The Clinical Diagnosis of

Temporomandibula. Disorders in the

Orthodontic Patmnt
Daniel M. Laskin

Because many of the diseases and disorders that affect the temporoman-
dibular joint (TMJ) and associated masticatory muscles occur in the age
group of patients generally seen by the orthodontist, their recognition is of
great importance in planning and performing orthodontic therapy. This ar-
ticle discusses the diagnosis and clinical significance of the various condi-
tions that may be encountered. (Semin Orthod 1995;1:197-206.)
Copyright © 1995 by W.B. Saunders Company

ile basis for the successful m a n a g e m e n t o f
T any t e m p o r o m a n d i b u l a r disorder is the es-
tablishment o f an accurate diagnosis. Without
an accurate diagnosis, m a n a g e m e n t o f the con-
dition becomes empirical r a t h e r than rational,
a n d the c h a n c e o f successful t r e a t m e n t is
greatly d i m i n i s h e d . U n f o r t u n a t e l y , despite
many years of clinical investigation, there is
still considerable confusion about the classifi-
cation o f disorders that inw)lve tile t e m p o r o -
m a n d i b u l a r joint (TMJ) and associated struc-
tures. It is not that logical classifications |lave
not been developed. 1'~ T h e problem is that
one continues to see a failure of these classifi-
cations being used as the basis for clinical man-
agement, and patients with diverse problems
continue to be treated as if their pain and dys-
function were caused by a single disease.
Historically, this diagnostic dilemma began
m o r e than 60 years ago w h e n Costen :* de-
scribed a series o f signs and symptoms that he
related to the TMJ and related structures, and
was uhimately n a m e d Costen's syndrome. Al-
t h o u g h the n a m e changed over tile years f r o m
Costen's s y n d r o m e to TMJ s y n d r o m e to cran-
iomandibular syndrome, the u n d e r l y i n g idea
From the Department oJ Oral and Maxillo]acial Smgery, and
MCV Temporomandibular Joint and Facial Pain Research Cen-
ter, Medical College of Virginia, Virginia Commonwealth Uni-
versity, Richmond, VA.
Address correspondence to Daniel M. Laskin, DDS, MS, De-
partment of Oral and Maxillofacial Surgeu, Medical College of
Virginia, PO Box 980566, Richmond, VA 23298-0566.
Copyright © 1995 by W.B. Saunders Company
1073-8746/95/0104-000255.00/0
that this was a single disease entity c o n t i n u e d
to p e r m e a t e clinical practice.
In 1969 Laskin 4 c h a l l e n g e d this c o n c e p t
when he p r o p o s e d that within this heteroge-
nous population o f patients there was a distinct
g r o u p whose problem was related to the mas-
ticatory muscles r a t h e r than to the T M ] , and
s u g g e s t e d the n a m e m y o f a s c i a l p a i n - d y s -
function (MPD) s y n d r o m e for this condition.
A h h o u g h this concept b r o u g h t some clarity
to the field, it was still not unusual to hear
practitioners speak about T M | patients and to
see the term used generically to describe pa-
dent populations in both clinical and research
studies.
In 1982, the American Dental Association
sponsored a c o n f e r e n c e on the subject that re-
sulted in a r e c o m m e n d a t i o n that the umbrella
term for ttle conditions involving the T M J and
associated structures should be " t e m p o r o m a n -
dibular disorders (TMD)," with subcategories
e n c o m p a s s i n g masticatory muscle pain a n d
dysfunction (MPD) and the true pathology o f
the t e m p o r o m a n d i b u l a r j o i n t ( T M J disor-
ders). 5 However, despite the [act that this pro-
posed classification has had wide acceptance, it
has still not resolved the diagnostic dilemma.
A h h o u g h most clinicians now speak o f T M D
patients rather than TMJ patients, the treat-
m e n t used often has not changed to reflect the
h e t e r o g e n e i t y o f the c o n d i t i o n s i n v o l v e d .
Moreover, there continues to be confusion in
the literature; it is not easier to distinguish a
c u r r e n t g r o u p o f T M D patients f r o m a f o r m e r
g r o u p o f T M J patients with respect to what
their specific problem(s) might be.

Seminars in Orthodontics, Vol 1, No 4 (December), 1995: pp 197-206 197

198 Diagnosis of TMD in Orthodontic Patients
This article provides a brief description of
the various temporomandibular disorders so
that the clinician is able to establish an accurate
diagnosis on which to base rational therapy.
Although many of these conditions are limited
only to the structures of the TMJ, others also
involve adjacent structures. Moreover, in some
patients, the TMJ involvement can be part of a
more generalized pattern of malformation. In
all instances, when d a m a g e occurs to the
condyle in a growing child, one can expect to
see secondary mandibular and facial defor-
mity.
Pathology of the
Temporomandibular Joint
The conditions that involve the TMJ are no
different than those that involve other joints of
the body. Thus, one may see congenital and
developmental anomalies, acute traumatic in-
juries, neoplasia, all of the various forms of
arthritis, and internal derangements of the
TMJ. Of the various conditions, those of great-
est interest to the orthodontist are the congen-
ital and developmental disturbances, degener-
ative and rheumatoid arthritis, and derange-
ments of the intra-articular disc. Some of these
conditions are of concern because they can
produce facial skeletal deformities and severe
malocclusions in the growing child, whereas
others can cause pain and dysfunction in chil-
dren as well as young adults.
Congenital Anomalies
The various congenital anomalies that affect
the region of the TMJ are a diagnostic as well
as a therapeutic challenge to the orthodontist.
Although they may share some clinical fea-
tures, there are distinct differences that make
each uniquely different from the others. 6
Hemifacial microsomia (first and second arch syn-
drome, lateral facial dysplasia). This congenital
a n o m a l y is c h a r a c t e r i z e d by h y p o p l a s i a
or agenesis of the tissues in the region of the
first and second branchial arch. Although it
is usually unilateral, bilateral cases have been
reported. 7 The faces of the latter patients,
however, are asymmetrical, a feature that gen-
erally distinguishes them from patients with
Treacher Collins syndrome.
The mandibular deformity generally in-
volves the TMJ and mandibular ramus, rarely
extending beyond the antegonial notch. There
are also associated abnormalities of the exter-
nal, middle, and inner ear; the temporal bone;
the parotid gland; the muscles of mastication;
and the facial nerve. Because of the absent or
hypoplastic condyle, the mandible deviates to
the affected side and the unaffected side is flat-
tened and elongated. Associated with the skel-
etal deformity is a malocclusion which, along
with the facial deformity, becomes worse as
growth continues.
Goldenhar's syndrome (oculoaurieulovertebral dys-
ostosis). The facial asymmetry and malocclu-
sion observed in patients with this syndrome
are similar to that which occurs with hemifacial
microsomia. However, in addition there are fa-
cial skin tags, epibulbar dermoids, and verte-
bral anomalies. In approximately half the cases
there are also anomalies of the cardiovascular
and genitourinary systems, and in a small per-
centage of patients there is a cleft palate.
Treacher Collins syndrome (mandibulofaeial dys-
ostosls). In comparison with the first and sec-
ond arch s y n d r o m e and Goldenhar's syn-
drome, which are usually unilateral, Treacher
Collins syndrome usually presents as a sym-
metrical bilateral facial deformity character-
ized by a hypoplastic mandible, deficient malar
bones, low-set deformed ears, and an antimon-
goloid slant to the palpebral fissures. Although
joint function is generally normal, the condyles
are usually small, the mandibular body and ra-
mus are short, and there is antegonial notching
and a downward bowing of the lower border of
the mandible. Although the deformity is clas-
sically symmetrical, asymmetrical cases have
been reported, 8 and in such patients it may be
difficult to distinguish between Treacher Col-
lins syndrome and bilateral facial microsomia.
Hallerman-Streiff syndrome (oeulomandibulodys-
cephaly). T h e facial d e f o r m i t y in this syn-
drome resembles Treacher Collins syndrome
but, in addition, one finds scaphocephaly, con-
genital cataracts, and proportionate dwarfism.
The face is small in comparison to the skull,
the m a n d i b l e is narrow, a n d the nose is
beaked, leading to a bird-like facial appear-
ance. The TMJ, which is located more anteri-
orly than normal, is hypoplastic and the
condyles are small or absent. Despite the ante-
riorly displaced joints, however, the underde-
 Daniel M. Laskin
velopment of the mandibular ramus and body
results in a Class II malocclusion and often an
anterior open bite.
Developmental Anomalies
Injury to the TMJ in the growing child by such
conditions as trauma, infection, or irradiation
can also cause c o n d y l a r hypoplasia, with
growth arrest or retardation and facial asym-
metry similar to that observed with the congen-
ital hypoplasias. However, because of the later
onset, the morphological changes are usually
less severe, and the other syndromic phenom-
ena are not present. Condylar hyperplasia and
mandibular overgrowth can also occur in some
individuals. However, unlike condylar hy-
poplasia, which is usually recognized at an
early age, condylar hyperplasia is usually not
recognized until the late teens or early 20s
when condylar growth continues beyond the
normal time.
Condylar hypoplasia. Condylar hypoplasia
produces a facial deformity on the affected
side characterized by a short and wide mandib-
ular ramus, a short mandibular body, fullness
of the face, and deviation of the chin. On the
unaffected side the body of the mandible is
elongated and the face is fiat. Malocclusion de-
velops from the mandibular deviation. When
there is a bilateral growth arrest, there is usu-
ally a symmetrical underdevelopment of the
mandible and a micrognathic appearance.
Diagnosis is based on the history of a pro-
gressive facial asymmetry beginning during
the growth period, generally associated with an
injury; radiographic evidence of condylar un-
derdevelopment; and increased antegonial
notching. 7 The last is important in helping to
distinguish condylar hypoplasia and growth
retardation from condylar hyperplasia and
mandibular overgrowth.
Unilateral condylar hyperplasia. This disorder
of unknown origin is characterized by persis-
tent or accelerated unilateral condylar growth
at the time when growth should be diminishing
or ended. The slowly progressive unilateral en-
largement of the mandible causes a cross-bite
malocclusion, facial asymmetry, and shifting of
the midpoint of the chin to the unaffected side.
Concomitant with the increased downward
and forward growth of the mandible, which
carries the teeth with it, there is compensatory
199
eruption of the maxillary teeth and downward
growth of the maxillary alveolar process, as
well as upward growth of the mandibular al-
veolar process in an attempt to maintain the
occlusion. The latter often leads to a convex
appearance of the inferior mandibular border
on the affected side. This is in contrast to the
antegonial notching observed with condylar
hypoplasia.
Radiographically the TMJ appears normal
or there may be symmetrical enlargement of
the condyle and elongation of the mandibular
neck. 9 Because a chondroma or osteochon-
droma of the condyle can produce signs and
symptoms similar to unilateral condylar hyper-
plasia, they must be ruled out in the differen-
tial diagnosis. The latter generally grow more
rapidly, causing quicker changes in facial sym-
metry. Moreover, because of the rapid growth,
dental compensation may not occur and an
open bite develops. Another distinguishing
characteristic is the fact that with a chondroma
or osteochondroma the condyle is asymmetri-
cally rather than symmetrically enlarged.
The Arthritides
All of the various forms of arthritis that can
affect the other joints of the body can also in-
volve the TMJ. The commonest forms seen are
degenerative and rheumatoid arthritis. How-
ever, in some instances, infectious and trau-
matic arthritis, as well as the rarer types such as
psoriatic arthritis, ankylosing spondylitis, gout,
and pseudogout can be encountered. 1°
Rheumatoid Arthritis. As many as 50% of pa-
tients with rheumatoid arthritis will show some
involvement of the TMJ. 1I'12 The degree of
involvement may vary from transient episodes
of pain, swelling, and limited movement to se-
vere damage of the periarticular and articular
structures resulting in fibrous or bony ankylo-
sis. The disease has a female to male predilec-
tion of approximately 3:1.12
The distribution of rheumatoid arthritis, in
comparison with that of degenerative arthritis,
generally tends to be symmetrical. Moreover,
whereas degenerative arthritis can be limited
to only the TMJ, rheumatoid arthritis usually
begins in the peripheral joints (wrists, elbows,
ankles) and the clinical findings are more gen-
eralized (Table 1).
Patients with involvement of the TMJ usu-
200 Diagnosis ~ TMD in Orthodontic Patients

Table 1. General Features of Rheumatoid Arthritis and Osteoarthritis

Rheumatoid Arthritis Osteoarthrit~*
Joint inw~lvement Symmetric Asymmetric or symmetric
Joints usually involved Wrists, hands, elbows, ankles Hips, knees, spine, hands
Joint tenderness Usual None or mild
Morning stiffness >3(1 nfinutes <3() minutes
[land joints commonly involved Proximal interphalangeal attd Distal interphalangeal
metacarpophalangeal
Type of hand swelling Soft Bony hard
Sedimentation rate Usually elevated Normal
Rheumatoid fa.ctor Positive (70% to 80%) Negative
Anemia Hypochronfic, normocytic None
Extra-articular findings May be present None
Radiographic findings Erosive changes Erosive anti exophytic changes
Gender distribution Female 3:1 Equal

ally complain of a deep, dull, aching pain in
the p r e a u r i c u l a r region that is exacerbated by
function, swelling of the preauricular tissues
d u r i n g the acute phases, and progressive lim-
itation o f jaw m o v e m e n t . When severe destruc-
tion o f the condyle occurs in the late stages, the
patient may develop a progressive Class II mal-
occlusion and an anterior o p e n bite caused by
loss o f ramal height. T h e radiographic fea-
tures o f r h e u m a t o i d arthritis o f the T M l in-
clude a loss o f the intra-articular joint space,
condylar destruction, and erosion o f the glen-
old fossa. '~
W h e n r h e u m a t o i d arthritis is suspected on
the basis o f the clinical and radiographic find-
ings, laboratory tests can be used to confirm
the diagnosis.l~ T h e most commonly used test
is for r h e u m a t o i d factor, which is positive in up
to 80% o f the patients. T h e erythrocyte sedi-
mentation test, although not specific for rheu-
matoid arthritis, is positive in about 90% o f
patients d u r i n g the acute stages o f the disease.
O t h e r tests for r h e u m a t o i d arthritis include
the presence o f antinuclear antibodies, which
are f o u n d in 15% to 50% o f patients, and
H L A - D W 5 and HLA-DR8, which are f o u n d in
50% o f r h e u m a t o i d patients.
Although r h e u m a t o i d arthritis generally oc-
curs in patients between 40 and 60 years o f
age, 12 there is also a juvenile f o r m occurring in
patients u n d e r 16 years o f age. It is estimated
that the n u m b e r of children affected in the
U n i t e d S t a t e s r a n g e s f r o m 3 0 , 0 0 0 to
250,000. I4 T h u s , such patients may occasion-
ally be e n c o u n t e r e d by the orthodontist. T h e
disease occurs p r e d o m i n a t e l y in girls, and has
two peaks o f onset, one between the ages o f 1
and 3 years and the o t h e r between the ages o f
8 and 12 years, l:~
Juvenile r h e u m a t o i d arthritis is classified
into three subtypes: systemic (Still's disease),
polyarticular, and pauciarticular, l:~ Although
the TMJ can be involved in any o f these sub-
types, it is most often affected by the polyartic-
ular form. T h e clinical features include T M ]
pain, tenderness, and decreased range o f mo-
tion. Because the disease process destroys the
condylar growth site, a characteristic feature is
micrognathia and a Class II relationship, fle-
quently r e f e r r e d to as a birdface deformity.
T h e severity o f this d e f o r m i t y is related to the
age o f onset o f the disease and its duration.
Ankylosis is m o r e c o m n t o n with juvenile rheu-
matoid arthritis than with the adult onset type.
T h e r a d i o g r a p h i c findings with j u v e n i l e
r h e u m a t o i d arthritis resemble those observed
in adult disease. T h e s e include erosion o f the
articular surface o f the condyle, tlattening and
erosion o t the articular eminence, and loss of
the joint space, t5 Because o f the growth defi-
ciency, there is micrognathia, increased ante-
gonial notching, and ti-equently an a n t e r i o r
o p e n bite. T h e laboratory findings are incon-
sistent and vary with the subtype. R h e u m a t o i d
factor is positive in 5% to 20% o1 patients,
mostly those with the pauciarticular and poly-
articular forms, and the antinuclear antibody
test is positive mainly in patients with the pau-
ciarticular f o r m (60% to 88%).1°
Degenerative arthritis (degenerative joint disease,
osteoarthritis, osteoarthrosls). Degenerative ar-
thritis is the c o m m o n e s t disease affecting the
TMJ. Radiographic evidence has b e e n n o t e d in
14% to 44% o f asymptomatic persons 16 and it
 Daniel M. Lashin 201

has b e e n n o t e d histologically in 40% to 60% of dition is most frequently unilateral, a l t h o u g h it

studied populations. (7.is H o w e v e r , only 8% to
16% o f the p o p u l a t i o n have clinical s y m p -
tOIIlS. I9.20
D e g e n e r a t i v e arthritis can occur in either a
p r i m a r y or secondary form. 9 P r i m a r y disease
is a g r a d u a l l y d e v e l o p i n g p r o c e s s , a n d is
caused by the n o r m a l wear and tear to which
the joint is subjected. It usually occurs in per-
sons older than 50 years and the large weight-
bearing joints are most c o m m o n l y involved.
W h e n the disease involves the hands, the most
frequently affected joints are the distal inter-
phalangeai.joints, p r o d u c i n g the ctlaracteristic
e n l a r g e m e n t s k n o w n as H e b e r d e n ' s nodes.
W h e n the p r o x i m a l i n t e r p h a l a n g e a l joints are
involved, the e n l a r g e m e n t s are called Bouch-
ard's nodes. P r i m a r y d e g e n e r a t i v e disease o f
the T M J is generally a s y m p t o m a t i c , a l t h o u g h
patients m a y occasionally c o m p l a i n o f j o i n l
stiffness, crepitation, a n d mild pain. It usually
occurs bilaterally.
Secondary d e g e n e r a t i v e .joint disease is ob-
served most often in persons between 20 years
and 40 years o f age, a l t h o u g h it can occtJ.r (lur-
ing the teens. It is caused by a s p e e d i n g u p of
the d e g e n e r a t i v e process by t r a u m a , persistent
p a r a f u n c t i o n , or increased stress on the joint
p r o d u c e d by loss of teeth or severe malocclu-
sion. It is characterized by TIM] p a i n , j o i n t ten-
derness, limitation o f m o u t h o p e n i n g and, in
the late stages, crepitation. W h e n associated
with myofascial pain a n d dysfunction (MPD),
there is usually masticatory muscle t e n d e r n e s s
a n d the s y m p t o m s are m o r e severe. In contrast
to p r i m a r y d e g e n e r a t i v e .joint disease, the con-
may b e c o m e bilateral in the late stages, and
i n v o l v e m e n t o f o t h e r joints is u n c o m m o n .
T h e r a d i o g r a p h i c c h a n g e s are similar in
both the p r i m a r y a n d s e c o n d a r y f o r m s o f de-
generative j o i n t disease. ``)T h e earliest c h a n g e is
s u b c h o n d r a l sclerosis. As the condition p r o -
gresses, there is c o n d y l a r flattening a n d lip-
ping, erosion, or o s t e o p h y t e f o r m a t i o n . Occa-
sionally, in the late stages, b r e a k d o w n o f the
s u b c h o n d r a l b o n e gives rise to a b o n e . " c y s t "
within the condyle. W h e n the intra-articular
disc becomes involved, there will be n a r r o w i n g
o f the j o i n t space. T h e r a d i o g r a p h i c c h a n g e s
are generally m o r e severe in the s e c o n d a r y
than in the p r i m a r y f o r m of d e g e n e r a t i v e j o i n t
disease. T h e distinguishing features between
d e g e n e r a t i v e arthritis and r h e u m a t o i d arthritis
are described in Tables 1 and 2.
Internal Derangements
I n t e r n a l d e r a n g e m e n t o f the T M J can be de-
fined as an a b n o r m a l relationship between the
intra-articular disc and the condyle w h e n the
teeth are in occlusion. Originally this was con-
sidered to involve an a n t e r i o r or a n t e r o m e d i a l
displacement, with the posterior b a n d t o r w a r d
o f the 12 o'clock position. H o w e v e r , because it
has now been shown that a f b r w a r d position is
not always associated with clinical signs or
s y m p t o m s , 21 a move logical definition would
be that an internal d e r a n g e m e n t is a condition
characterized by either an a b n o r m a l a n a t o m i c
disc-condyle relationship, or a n o r m a l relation-
ship associated with disc immobility, that re-

Table 2. Distinguishing Clinical Features of Rheumatoid Arthritis and Osteoarthritis of the

Temporomandibular Joint
Rheumatoid Arthritis Osteoarthritis

Incidence 50% of patients 20% to 30% of patients

I.ocation Usually bilateral
Signs Bilateral preauricuIar swelling and
tenderness; moderate to severe
limitation of jaw movement; anterior
open bite and retrognathia in late
stages
Symptoms Constant preauricuIar pain; joint
stiffness; crepitant joint noises;
progressive restriction of jaw motion
Radiographic changes Erosion of condyle and fossa; loss of
joint space
Often unilateral
Occasional joint tenderness; mild to
rnoderate jaw limitation; popping,
clicking, or crepitant sounds; no
occlusal or facial changes
Dull, aching preauricular pain,
exacerbated by function; popping,
clicking, or crepitant sounds; some
restriction of jaw motion
Subchondral scerosis; condylar
flattening; marginal lipping;
osteophyte formation
202 Diagnosis of TMD in Orthodontic Patients
sults in clinical symptoms o f pain a n d / o r dys-
function.
Internal d e r a n g e m e n t s can be classified into
f o u r stages. T h e earliest stage involves an in-
c o o r d i n a t i o n phase, which is not associated
with joint pain or noise, and is only recognized
when patients are asked if their jaw joint moves
smoothly and they reply that they feel a slight
catching or binding sensation. In some patients
the incoordination phase is eventually followed
by the onset o f limited m o u t h o p e n i n g associ-
ated with adhesion o f the disc to the fossa in a
relatively n o r m a l position (Fig 1). However, in
most patients the next stage is anterior or an-
teromedial displacement of the disc, which re-
turns to a normal relationship with the condyle
d u r i n g the o p e n i n g m o v e m e n t and is associ-
ated with a clicking or p o p p i n g sound (Fig 2).
If the d e g r e e of disc displacement progresses,
reduction to a n o r m a l relationship on m o u t h
o p e n i n g does not occur, the patient's jaw is
locked, and o p e n i n g is initially limited to 23 to
25 m m (Fig 3). Because r e t u r n o f the disc to its
normal relationship does not occur, this stage
is not characterized by joint clicking or pop-
ping. I f a separation or tear occurs at the point
o f a t t a c h m e n t o f the retrodiscal tissue to the
disc, however, crepitus may be h e a r d as the
condyle rubs directly against the articular em-
inence.
Although most stages o f internal derange-
m e n t can be recognized by the clinical signs
and symptoms, in instances when there is un-
certainty the disc can be visualized using mag-
netic resonance imaging (MRI). 22 Lateral im-
Figure 1. Adhesion of the intra-articular disc caus-
ing limitation of mouth opening. (A) The disc is
adherent to the articular eminence in a normal po-
sition wimn the mouth is closed. (B) During mouth
opening the disc does not move and this limits
condylar translation. Because the condyle only ro-
tates, opening is limited to 25 to 30 mm. (Reprinted
with permission from Kaplan AS, Assael LA. Tem-
poromandibular Disorders: Diagnosis and Treat-
ment, Philadelphia, PA: Saunders, 1991).
A
C,os,n0
Click
B
ning
t '" Chck
Figure 2. Diagram showing anterior displacement
of the intra-articular disc with reduction on opening
the mouth. A clicking or popping sound occurs as
the disc returns to its normal position in relation to
the condyle. During closure the disc again becomes
anteriorly displaced, sometimes accompanied by a
second sound (reciprocal click). (Modified with per-
mission from McCarty W. Diagnosis and treatment
of internal derangements of the articular disc and
mandibular condyle. In: Solberg WK, Clark GT, ed-
itors. Temporomandibular Joint Problems: Biologic
Diagnosis and Treatment. Chicago IL: Quintes-
sence, 1980: 155).
ages m a d e at varying degrees o f m o u t h open-
ing p r o v i d e a series o f static views o f the
dynamic disc-condyle relationship. W h e n the
images are m a d e in an a n t e r o p o s t e r i o r direc-
tion, lateral or medial disc displacement can
also be observed. A l t h o u g h tears or separa-
tions in the disc-retrodiscal tissue j u n c t i o n can
sometimes be observed o n MRI, a r t h r o g r a p h y
is the most reliable diagnostic m e t h o d for this
purpose.
Considerable attention has been given in the
literature to the clinical significance o f recip-
rocal clicking o f the T M J (Fig 2), with the im-
plication that it is a m o r e serious situation than
the m e r e presence o f a click on o p e n i n g o f the
mouth. Actually, the same changes in the disc-
condyle relationship occur w h e t h e r o r not a
click is h e a r d o n m o u t h closure. 23 In patients
whose TMJ clicks every time they o p e n their
m o u t h , the disc has to slip o f f the condyle dur-
ing m o u t h closure so that the process can re-
peat itself. T h e d i f f e r e n c e is that, in some pa-
 Daniel M. Laskin
D C
Figure 3. Diagram showing anterior displacement
of the intra-articular disc without reduction on at-
tempted mouth opening. The displaced disc acts as
a barrier and prevents full translation of the
condyle. (Modified with permission from McCarty
W. Diagnosis and treatment of internal derange-
ments of the articular disc articular disc and man-
dibular condyle. In: Solberg WK, Clark GT, editors.
Temporomandibular Joint Problems: Biologic Di-
agnosis and Treatment. Chicago, IL: Quintessence,
1980: 151).
tients, the passage of the condyle over the pos-
terior band as the disc again slips forward
d u r i n g closure is associated with a cticking
sound, but in others it occurs silently and can
only be detected by the slight j a r r i n g sensation
felt by palpation over the joint or the mandib-
ular angle. Thus, the presence or absence of
reciprocal clicking does not seem to have any
real clinical significance.
Avascular Necrosis
Avascular necrosis is the death of bone second-
ary to the loss of its vascular supply. It was first
described in the femoral head, where it gener-
ally results from disruption of the blood supply
caused by a fracture of the femoral neck. How-
ever, it has also been claimed that nontrau-
matic avascular necrosis of the f e m u r can be
associated with systemic corticosteroid therapy,
excessive alcohol use, and sickle cell disease. 24
On MRI the normal strong signal caused by
the hydrogen-rich fat content of the marrow
decreases when avascular necrosis of the fe-
mur occurs, and this allows early detection.
T h e finding of a similarly decreased mar-
203
row signal in the condyle and condylar neck o f
some patients with internal d e r a n g e m e n t s has
ted to the suggestion that such d e r a n g e m e n t s
can cause avascular necrosis in T M J . u5'26
Based on the rich blood supply provided to the
condyloid process via the inferior alveolar ar-
tery, the periosteal vasculature, and the lateral
pterygoid muscle, however, it is unlikely that a
traumatic etiology can be implicated in these
cases. In fact, avascular necrosis has not been
shown to occur even when there are displaced
fractures of the condyloid process, whereas it is
a c o m m o n occurrence with displaced subcapi-
taI and high transcervical femoral neck frac-
tures.
Fat emobolism has also been proposed as a
cause of vascular necrosis in the femur. T h e
source of these emboli has been postulated to
be either alcohol-related or high dose steroid-
related fatty liver disease, or a coalescence of
endogenous plasma lipoproteins. 24 However,
none of these conditions are c o m m o n in the
usual age group developing internal derange-
ments of the TMJ.
It thus appears that if avascular necrosis
does occur in the t e m p o r o m a n d i b u l a r j o i n t it is
a rare p h e n o m e n o n . Although there may be
MRI changes observed in the condyloid pro-
cess that resemble avascular necrosis of the fe-
mur, there is no histologic p r o o f of such a sim-
ilarity, and it is probable that the decreased
marrow signal observed on MRI generally rep-
resents fibrosis or osteoporosis rather than an
avascular necrosis. 27 Until better documenta-
tion is provided of the presence of a true avas-
cular necrosis in the condyle, therapy should
be directed solely toward m a n a g e m e n t of the
primary condition (internal d e r a n g e m e n t , de-
generative joint disease).
Myofascial Pain and Dysfunction
It is now recognized that many of the patients
who, in the past, were diagnosed as having a
TMJ disorder actually were s u f f e r i n g f r o m
masticatory MPD. It is easy to u n d e r s t a n d how
such confusion could have occurred. In the
first place, the major symptoms (pain and dys-
function) of many forms of TMJ pathology
and those of masticatory muscle involvement
are similar in character and location. Secondly,
patients with p r i m a r y T M J p a t h o l o g y fre-
204 Diagnosis of TMD in Orthodontic Patient~
quently develop secondary muscle symptoms
caused by protective splinting of the jaw. Fi-
nally, patients with long-standing MPD associ-
ated with chronic parafunctionaI habits, partic-
ularly clenching, can develop secondary or-
ganic changes in the TMJ. However, despite
these overlapping phenomena; a recognition
of the clinical signs and symptoms of MPD,
plus a careful analysis of the patient's history,
should enable the clinician to make a correct
diagnosis of the primary problem. Generally
this involves distinguishing MPD from second-
ary degenerative joint disease (Table 3) and
u n d e r s t a n d i n g its relationship to internal de-
rangements of the TMJ. Because these condi-
tions occur most frequently in young women, a
major c o m p o n e n t of the orthodontists' patient
population, the clinician needs to be cognizant
of their presence before beginning treatment
and should be aware of the fact that their de-
velopment d u r i n g therapy is usually coinciden-
tal. 2~
T h e most c o m m o n symptom of MPD is pain
of unilateral origin. 29 In contrast to the pain
associated with joint disease, which is well lo-
calized, the pain of muscular origin is more
diffuse, a n d patients are usually unable to
identify the specific site involved. W h e n asked
to locate the source of the pain, they will gen-
erally place their h a n d on their face rather
than place a finger on the exact area. This is an
i m p o r t a n t d i s t i n g u i s h i n g criterion between
muscle and joint disorders.
Although myofascial pain is poorly local-
ized, the patient's description of the character
of the pain can help the clinician determine the
muscles that are involved. T h e masseter is the
most frequently involved muscle, and the pa-
tient usually refers to the pain as a jawache.
T h e temporalis, which is the next most com-
monly involved muscle, produces pain on the
Table 3. Distinguishing Features of Degenerative Arthritis and Myofascial Pain and Dysfunction
DegenerativeArthritis
Type of pain Dull, aching, preauricular pain,
increased with function
Localization of pain Well localized
Joint tenderness Always present
Muscle tenderness Occasional (splinting)
Limitation of mouth opening Mild to moderate
Joint noise Frequent popping, clicking, or
crepitant sounds
Radiographic TMJ changes Present
side of head that is generally interpreted by the
patient as a headache. Involvement of the lat-
eral pterygoid causes pain that feels like an
earache and/or a pain behind the eye, whereas
medial pterygoid involvement causes discom-
fort when swallowing, the feeling of a painful,
swollen gland beneath the angle of the mandi-
ble, and a sensation of stuffiness or a full feel-
ing in the ear.
T h e pain associated with MPD is usually
constant, but it is often more severe on arising
in the morning or gradually worsens as the day
progresses. It is generally exacerbated by man-
dibular function, especiaIly chewing and exces-
sive talking. T h e pain also tends to become re-
gional with time, and spreads to the cervical
region and later to the shoulders and back.
Masticatory muscle tenderness is a n o t h e r
c o m m o n finding in MPD patients, 29 and its
presence can be used to confirm the source of
the pain in those muscles accessible to palpa-
tion (masseter, temporalis, medial pterygoid).
T h e most c o m m o n sites of tenderness are near
the angle of the mandible, in the belly and an-
terosuperior aspect of the masseter, in the an-
terior temporal region, and over the temporal
crest on the anterior aspect of the coronoid
process.
T h e third c o m m o n symptom of MPD is lim-
itation of mandibular movement. 29 T h e r e is
inability to open the m o u t h as wide as usual
and the mandible deviates to the affected side
when opening is attempted. T h e r e is also re-
duced excursion to the unaffected side. T h e
degree of limitation in mandibular m o v e m e n t
is usually correlated with the severity of the
pain.
Clicking or popping sounds in the TMJ are
another finding in some patients with MPD.
Intermittent clicking or popping can accom-
pany the lateral pterygoid spasm that occurs in
MPD
Dull, aching, radiating pain, increased
with function
Poorly localized
Generally absent
Always present
Moderate to severe
Occasional clicking or popping sounds
Absent
 Daniel M. Laskin
some of these patients, whereas the frictional
changes introduced by a chronic clenching
habit are the cause when the joint sounds are
persistent. The presence ofjoint sounds alone,
however, is not sufficient to make a diagnosis
of MPD. 4'3° They must be accompanied by
pain and tenderness in the masticatory muscles
that began before rather than after the onset
of the clicking or popping, as would occur in
patients with a primary internal derangement
and secondary muscle splinting.
In addition to the three common symptoms
of diffuse pain, masticatory muscle tenderness,
and limited mouth opening, most patients with
primary MPD usually have an absence of clin-
ical or radiographic evidence of pathological
changes in the TMJ. 4'3° These negative char-
acteristics are important in establishing the di-
agnosis because they help confirm that the pri-
mary site of the problem is not in the articular
structures.
Nonarticular Conditions Mimicking
Temporomandibular Disorders
Although an understanding of the signs and
symptoms of the various temporomandibular
disorders should generally enable the clinician
to make an accurate diagnosis, it is still impor-
tant to be aware of the various nonarticular
conditions that also need to be considered in
the initial differential diagnosis. There are a
number of conditions besides TMJ pathology
and MPD that can cause similar symptoms of
facial pain and mandibular dysfunction. Those
causing similar pain include pulpitis, pericoro-
nitis, otitis, parotitis, maxillary sinusitis, tri-
geminal neuralgia, atypical facial neuralgia,
temporal arteritis, Trotter's syndrome (naso-
pharyngeal carcinoma), and Eagle's syndrome.
Conditions that can cause mandibular limita-
tion and dysfunction include chronic odonto-
genic infections, chronic nonodontogenic in-
fections, myositis, myositis ossificans, posttrau-
matic or postsurgical scarring, neoplasia,
scleroderma, hysteria, extrapyramidal reac-
tions produced by psychotropic drugs, and
mechanical obstruction caused by posttrau-
matic depression of the zygomatic arch or os-
teochondroma of the coronoid process. Al-
though some of these conditions also cause
205
pain, the main complaints are usually related
to altered jaw function.
The differences in the history and clinical
and radiographic findings should help the cli-
nician distinguish TM~ pathology and MPD
from the various nonarticular conditions that
produce relatively similar signs and symptoms.
Although it is not the purpose of this article to
discuss the specific differential diagnosis of
these conditions, it is essential that one is fa-
miliar with this information, which is readily
available in the literature.
Conclusions
Ahhough not all orthodontists may wish to be-
come directly inwflved in the treatment of pa-
tients with MPD, they will encounter such pa-
tients in their practice. It is therefore essential,
when it is present, that they recognize the con-
dition before beginning orthodontic treatment
so that patients will not consider it a conse-
quence of their therapy. The same is true for
TMJ problems such as internal derangement
or secondary degenerative joint disease. More-
over, when these conditions arise during orth-
odontic treatment, the orthodontist must also
realize that they are generally unrelated to
such therapy. ~:~ However, they may require
modifications in treatment procedures that can
aggravate the situation. Finally, the orthodon-
tist will play a major role in the management of
patients with malocclusions and facial asymme-
tries associated with congenital and develop-
mental anomalies. Because the orthodontist
may he the first doctor to see such patients, he
or she must not only be able to make the cor-
rect diagnosis, but also must understand the
chronology of the underlying growth distur-
bances so that this can be integrated into the
final treatment plan.
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