hypertrophicform)

Characteristic feature:

I. Cellular organization: Still haphazard, but with reduced cell

proliferation throughout and no hypertrophic zone of chondrocytes
resulting in reduced cartilage thickness.

II. Matrix formation: Increase of cartilage matrix relative to cell

population:

III. Calcification pattern: Calcified cartilage forms a broad continuous

line across the lower border.

IV. Mechanism of erosin: none, absence of chondrolastic resorption.

V. Capillary patterns: haphazard with no capillary penetration of

cartilage.

VI. Bone forming process: A type of intramembranous bone formation

resulting in an abundance of subchondral bone merging directly with
the lower border of cartilage.

VII. Growth mechanism : non adaptive and non reactive.

TMJ is known as a secondary joint. Reasons being

1). The original joint developed within the bronchial arch system at the
junction of the floor of the housing of a nerve cell concentration and the
first gill arch in primitive fishes. In our phylogenetic history the bronchial
arch system was the prior mandibular joint. During evolution neurons
became concentrated at one end, and structural stability was provided by

11
bilateral arch of the 1st bronchial cartilages. After that stage a new or
secondary association between the skull and the existing teeth – bearing
structure the dentary bone came into being in front of the original joining
“Secondary”, therefore may apply to joint in that it is later development
in our phylogenetic history.

2). All synovial joints of the body are formed earlier. The new
articulation between temporal bone and mandible is therefore secondary.”
Secondary” there may apply to the joint because of its being late in our
ontogentic development.

3). “Secondary” as an adjective. It refers to the “second” appearance of

the cartilageous components of the joint. New cattilage formation beings
as a secondary event in 4 regions condylar process, coronoid process,
symphysis and gonial region. Other 3 except condylar cartilage
disappears around birth.

4). Late differentiation of original mesenchymal tissue from which the

cartilage originates – so “secondary” primary cartilage are covered by a
thin perichondrium. Secondary cartilage is covered by a fully developed
thin mesenchymal tissue layer.

5). Primary epiphyseal catilage reacts during development primarily to

overall systemic growth stimuli such as hormones. In contrast condylar
cartilage only secondarily follows these overall stimuli after additional
growth modulation by local factors. “Secondary” therefore applies to the
characteristic response of the condyle during growth.

Malocclusion and condylar cartilage:

The major problems which may involve the condylar cartilage and
are amenable to early orthodontic treatment are

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 1) Retrognathic, 2) Prognathic mandibular growth problems 3) open
bite 4) function crossbites 5) Deepbite.

The prepubertal growth and the hypertrophic form are nonadaptive

and as such, if not completely lacking in its adaptive remodeling capacity,
is almost totally unresponsive to external forces and pressures. Thus, the
nonhypertrophic or mature form of the condylar cartilage is not likely to
respond to changes in its environment, so any gross skeletal malocclusion
in adults preferably should be treated by a combination of orthodontic
and surgical intervention.

Remodelling of TMJ during orthodontic treatment:

As early as in 1930, 40 and 41 Breitner found that histological

changes could be observed in the condyle and the glenoid fossa as a result
of specific mechanical forces acting on the teeth, similar to orthodontic
appliances and functional appliances.

Derichsweiler (1958) and Baume (1961) found similar result with

experiments on monkeys. Lieb (1968) claimed that it is possible to
correct class II with a suitable appliance but that it is still obscure how,
and where in the dentofacial complex the transformation occurs which
results in occlusal changes. He suggested the following mechanisms:

1) Frontal displacement of the whole mandible at the TMJ as a result

of a corresponding change in the glenoid fossa

2) Increase of the sagittal growth of the mandible

3) Change of mandible morphology

4) Retardation of the natural frontal development of the maxillary

complex

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 5) Alveloar transformation by distal movement of upper teeth and
mesial movement of lower teeth.

Folke and stallard (1966) studied the effect of distal displacement of

mandible in rats with the aid of inclained planes cemented to lower
incisors. “Gross alterations” were observed in the anterior part of the
condyle, especially near the attachment of lateral pterygoid muscle while
no morphological changes were seen at the fossa or the disk. Ingervall
(1972) Ramjford (1966) Walden and Enlow (1971), Blaukenship and
ramjford (1976) reported their study on adult Rhesus monkeys and the
results were in contrast to the previous studies. They concluded that TMJ
in adult monkeys are more resistant to severe changes in occlusion.

Disease of the temporomandibular joint

Developmental abnormalities of temporomandibular joints:

It is divided into two groups

1) Under development

2) Over development.

Again underdevelopment divided into two groups

1) Unilateral under development

2) Bilateral under development.

Causes for unilateral underdevelopment

a). Prenatal growth disturbance condylar hypoplasia

b). Postnatal growth disturbance.

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This is due to

i. Trauma

ii. Infection

iii. Radiation

iv. Idiopathic

Causes of Bilaterla underdevelopment:

1) Prenatal growth disturbance: divided into two groups

a. Heriditary

b. Non hereditary.

a) Heriditary: Chromosomal anamolies (Turner’s syndrome)

 Achondroplasia

 Mandibulofacial dystosis

b) Non Heriditary:

 Robin syndrome

 Moebins syndrome

 Arthronigodysplasia congenital

 Radiation of fetus.

(2) Post natal growth disturbance.

 Endocranie  hypothyroid

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  Hypopituitory.

 Dietary deficiency of vitamin D

 Rheumatoid arthritis.

Causes:

1) Local cuases

2) Systemic causes.

Local cuases:

Trauma  forceps or breech deliveries below to chin.

Infections  Primary infection and condylar cartilage rareotitis

media, scarlet fever, upper respiratory tract infection, dental,
hematogenous.

Radiation: In the region of growing condyle

Systemic causes of unilateral underdevelopment:

Hereditary: Archondroplasia, dysfunction of cartilage.

Prenatal : Rheumatoid arthritis gonorrhea,

Syphilis etc

Dietary: Vitamin D

Endocrine : Hypothyroidism

Hypopitutarism.

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Over development:

This is divided into 2 groups.

1) Unilateral over development

2) Bilateral over development

1) Causes of unilateral over development.

Developmental  Condylar hyperplasia, hypertrophy

 Hemifacial

Neoplastic  Chondroma

 Osteochondroma

 Fibrous dysplasia.

2) Causes of Bilateral over development:

Hereditary

 Klinefelter’s syndrome

 Diffusion

 Developmental true

 Prognathism

Endocrine

 Gignathism

 Acromegaly

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Treatment

If there is obstruction of movements the capsule has to be opened

and trimming of excess bone done.

ARTHRITIES:

It is a inflammation of the joint

Causes of Arthrities

 Infectious arthritis

 Rheumatoid arthritis

 Degenerative arthritis

 Hyper utricemia arthritis

 Traumatic arthritis.

Infections Arthrities:

The most common form of infections TMJ arthritis is that caused

by direct extension of infection into the joint as a result of an adjacent
cellulites or osteomyllitis.

Clinical features:

Severe pain in the joint, with extreme tenderness on palpation of

manipulation over the joint area.

Treatment:

Advice antibiotics and anti-inflammatory drugs to the patients.

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Rheumatoid Arthritis:

It is a disease of unknown etiology which commonly begins in

early adult life and effects women more frequently than mens in a ratio of
at least 2 to 1%

Clinical features:

Slight fever, loss of weight and fatigability. The joints affected are
swollen and patient complains of pain and stiffness.

Treatments:

There is no specific treatment. Anti-inflammatory drugs and

cortico steroids are beneficial. Surgical intervention in the form of
condylectomy may be necessary to region movement.

Degenerative or Osteo-arthritis

Due to repeated micro trauma, repeated malpositioning of the

condyle, chronic spasm of one or more of the muscles of the jaws.

Clinical features:

Complain of clicking and snapping in the TMJ, but pain is not

necessarily a feature. Sublaxation of the condyle may also occur. In
addition there may be accompany inflammation changes.

Treatment:

There is no treatment for this slowly progressive type of arthritis

other than condylectomy.

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Traumatic Arthrities:

Causes:

Trauma from a blow excessive opening of the mouth, endotracheal

incubation causing stretching or tearing of capsular tissues.

Features:

Pain pre-auricular tenderness, limitation of movements when

unilateral chin deviates to the affected side while opening of mouth.

Treatment:

Limitations of jaw movements either voluntary or by inter

maxillary ligation.

ANKYLOSIS:

Defined as an abnormal immobility of the articulating bones.

Classification:

Divided into two groups

1) False Ankylosis

2) True Ankylosis.

1) Flase :

a. Fibrous

b. Extra capsular

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 c. Psedo

Extra capsular:

a. Infection

b. Tetanus

c. Epilepsy

d. Hysterical trismus

e. Sub mucous fibrousis

2) True Ankylosis (Intra capsular or bony ankylosis)

Causes

a. Birth trauma

b. Hemarthrosis

c. Supperative arthritis

d. Rheumatoid arthritis

e. Osteomylitis

f. Untreated fractures of condyle and

g. Tumors.

Treament:

Forceful opening or surgical intervention of the fibrous

connections in the joint are less satisfactory methods. The most

21
satisfactory result is gained from osteo arthrotomy. The other routine
general procedures available are

 Condyletomy

 Osteo arthrotomy

 Gap arthroplasty

 Osteo orthroplasty.

In fibrous ankylosis, use of specially devised activators have been

found to be encouraging.

Bell suggested the term temperomandibular disorders which is

commonly used and also adopted by ADA.

Theories:

1) Mechanical displacement theory:

Condylar displacement after loss of molars and premolars caused

TMD by impingement on the auriculotemporal nerve and related
structure (ear).

Prentiss, Moson, Costen, Gerber, Tempel were of this opinion.

2) Neuromuscular theory:

Functional disharmony between dental occlusion and the TMJ is

considered by many clinician as the most common etiologic factor.
Geering, carisson et al, Ramjford, olsson Christensen supported this
theory.

3) Psychophysiologic theory:

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 According to this theory the primary factor for the pain dysfunction
symptoms is the spasm of the masticatory muscles (Franks, Laskin)

4) Muscle Theory:

The imbalance between lack of adequate muscle exercise and over

stimulation – contributes for TMD. (Krans, Swanson, Bell).

5) Psychological theory:

Claims that emotional, behavioral and personality characteristics

are the causative factors (Moulton, McCall et al. Lefer, Lupton, Doms et
al).

6) Miscellaneous:

Orthodontic theory Larson and Ronnerman (1981) – EJO 18 fixed

5 final (activator)

They concluded that extensive ortho treatment can be performed

without fear of creating complications of TMJ.

Janson and Hasund (81) – EJO – Cl II div 1 cases. 30 extraction

and 20 non extraction with headgear. Dysfunction mild to moderate but
no significant risk of developing TMD even with severe malocclusion.

Sadowsky and Begole (1980) – AJO

Pancherz (1985) – AJO – Cl II div – 1 – 22 patients (Herbst)

Tenderness on palplation doubled during initial 3 months treatment

but symptoms disappeared after appliance removal.

Dibbetts and Vauder Weele (87) AJO 72 fixed (Begg’s) and

extraction 63 functional symptoms, objective signs and radiographic

23
changes in condyles supported that orthodontic treatment does not induce
TMD.

Classification of TMD according to Bell W.E.

I Masticatory muscle disorders:

a. Protecitive muscle disorders.

b. Masticartory myospasm.

i. Elevator muscle spasm

ii. Lateral pterygoid muscle spasm.

c. Masticatory myositis.

II Disc – Interference Disorders:

a. Class I interference

b. Class II interference

c. Class III interference.

i. Excessive passive interarticular pressure

ii. Structural irregularity.

iii. Non-inflammatory degenerative joint disease.

iv. Internal derangement.

 Disc-condyle adhesion.

 Damaged articular disc

 Displaced articular disc

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  Detached superior retrodiscal lamina.

d. Class IV interference (hypermobile sublaxation)

e. Class V interference (Spontaneous anterior dislocation>)

III Inflammatory disorders:

b. Synovitis and capsulitis.

c. Retrodiscitis.

d. Inflammatory arthritis.

i. Degenerative arthritis

ii. Traumatic arthritis.

iii. Infectious arthritis.

iv. Rheumatoid arthritis.

v. Hyper uricemia.

IV Chronic mandibular Hypomobilitis:

a. Pseudo ankylosis.

b. Contractured – elevated muscle

i. Myostatic contracture.

ii. Myofibrotic contracture

c. Ankylosis.

i. Firbous ankylosis.

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 ii. Osseous Ankylosis

iii. Total fixation of the joint.

V Growth Disorders.

a. Aberration of deviation.

b. Acquired changes in structure.

c. Neoplasia

i. Benign tumor

ii. Malignant tumor.

Diagnosis:

Making an accurate diagnosis is the most important single step in

the management of TMD of all types without it, therapy is empirical at
best and becomes little more than a trial and error procedure.

The clinical symptoms that comprise the patient chief complaint

should be clearly identified. They should be reported into clinically
recognizable groups:

1) Masticatory pain.

2) Restricted range of motion.

3) Disc interference during translatory cycles.

4) Acute malocclusion.

By utilizing these cardinal symptoms TMD’s can be classified as

1) Masticatory muscle disorders.

26
 2) Disc interference disorders.

3) Inflammatory disorders.

4) Chronic mandibular hypomobilities.

5) Growth disorders of the joint.

The most common signs of joint disorders are

a) Joint sounds:

Heard during various jaw movements clicking and crepitation.

Clinical Examination:

 Ausculation

 Palpation – Explained later

 Functional analysis – for any deviations during movements.

Intercapsular interference in normal jaw movement:

This may be seen as a catching of the joint or even as an

intermittent or permanent locking of the joint pain may or may not
accompany these signs.

Confirmation of diagnosis:

 Radiography  Analgesic blocking – to differentiate primary pain

and referred pain.

 Sonography

 Study casts

 Thermography

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  Condyle path registration

 OPG

 Arthrotomography

 MRI

 Nuclear scanning.

OPG:

Panoramic viewing of the teeth and jaws including the TMJ

provides useful screening visualization of the masticatory structure. Since
it is done in a single static positon, its value is seriously limited. It often
furnishes clues that justify more adequate radiographic examination of
the joints.

Management of TMD’s :

The 3 main objectives of treatment of mandible dysfunction are

1) Control of pain and discomfort.

2) Lowering of psychological stress or tension.

3) Elimination of TMJ and occlusal disharmony.

Dental Methods:

1) Occlusal bite planes and splints.

2) Occlusal adjustment.

3) Occlusal reconsruction.

Condylar positioning after orthodontic surgery:

28
 Clinician treating patients with traumatic injuries involving
mandible condyle or TMJ are familiar with the tremendous anatomic
variations that can be tolerated by some individuals. Conversely, very
minor changes in mandible condyle- disc – glenoid fossa relationships
may not be tolerated by some individuals. The factors which contribute to
this intolerance are unknown.

There is some evidence that suggest that patients with posterior

position of the condyle are more likely to have symptoms than are others
who do not conversely, patients in whom the condylar position is altered
to a slightly anterior or anterior inferior position relative to the normal
position may be more tolerant, with relatively normal function and little
discomfort. As yet, no particular technique used to reposition the
mandible condyle to glenoid fossa during orthodontic surgery.

Herper R P (1990 AJO) analyzed TMJ function after orthodontic

surgery using condylar path tracings (axiograph) – Functional adaptation
of TMJ was found to be more favourable for mandible reduction and
maxillary impaction than for mandible reduction and maxillary impaction
than for mandible advancement or combined upper and lower jaw
procedures.

29
 CONCLUSION:

To quote Zarb : “Compelling evidence correlating tooth position

irrefutable with increased risk of TMJ dysfunction is not available”.

Whether this is true or not, as orthodontist, our aim should not only
be to improve aesthetics but also to provide a functionally stable
occlusion and TMJ.

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