Download Magnetic resonance imaging of the lateral pterygoid muscle in

Document related concepts

Anatomical terminology wikipedia , lookup

Transcript
MAGNETIC RESONANCE
IMAGING OF THE LATERAL
PTERYGOID MUSCLE IN
TEMPOROMANDIBULAR
DISORDERS
XIAOJIANG
YA NG
Department of Prosthetic Dentistry and
Stomatognathic Physiology and
Department of Oral and Maxillofacial
Surgery, Institute of Dentistry,
Department of Diagnostic Radiology,
University of Oulu
OULU 2002
XIAOJIANG YANG
MAGNETIC RESONANCE IMAGING
OF THE LATERAL PTERYGOID
MUSCLE IN TEMPOROMANDIBULAR
DISORDERS
Academic Dissertation to be presented with the assent of
the Faculty of Medicine, University of Oulu, for public
discussion in the Auditorium I of the Institute of
Dentistry, on April 19th, 2002, at 12 noon.
O U L U N Y L I O P I S TO, O U L U 2 0 0 2
Copyright © 2002
University of Oulu, 2002
Reviewed by
Docent Pentti Kemppainen
Docent Osmo Tervonen
ISBN 951-42-6643-9
(URL: http://herkules.oulu.fi/isbn9514266439/)
ALSO AVAILABLE IN PRINTED FORMAT
Acta Univ. Oul. D 668, 2002
ISBN 951-42-6642-0
ISSN 0355-3221
(URL: http://herkules.oulu.fi/issn03553221/)
OULU UNIVERSITY PRESS
OULU 2002
Yang, Xiaojiang, Magnetic resonance imaging of the lateral pterygoid muscle in
temporomandibular disorders
Department of Prosthetic Dentistry and Stomatognathic Physiology, Institute of Dentistry, and
Department of Oral and Maxillofacial Surgery, Institute of Dentistry, University of Oulu, P.O.Box
5281, FIN-90014 University of Oulu, Finland, Department of Diagnostic Radiology, University of
Oulu, P.O.Box 5000, FIN-90014 University of Oulu, Finland
Oulu, Finland
2002
Abstract
The fact that the lateral pterygoid muscle (LPM) and related symptoms play an important role in
temporomandibular disorders (TMD) is widely recognized. In the study reported here, the LPM was
investigated by magnetic resonance imaging (MRI) of patients with TMD. The visibility of the LPM
in MRI with different projections was analyzed and a new imaging projection, condyle-the lateral
pterygoid muscle projection (CLPM), for the LPM in MRI was introduced. Normal and abnormal
findings of the LPM was compared with clinical symptoms of TMD.
Compared with sagittal imaging of temporomandibular joint (TMJ), CLPM images and most of
the oblique sagittal imaging were able to show the LPM clearly. Hypertrophy, atrophy and
contracture of the LPM were found in TMJs either with disc in normal position or with disc
displacements. Pathological changes of the superior belly and hypertrophy of the inferior belly
combined with various pathological changes of the superior belly were the most frequently observed
abnormal imaging findings of the LPM in TMD. The pathological changes of the LPM were
associated with the main clinical symptoms of TMD. In patients with symptomatic condyle
hypermobility, the pathological changes of the LPM and related symptoms were associated with the
clinical symptoms of TMJs with disc in normal position. The imaging abnormalities of the LPM were
common in TMJs with disc displacements and seemed to be fewer in condyle hypomobility cases in
TMJs with anterior disc displacement with non-reduction (ADDnr). However, normal imaging of the
LPM was also found in TMJs with severe osteoarthritic changes and disc displacement.
The recognition of muscle alterations may lead to a more specific diagnosis and improve the
understanding of the clinical symptoms and disease pathophysiology of TMD.
Keywords: TMJ, TMD, lateral pterygoid muscle, MRI
Acknowledgement
I would like to express my deep and sincere gratitude to my supervisor, Professor Aune
Raustia, D.D.S., Ph.D., Head of the Department of Prosthetic Dentistry and
Stomatognathic Physiology, Institute of Dentistry, University of Oulu. Her wide
knowledge and her logical way of thinking have been of great value for me. Her
understanding, encouraging and personal guidance have provided a good basis for the
present thesis.
I am deeply grateful to my supervisor, Professor Kyösti Oikarinen, D.D.S., Ph.D.,
Head of the Department of Oral and Maxillofacial Surgery, Institute of Dentistry,
University of Oulu, for his detailed and constructive comments, and for his important
support throughout this work.
I wish to express my warm and sincere thanks to Professor Min Hong, D.D.S.,
Ph.D., Head of the Department of Oral and Maxillofacial Surgery, General Military
Hospital, Beijing, China, who introduced me to the field of oral maxillofacial surgery
and Professor Kurt Schellhas, M.D., Director of Neuroimaging and Spinal Injection
Procedures, Center for Diagnostic Imaging, Minnesota, USA, whose letters gave me
important guidance during my first steps into MR imaging studies. Their ideals and
concepts have had a remarkable influence on my entire career in the field of
temporomandibular joint research.
I owe my most sincere gratitude to Professor Eric Fossion MD, LDS, and Professor
Antoon De Laat, LDS, GHO, who gave me the opportunity to work with them in the
Department of Oral and Maxillofacial Surgery at the Catholic University of Leuven in
Belgium and gave me untiring help during my difficult moments.
I warmly thank Dr. Hannu Pernu, D.D.S., M.D., for his valuable advice and friendly
help. His extensive discussions around my work and interesting explorations in
operations have been very helpful for this study.
My warm thanks are due to Professor Juhani Pyhtinen, M.D., Ph.D., and Professor
Changzu Fan, M.D., who directed me in magnetic resonance imaging studies. Their
kind support and guidance have been of great value in this study.
My sincere thanks are due to the official referees, Docent Pentti Kemppainen,
D.D.S., Ph.D., and Docent Osmo Tervonen, M.D., Ph.D., for their detailed review,
constructive criticism and excellent advice during the preparation of this thesis.
I wish to thank Mr. Ahti Niinimaa, M.Sc., Ph.D., and Mr. Risto Bloigu, M.Sc., for
their guidance in statistical analysis, and Dr. Petri Tiilikainen, D.D.S., for his essential
assistance in reviewing the patient files of this study.
I am grateful to Docent Kimmo Lehtimäki, D.D.S., Ph.D., for attracting me to
Finland and for interesting discussions on the operations of the temporomandibular
joint.
I also wish to thank Mrs. Anna Vuolteenaho, M.A., for revising the English of my
manuscript. Ms Liisa Kärki, Ms Seija Leskelä and Ms Taru Kaleva are thanked for their
excellent photographic work, and Ms Sinikka Vuoti and Ms Eija Takkula for their
sympathetic help in secretarial work.
During this work I have collaborated with many colleagues for whom I have great
regard, and I wish to extend my warmest thanks to all those who have helped me with
my work in the Department of Prosthetic Dentistry and Stomatognathic Physiology in
Oulu, in the Department of Oral and Maxillofacial Surgery and in the Department of
Diagnostic Radiology at the University of Oulu, at Tampere University Hospital, at
Leuven University Hospital in Belgium, and at General Military Hospital in Beijing,
China.
I owe my loving thanks to my wife Xiaoping Liang, my sons Zou yi Yang and Zichao
Liang. They have lost a lot due to my research abroad. Without their encouragement
and understanding it would have been impossible for me to finish this work. My special
gratitude is due to my brother, my sisters and their families for their loving support. My
loving thanks are due to Raili and Pentti Rantanen. They let me own a happy family in
Finland.
The financial support of the University of Oulu is gratefully acknowledged.
Oulu, Finland, February 2002
Xiaojiang Yang
Abbreviations
ADDnr
ADDr
CT
EMG
LPM
MR
MRI
PD
RF
TE
TMD
TMJ
TR
anterior disc displacement with non-reduction
anterior disc displacement with reduction
computed tomography
electromyography
the lateral pterygoid muscle
magnetic resonance
magnetic resonance imaging
proton-density
radiofrequency
echo delay time
temporomandibular disorders
temporomandibular joint
pulse repetition time
List of original publications
This thesis is based on following articles, which are referenced to in the text by Roman
numerals:
I.
II.
III.
IV.
Yang XJ, Hong M, Hu XH. (1992) A New MRI Projection for the
Temporomandibular Joint and Lateral Pterygoid Muscle. J
Craniomandibular Disorders: Facial & Oral Pain. 6(1): 32-9
Yang XJ, Pernu H, Pyhtinen J, Tiilikainen PA, Oikarinen KS, Raustia
AM: (2001) MRI Findings of Lateral Pterygoid Muscle in the Patients
with Symptomatic Temporomandibular Joint Hypermobility. J
Craniomandibular Practice 19 (4):260-268.
Yang XJ, Pernu H, Pyhtinen J, Tiilikainen PA, Oikarinen KS, Raustia
AM: MR Abnormalities of the Lateral Pterygoid Muscle in Patients with
Nonreducing disc Displacement of the Temporomandibular Joint. J
Craniomandibular Practice, in press.
Yang XJ, Pernu H, Pyhtinen J, Tiilikainen PA, Oikarinen KS, Raustia
AM:
Disc
Displacement
in
Patients
with
Symptomatic
Temporomandibular Joint Hypermobility – A MRI Study of 153 TMJs. J
Craniomandibular Practice (submitted).
Contents
Abstract
Acknowledgements
Abbreviations
List of original publications
1 Introduction ........................................................................................................... 15
2 Review of literature ............................................................................................... 16
2.1 Diagnostic criteria of TMD............................................................................. 16
2.2 Imaging of TMJ .............................................................................................. 17
2.2.1 Plain film radiography ............................................................................. 17
2.2.2 Panoramic radiography............................................................................ 18
2.2.3 Tomography............................................................................................. 18
2.2.4 Arthrography ........................................................................................... 19
2.2.5 Computed tomography ............................................................................ 20
2.2.6 Magnetic resonance imaging ................................................................... 20
2.2.6.1 Physical principles ............................................................................ 20
2.2.6.2 MRI of TMJ...................................................................................... 21
2.3 Lateral pterygoid muscle (LPM)..................................................................... 22
2.3.1 Anatomy of the LPM ............................................................................... 22
2.3.2 Electromyography of the LPM ................................................................ 23
2.3.3 Clinical examination of the LPM............................................................. 24
2.3.4 Imaging of the LPM................................................................................. 24
2.3.4.1 Imaging projections .......................................................................... 24
2.3.4.2 Imaging evaluation of skeletal muscle.............................................. 25
3 Aims of the study................................................................................................... 27
4 Materials and methods........................................................................................... 28
4.1 Materials ......................................................................................................... 28
4.1.1 General information on patients............................................................... 28
4.1.2 Information from patient files.................................................................. 29
4.2 Magnetic resonance imaging technique.......................................................... 29
4.2.1 MRI equipments and parameters ............................................................. 29
4.2.2 Imaging projections ................................................................................. 30
4.3 Grading of MRI findings ................................................................................ 30
4.3.1 Lateral pterygoid muscle ......................................................................... 30
4.3.1.1 Visibility of the LPM in MRI ........................................................... 30
4.3.1.2 Normal MRI findings of the LPM .................................................... 31
4.3.1.3 Abnormal MRI findings of the LPM ................................................ 31
4.3.2 Disc position ............................................................................................ 32
4.3.3 Morphology of the disc............................................................................ 32
4.3.4 Effusion ................................................................................................... 32
4.3.5 Osteoarthritis ........................................................................................... 32
4.3.6 Condyle mobility ..................................................................................... 32
4.4 Statistical methods .......................................................................................... 33
5 Results ................................................................................................................... 34
5.1 Visibility of LPM in MRI ............................................................................... 34
5.2 MRI findings of the LPM in patients with TMD ............................................ 35
5.3 MRI findings of the LPM and clinical symptoms........................................... 37
5.4 Imaging findings of the LPM, disc position and condyle mobility in MRI .... 38
5.5 Pathological changes of the LPM in different types of TMD ......................... 40
5.5.1 Pathological changes of the LPM in TMJ hypermobility ........................ 40
5.5.2 Pathological changes of the LPM in TMJs with ADDnr ......................... 40
6 Discussion.............................................................................................................. 42
6.1 Methodological considerations ....................................................................... 42
6.1.1 Subjects.................................................................................................... 42
6.1.2 Methods ................................................................................................... 43
6.2 Visibility of the LPM in MRI ......................................................................... 44
6.3 Pathological changes of the LPM and clinical symptoms of TMD ................ 46
6.4 Pathological changes of the LPM in different types of TMD ......................... 47
6.4.1 Pathological changes of the LPM and disc displacements....................... 47
6.4.2 Symptoms of the LPM in TMJs with disc in normal position ................. 48
6.4.3 Pathological changes of the LPM in TMJ hypermobility ........................ 49
6.4.4 Pathological changes in the two bellies of the LPM ................................ 50
6.4.5 Pathological changes of the LPM in late stage of TMD .......................... 51
7 General discussion................................................................................................. 53
8 Conclusions ........................................................................................................... 56
9 References ............................................................................................................. 57
10 Appendix: Figures ............................................................................................... 69
11 Original Papers .................................................................................................... 80
1 Introduction
Temporomandibular disorders (TMD) are pain and dysfunction syndromes involving
the temporomandibular joint (TMJ) and/or muscles of mastication. The symptoms of
TMD include clicking of TMJ, pain, and abnormal movement of mandible.
Displacements of the disc appear in TMJ, and various degenerative changes can occur
in the condyle and disc. The diagnosis of TMD is one of the focuses in dental clinical
practice.
In the past decades, imaging diagnosis of TMJ has developed very fast. These
advances have included arthrography, computed tomography (CT) and magnetic
resonance imaging (MRI). Among these methods, it has been presented that MRI can
give more accurate information of TMJ, e.g. on disc displacement, osteoarthritic
changes of condyle, deformities of the disc, and pathological situations of surrounding
soft tissues of TMJ. MRI findings have also been compared with surgical findings,
anatomical and histological observations of autopsy specimens. It has been suggested
that MRI is the best method in imaging diagnosis of TMD.
The studies presented on MRI have mainly discussed the disc displacements of TMJ.
However, it has been found that pain and dysfunction symptoms of TMJ vary in
patients with or without disc displacements. Alterations of the clinical symptoms of
TMJ cannot always be explained only by disc displacements. The function and
dysfunction of masticatory muscles should also be taken into account.
Previous studies have shown that the lateral pterygoid muscle (LPM) may play an
important role in TMD. Stable and reliable methods to evaluate the LPM are still
lacking. MRI has been confirmed as an important tool in diagnosing muscular diseases.
In the study reported here MRI was used in imaging diagnosis of the LPM with the aim
of detecting pathological changes of the LPM in patients with TMD and of discussing
the correlations of the imaging abnormalities with the clinical symptoms.
2 Review of literature
2.1 Diagnostic criteria of TMD
A multitude of terms have been used to describe patients presenting with pain and
dysfunction of the temporomandibular joint (TMJ) and related masticatory muscles:
Costen’s syndrome (Costen 1934), dysfunctional temporomandibular joint and muscle
pain (Ramfjord 1961), myofascial pain dysfunction (MPD) (Laskin 1969),
temporomandibular joint syndrome (Carraro et al. 1969), mandibular dysfunction
(Thompson 1971) and craniomandibular disorders (McNeill 1990). These terms
include several entities that have different etiology, but present with similar signs and
symptoms (Westesson 1993).
Temporomandibular disorders (TMD) are one subgroup of any of these terms, and
they embrace a number of clinical problems that involve the masticatory muscles
and/or the temporomandibular joint (Laskin 1969, Agerberg & Carlsson 1975, McNeill
et al. 1990, Westesson 1993). This term is most frequently used in clinical practice
(Raustia et al. 1994, Eberhard et al. 2000, Steed & Wexler 2001).
The studies of internal derangement of TMJ (TMJID) focus on displacement of the
disc in temporomandibular joint (Farrar 1978, Wilkes 1978a,b). Wilkes defined the
criteria of TMJID in 1978. The criteria were based on clinical symptoms, surgical
findings, radiological findings, and they were later combined with MRI findings of
TMJ (Wilkes 1989, Schellhas 1989a). In past decades, a number of reports have been
presented indicating that the disc displacement is associated with the pain and
dysfunctional symptoms of TMJ (Farrar & McCarty 1979, Schellhas 1989a, Katzberg et
al. 1996, Emshoff et al. 2001). The studies also showed that the disc displacement
correlated with disc deformity (Yoshida et al. 2000, Taskaya-Yilmaz & Ogutcen-Toller
2001) and osteoarthritic changes of the hard tissues in TMJ (Westesson 1985, Kurita et
al. 2000, Bertram et al. 2001). The pathological evidence in TMJs with disc
displacement have been confirmed by histological (Larheim et al. 1999, Leonardi
17
2001) and anatomical studies in autopsy specimens (Westesson & Rohlin 1984a,
Widmalm et al. 1992, Kondoh et al. 1998).
However, some questions have arisen based on the clinical studies. In Wilkes’s
criteria, the internal derangement of TMJ was described as a progressing procedure in
radiological stages; oppositely, clinical symptoms show as a chronically released
procedure (Wilkes 1989). The symptoms of some patients might be relieved after
conservative or surgical treatment, but the severe disc displacement and degenerative
changes of TMJ might still exist (Montgomery et al. 1992, Sato et al. 1999, Nishimura
2001). Other reports found that the symptoms of the patients with severe disc
displacement of TMJ might be resolved even without any treatment (Lundh et al. 1992,
Kurita at al. 1998, Sato et al. 1998). On the other hand, pain and dysfunction symptoms
have also been found in TMJs without disc displacement (Benito et al. 1998). The
results of these studies indicate that the disc displacements of TMJ cannot always
explain the alterations of the clinical symptoms. If the views only encompass disc
displacement, it may not be enough for the diagnosis and treatment of TMJ problems.
The function and dysfunction of the masticatory muscles in TMD should also be taken
into account (Helkimo 1974a,b, Solberg 1986a, Katzberg et al. 1996, De Laat 1998,
Greene 2001). Identification of pathological changes of masticatory muscles is still
lacking in diagnostic criteria of TMD, and more evidence of pathological changes of
the masticatory muscles in TMD is needed.
2.2 Imaging of TMJ
Most studies agree that TMD cannot be diagnosed only on the basis of findings by
clinical examinations. Imaging diagnosis is very important (Wilkes1989a,b, Westesson
et al. 1989, Gibbs et al. 1998). There are a number of imaging techniques, ranging
from plain-film to MRI, that have been used in diagnosis of TMD. Arthroscopy is
applied as a treatment for TMD rather than a diagnosis technique (Barkin & Weinberg
2000, Holmlund et al. 2001). Nuclear medicine imaging is rarely used for clinical
diagnosis of TMD (Matin 1983). These two methods are therefore not included in this
review.
2.2.1 Plain film radiography
Plain films of TMJ are made with a stationary x-ray source and film. In order to avoid
superimposition of adjacent anatomic bony structures making visualization of all parts
of TMJ, different projections of transcranial films have been applied, which include
oblique transcranial view, transmaxillary view, submental-vertex view and
transpharyngeal view (DelBalso 1990, Kopp & Rockler 1979, Kononen & Kilpinen
1990, Williamson et al. 1999). Transcranial plain films have been used in the past to
18
diagnose TMD by evaluating the position of the mandibular condyle in the glenoid
fossa and condylar osseous changes (Weinberg 1979, van Sickels et al. 1983, Kononen
& Kilpinen 1990). However, some studies have reported that the relationship between
the condyle and the glenoid fossa could not be accurately evaluated in transcranial film
by comparing with tomography of TMJ (Pullinger et al.1985, Knoernschild et al.
1991). Concordance in the degree of condylar displacement was found in only 60% of
the cases when comparing transcranial film and tomography (Pullinger & Hollender
1985). Currently, transcranial plain film is suggested to be a method for detecting
condylar fractures rather than a method for diagnosing TMD (Lindqvist et al. 1988,
Brooks et al. 1997, Thoren et al. 2001).
2.2.2 Panoramic radiography
Panoramic radiography used to be considered a good imaging method for evaluating
TMJ since information about the teeth and other parts of the jaws were also shown on
the image (Kononen & Kilpinen 1990, Howard 1990). However, the relationship
between the condyle and glenoid fossa cannot be evaluated in the panoramic film
because the fossa cannot be seen with superimposition of the base of the skull and
zygomatic arch. The morphology of the condyle becomes wider than the anatomic
structure of the condyle (DelBalso 1990). The agreement between panoramic
radiographs and lateral tomograms on osseous changes of the condyle is 60% to 70%
(Habets et al. 1989, Ludlow et al. 1995). Panoramic radiography has also been used in
evaluating condyle fractures (Silvennoinen et al. 1998).
2.2.3 Tomography
Tomography of TMJ is generated through the synchronous movement of the x-ray tube
and film cassette through an imaginary fulcrum located in the center of the desired
imaging plane. Linear tomography and complex tomography are involved (DelBalso
1990).
Osseous changes in TMJ. Several studies have attested that tomography is a good
method for depicting the osseous changes with arthrosis in TMJ (Berrett 1983,
Rosenberg & Graczyk 1986). In studies of TMJ specimens obtained at autopsy,
tomography has been shown to represent the anatomic structures better than
transcranial radiography (Lindvall et al. 1976, Eckerdal & Lundberg 1979). Observer
performance studies in the assessment of tomographic images have shown a 60% to
80% interobserver agreement and a similar intra-observer agreement (Kopp & Rockler
1978, Petersson & Rohlin 1988, Rohlin & Peterson 1989, Cholitgul et al. 1990).
Condyle position. For evaluation of condyle position in glenoid fossa of TMJ,
tomography has been reported to be more reliable than plain film and panoramic
19
radiography in a study comparing the three methods (Ludlow et al. 1995). Tomography
has been used for evaluating the condyle position and joint space in many reports
(Knoernschild et al. 1991, Kuboki et al. 1999, Ozawa et al. 1999). However, numerous
studies have shown that condyle position appears to be highly variable in both
asymptomatic (Pullinger et al. 1985, Blaschke & Blaschke 1981) and symptomatic
subjects (Brand et al. 1989, Pullinger et al. 1986). On the other hand, the relationship
between the condyle position and disc displacement is uncertain. The condyle position
is not reliable in estimating the disc displacement of TMJ and related symptoms
(Katzberg et al. 1983, Bonilla-Aragon et al. 1999, Kurita et al. 2001). Clinically,
condyle position is still an important aspect in orthognathic surgery (Williamson et al.
1999, Arat et al. 2001) and orthodontic studies (Major et al. 1997, Zhou et al. 1999).
The major disadvantage of tomography is the lack of visualization of the soft tissue of
TMJ, a problem shared with plain film radiography.
2.2.4 Arthrography
The technique of TMJ arthrography was introduced in the 1940s (Nørgaard 1947), but
it was not extensively used until the late 1970s (Westesson et al. 1980, Westesson
1993). Arthrography improved rapidly after the late 1970s (Wilkes 1978, Farrar &
McCarty 1979, Katzberg et al. 1979). There are two technical methods for
arthrography of TMJ. In single-contrast arthrography, radiopaque material is injected
into either the lower or upper joint space, or into both compartments (Wilkes 1978a,b,
Brand 1990). In double-contrast arthrography, a small amount of air is injected into the
joint space after the injection of contrast materials (Westesson et al. 1980, Westesson
1982, Ma 1987). A comparative study reported that there was no statistically
significant difference in the diagnostic accuracy between these two techniques
(Westesson & Bronstein 1987).
Several studies have shown that arthrography is an accurate imaging method for
evaluating anterior disc displacement. The accuracy for diagnosing the position of the
disc ranged from 84% to 100% compared with the corresponding cryosectional
morphology and surgical findings (Westesson & Rohlin 1984b, Westesson et al. 1986,
Tanimoto et al. 1989, Schellhas et al. 1988). Perforation and adhesion of the disc can
also be shown by this technique (Helms et al. 1980, Westesson et al. 1986, Schellhas et
al. 1988, Ryan et al. 1990). These studies have given important evidence for diagnosis
and identification of TMJ internal derangement (Wilkes 1989). Arthrography is based
on plain film (Helms et al. 1980, Van Sickels et al. 1983) and tomography (Wilkes
1978a,b, Katzberg et al 1979). A recent study reported that using the arthrography
technique might improve the accuracy of diagnosing perforations and adhesions of the
disc in magnetic resonance imaging of TMJ (Toyama et al. 2000).
There are some advantages of this technique. Arthrography is a method that depends
upon more technical training and experience in the observation of images, it also has
minimally invasive (Westesson et al. 1993).
20
2.2.5 Computed tomography
In the 1980s, computed tomography (CT) began to be applied in the diagnosis of TMJ
ankylosis (Kaban & Bertolami 1981), condyle fracture (Avrahami et al. 1984, Sahm &
Witt 1989), disc displacement (Helms et al. 1982, Thompson et al. 1984) and osseous
changes (Larheim & Kolbenstvedt 1984, Katzberg et al. 1984, Cohen et al. 1985).
In an earlier report, the accuracy for disc displacement was high (81%) when
comparing imaging observations of CT and surgical findings (Thompson et al. 1984).
Some reports considered that CT might replace the technically difficult and invasive
arthrography in the diagnosis of disc displacement in TMD (Helms et al. 1982,
Avrahami et al. 1984, Cohen et al. 1985). However, the accuracy of the disc
displacement was only 40%-67% in CT in studies of autopsy specimen materials
(Westesson et al. 1987b, Tanimoto et al. 1990). The accuracy of osseous changes of
TMJ in CT compared with cadaver material was 66%-87% (Tanimoto et al. 1990,
Westesson et al. 1987a). Some reports pointed out that radiographic evidence of
arthrosis may or may not be associated with clinical symptoms of pain dysfunction.
Thus patients without osseous changes in TMJ may have pain, and those with clear
signs of bony abnormalities may be pain-free (Westesson 1993, Brooks et al. 1992,
Bertram et al. 2001). CT was not considered as a good method for the diagnosis of
TMD in many later reports (Katzberg 1989, Kaplan & Helms 1989, Helms & Kaplan
1990, Westesson 1993, Brooks et al. 1997).
2.2.6 Magnetic resonance imaging
2.2.6.1 Physical principles
Magnetic resonance imaging (MRI) is unique in that there is no associated risk of
ionizing x-ray. For MRI, the patient placed in a strong static magnetic field. The
hydrogen nuclei, or protons, in the body align with the direction of the main magnetic
field, a short radiofrequency (RF) pulse at the proper frequency and duration is then
transmitted into the body. The protons absorb RF energy and flip over into a plane that
is at an angle with the direction of the main magnetic field, the protons reemit some of
the absorbed energy, which induces an electric current in a specially designed RF
receiver coil. The induced current, so-called the magnetic resonance (MR) signal, is
then transformed into an image by computerized mathematical methods
(Jarenwattananon & Gentry 1990).
An MR image is produced from signals coming from the hydrogen nuclei, or
protons, in the body. The contrast of the image is provided by differences in signal
intensity from protons in different tissues. Several parameters affect the signals
intensity: (1) amount of the hydrogen nuclei in tissue; (2) the characteristics of the
tissue, as determined by two different relaxation time constants (T1 and T2); (3) the
bulk flow of protons in tissues. Varying the pulse sequence imaging variables, such as
pulse repetition time (TR) or echo delay time (TE), allows discrimination of different
21
tissues. Special selected parameters can generate images in which contrast differences
are dependent on these factors. The most frequently used ones in TMJ images are T1weighted image (short TR and TE), T2-weighted image (long TR and TE) and protondensity (PD) image (long TR and short TE) (Jarenwattananon & Gentry 1990). Typical
values for T2 in tissue range from 0.02 to 0.30 seconds. In general, the more water a
tissue contains, the longer the T2. Thus, areas of long T2 can be interpreted as areas of
edema, effusion, or inflammation. Typical T1 values for tissue range from 0.2 to 3
seconds. Much of the power of MRI comes from the fact that various tissues have
different values of T1 and T2 and contrast can be varied over a wide range by adjusting
TE and TR (Kircos & Ortendahl 1990). For example, in T1-weighted and PD image,
the fibrocartilaginous disc is in low signal intensity. The lateral pterygoid muscle
(LPM) and bilaminar zone are of intermediate signal intensity. The position and
morphology of the disc can be clearly observed (Katzberg et al. 1985). However, in a
T2-weighted image, the disc, muscles and bilaminar zone are all in low signal intensity,
effusion (if it exists) of the bilaminar zone or in joint compartments can be well
observed with high-intensity signal (Schellhas & Wilkes 1989). Skeletal muscles,
fibrous, blood and fat tissues all have their own characteristic signal intensities in MRI
(Siegelman & Outwater 1999, Weinreb et al. 1985, Murphy et al. 1986).
2.2.6.2 MRI of TMJ
MRI with surface coil was introduced applied to TMJ imaging in the 1980s (Harms et
al. 1985, Katzberg et al. 1986, Schellhas et al. 1986). Several studies have compared
MRI of TMJ with arthrography and CT (Schellhas et al. 1988, Liedberg et al. 1996,
Trumpy et al. 1997). The MRI findings were also compared with anatomical and
histological observations (Westesson et al. 1987a,b, Larheim et al. 1999). In studies on
autopsy specimens, the accuracy of MRI in evaluating osseous changes in TMJ was
60% to100% (Westesson et al. 1987b, Hansson 1989, Tasaki & Westesson 1993) and
the accuracy in evaluating disc displacement was 73% to 95% (Westesson et al. 1987b,
Hansson 1989, Schwaighofer et al. 1990, Tasaki & Westesson 1993). All these studies
showed that MRI was the best method of imaging both the hard and soft tissues of the
TMJ (Raustia et al. 1995, Brooks et al. 1997, Gibbs et al. 1998).
Several studies have confirmed that disc displacement in MRI showed close
associations with clicking, pain and other dysfunction symptoms of TMJ (Katzberg et
al. 1996, Rammelsberg et al. 1997, Emshoff et al. 2001, Bertram et al. 2001). MRI was
considered as a golden standard to evaluate the disc position (Gibbs et al. 1998).
Whenever the clinical pain and dysfunction symptoms of TMJ were found to have no
relationship with disc displacement in MRI, a false-positive or false-negative imaging
diagnosis was suspected (Haley et al. 2001).
Although many studies agree that muscular pain is another major aspect of TMD
(Solberg 1986, Greene & Laskin 1988, Rauhala et al. 1999, Molina et al. 2000, Greene
2001, De Laat 2001), the evidence of pathological changes of the masticatory muscles
may have been ignored in imaging diagnosis. The results of some reports have shown
that MRI is not only an accurate method to detect the disc position but also a potential
technique to evaluate the pathological changes of the masticatory muscles in TMD
22
(Katzberg et al. 1985, Schellhas 1989b, van Spronsen et al. 1989, Westesson 1993,
Quemar et al. 1993). However, no reports concerning the relationship between the
abnormalities of the masticatory muscles in MRI and clinical symptoms have been
published.
2.3 Lateral pterygoid muscle (LPM)
2.3.1 Anatomy of the LPM
In the past decades, the lateral pterygoid muscle (LPM) has been given more attention
than other masticatory muscles in studies of TMJ problems.
According to Sicher (1965), the LPM arises with two bellies, the smaller superior
belly of the LPM (SLP) runs posteriorly from the infratemporal surface of the greater
sphenoid wing in an inferior and lateral direction to the crest of the eminence, where its
fibers become more horizontal and insert into the condyle and disc. The larger inferior
belly of the LPM (ILP) ran posteriorly and laterally from the outer surface of the lateral
pterygoid plate to insert into the pterygoid fovea. The two bellies are separated
anteriorly by a variably wide gap and fuse in front of the TMJ. The nerve to the LPM
branches off the masseteric or the buccal nerve. The blood supply is a branch of the
maxillary artery (Sicher 1965). Other report argued that there are three patterns of
nerve supply to the LPM. In the two most frequently observed patterns, both bellies of
the LPM were supplied from a common source that was derived from either the long
buccal or mandibular nerve. In the third pattern, independent branches to either belly
arose from deep temporal, long buccal or mandibular nerve (Aziz et al. 1998). The
results of Aziz’s study indicated that both bellies of the LPM were usual supplied by a
common proximate source, but each belly also received an independent nerve in every
case. The functional activities of the two bellies of the LPM might act as separate
muscles (Juniper 1981, Aziz et al. 1998).
The theory of internal derangement of TMJ involves anterior disc displacements,
which were in earlier studies considered to be brought about by the abnormal activities
of the superior belly of the LPM (Juniper 1984, Porter 1970, Osborn 1985). Some
anatomical studies supported this point of view by the observation that the superior
belly of the LPM inserts into the capsule and disc (Thilander 1964, Honee 1972).
However, later studies showed that the superior belly of the muscle inserted into the
condyle, capsule and disc (Bertilsson & Strom 1995, Naidoo 1996). Other reports
found that the insertion of the LPM might only be firmly attached but not inserted into
the disc (Wilkinson 1988, Heylings et al. 1995). The results of these studies presented
that from an anatomical point of view it was impossible for the superior belly of the
LPM to pull the disc forward independently from the condyle, leading to the disc
anterior displacement. Furthermore, other reports presented that not only the superior
belly but also the inferior belly of the LPM might have some fibers inserted into the
disc (Schmolke 1994, Bittar et al. 1994, Fujita et al. 2001). The relationship between
disc displacement and dysfunction of the LPM is still unclear. In a bilateral
23
comparative anatomical study of TMJ, Grunert et al. (2000) reported that an evident
hypertrophy of the superior belly of the LPM was found in the TMJs with disc
pathological changes or osseous changes of the condyle. The anatomical observation of
the auriculotemporal nerve showed that the pathological changes of the LPM might
compress or irritate the nerve and produce pain symptoms (Schmidt et al. 1998).
Although the results of these studies may lead to the realization that the LPM may have
a close association with TMJ disorders and involved symptoms, the clinical evidence
showing pathological changes of the LPM in patients is still lacking.
2.3.2 Electromyography of the LPM
Electromyography (EMG) is used for evaluating the functional activities of the LPM
(McNamara 1973, Lehr & Owens 1980, Widmalm et al. 1987, Wang et al. 2001).
Studies have reported EMG activities of the superior belly and/or inferior belly of the
LPM in different jaw positions (Mahan et al. 1983), on biting (Wood et al. 1986,
Hiraba et al. 2000) and other jaw movements (Gibbs et al. 1984, Murray et al. 1999,
Phanachet et al. 2001).
Studies concerning TMD have shown that abnormal electromyographic activities of
the LMP could be detected in the patients (Juniper 1984, Friedman 1997). The
abnormal EMG activities of the LPM were observed more obviously than those of
other masticatory muscles in TMD cases (Lafreniere et al 1997). These studies showed
that the LPM might play an important role in TMD. The basic evidence for
understanding and discussing the function and dysfunction of the LPM comes mostly
from the results of these studies.
However, many studies have found that EMG patterns of the LPM are not stable or
reproducible (Mahan et al. 1983, Gibbs et al. 1984, Hiraba et al. 2000). The main
reason is that it is difficult to place the electrodes correctly in the target belly,
especially in the superior belly, because of the deep location and small size of the LPM
(McNamara 1973, Mahan et al. 1983, Hiraba et al. 2000). If the insertion of the
electrode to the superior belly of the LPM is too high, too deep or in an unsuitable
angle, the electrode may be placed in the deep fibers of the anterior temporal muscles
or in the inferior belly of the LPM (Juniper 1981, Widmalm et al. 1984, Orfanos et al.
1996). Therefore, it was assumed that the electrodes from the superior LPM belly were
implanted in the other muscle or other belly. Data for superior belly of the LPM might
be discarded (Mahan et al. 1983). Some special devices were used in other studies,
which attempted to standardize the trajectory for electrode placement (Koole et al.
1990, Yoshida et al. 1999, Hiraba et al.2000), but the EMG patterns of each belly of
the LPM were still not well reproducible (Hiraba et al. 2000). Other report pointed out
that there was no evidence to confirm that the electrodes were placed in the target
belly, so CT was suggested to be used as an imaging guide for insertion of the electrode
(Orfanos et al. 1995). Clinically it seems impossible to make two or more CT scans on
the patients to locate the electrode. Even if the wires are initially accurately placed in
the target muscle, the wires may be displaced and enter the adjacent muscles during
24
EMG recording (Jonsson & Bagge 1968, Wood et al. 1986). How to make a stable and
reliable EMG for the LPM is still an open question.
2.3.3 Clinical examination of the LPM
Evaluating muscle status is of primary importance in the clinical examination of
patients with masticatory pain and TMD. Muscle palpation has been widely applied as
a reliable method (Solberg 1986b, Katzberg et al. 1996, Molina et al. 2000, Isselee et
al. 2001). Intraoral palpation of the inferior belly of the LPM was considered a
standard examination method to evaluate the LPM (Schwartz & Chayes 1966). Pain
and tenderness of the LPM were recorded in many reports when using this method
(Campell et al. 1982, Wanman & Agerberg 1986, Sindet-Pedersen 1988, Ai &
Yamashita 1992). Palpation pain of the LPM was reported significantly more than of
other masticatory muscles in patients with TMD (Gross & Gale 1983). This method is
still used and referred to in current studies (Molina et al. 2000, Liu et al. 2000).
However, other reports suspected that intraoral palpation of the inferior belly of the
LPM might give an unreliable evaluation by false palpation of the superficial belly of
the medial pterygoid muscle (Johnstone & Templeton 1980). The positive result of pain
in the LPM by intraoral palpation was found to be higher than by functional
manipulation of the LPM in both asymptomatic and masticatory pain groups (Thomas
et al. 1987). An anatomical study on specimens reported that it was nearly impossible
to palpate the inferior belly anatomically. False-palpations of the medial pterygoid
muscle and the deep tendon of the temporal muscle might have happened (Stratmann et
al. 2000). Functional manipulation or provocation of the LMP was suggested to
replace the intraoral palpation method (Thomas et al. 1987, Stratmann et al. 2000).
2.3.4 Imaging of the LPM
2.3.4.1 Imaging projections
The LPM can be observed in MR images of TMJ with different imaging projections.
The identifications of imaging projections for TMJ came from the concepts of
radiography and tomography practices (Aquilino et al. 1985, Gillespy & Helms 1986,
Farman & Farman 1999). In these techniques, the projections are dependent on head
position, x-ray source and mandible position. If any of them are changed, the
morphological structures of TMJ might be altered. Some special devices were
developed to connect the relationship between patients’ heads and imaging equipment
to obtain fine-quality images (Omnell & Petersson 1976). Some studies have found that
the true coronal or sagittal plane was not the best scanning plane for showing the TMJ
(Omnell & Petersson 1976, Rosenberg & Graczyk 1986). The plane, which is
25
perpendicular or parallel to the long axis of the condyle, might show the anatomic
structures of TMJ better. Individual oblique sagittal and oblique coronal planes were
suggested (Omnell & Petersson 1976, Rosenberg & Graczyk 1986). To find the true
sagittal and coronal plane was already difficult in radiographic or tomographic
techniques, so it was not easy to make oblique images of TMJ with these techniques
(Quemar et al. 1993).
MR images are made from signals that are obtained from the three-dimensional
gradient magnetic field. Slice position of MRI can be adjusted by changing the
frequency of RF excitation. Only protons on the selected plane that are excited by RF
will contribute to the image, so-called selective irradiation. RF can be selected in any
directions in the three axes of gradient fields (Kircos & Ortendahl 1990). In the MRI
technique, oblique images of TMJ are easy to be settled (Laurell 1987, Shellock &
Pressman 1989, Musgrave et al. 1991). Furthermore, MRI allows imaging planes to be
settled in any interesting section (van Spronsen et al. 1991, Chen et al. 2000). In some
studies the anatomical cross-section and coronal planes were applied to show the
masticatory muscles in CT or in MRI (Raustia et al. 1986, Kahl-Nieke & Fischbach
1999, van Spronsen et al. 1989). The anatomical cross-section and coronal plane was
nearly perpendicular or parallel to the long axis of the masseter muscle, temporal
muscle and medial pterygoid muscle. Later studies have used the selected scanning
plane in MRI that is perpendicular to the main fibers direction of these masticatory
muscles to obtain maximal cross-section of the muscles (van Spronsen et al. 1989, van
Spronsen et al. 1991).
The LPM can be observed on coronal and sagittal MR imaging of TMJ (van
Spronsen et al. 1989, Schellhas 1989b). Sagittal and oblique sagittal images of TMJ are
the most important images in TMD diagnosis, which can show disc, condyle, fossa and
sometimes the LPM on the same film (Katzberg et al. 1985, Schellhas 1989a,b, Benito
et al. 1998). However, there are no systematic reports on whether the anatomic
structures of LPM can be shown clearly in different imaging projections.
2.3.4.2 Imaging evaluation of skeletal muscle
Imaging evaluation of the skeletal muscles can be obtained by CT, ultrasonography and
MRI. However, CT and ultrasonography provide a limited capability for tissue
characterizations. Many tissues i.e. fat, fluid, and fibrous can be well identified by MRI
(Siegelman & Outwater 1999).
The characteristics of MR imaging signal intensity of normal and diseased muscle
tissues have been reported (Weinreb et al. 1985, Murphy et al. 1986). MRI diagnosis of
hypertrophy (Bertorini et al. 1994, Jacobs et al. 1994, Petersilge et al. 1995,
Thyagarajan et al. 1998), atrophy (Kader et al. 2000, Katz & Ropper 2000) and
contracture (Chen et al. 1998) of skeletal muscles were reported in studies dealing with
pain symptoms in the calf, lower back and shoulder. These pathological changes of the
muscles were found to be associated with pain and dysfunctional symptoms. MRI has
been accepted as an important tool to evaluate muscle diseases (Shellock &
Fleckenstein 2000).
26
Imaging evaluations of masticatory muscles have also been reported.
Ultrasonography has been applied in measuring the thickness of the masseter muscle
(Raadsheer et al. 1994). CT has been used in evaluating the density changes of the
masticatory muscles (Weijs & Hillen 1984, Raustia et al. 1986, van Spronsen 1989). A
previous study found that the density changes of the LPM in CT might be more
significant than those of other masticatory muscles in patients with TMD (Raustia et al.
1998). MRI has been reported in the diagnosis of hypertrophy of the masseter muscle
(Fyfe et al. 1999, Murakami et al. 2000, Kim et al. 2000) and temporal muscle
(Gniadecka et al. 1997). Schellhas (1989b) has discussed preliminarily the
characteristics of pathological changes of the masticatory muscles in MRI. Only a few
studies have referred to the normal and abnormal findings of the LPM in MRI
(Katzberg et al. 1985, Schellhas 1989b, Quemar et al. 1993). However, systematic
studies concerning pathological changes of the LPM in MRI are lacking, and there no
reports of the relationships between the pathological findings of the LPM and clinical
symptoms of TMD.
Previous studies have shown that the LPM plays an important role in TMD. It is still
difficult and unreliable to diagnose the dysfunction and pathological changes of the
LPM by EMG and clinical examination. It seems that MRI is a promising method for
obtaining more evidence of the pathological changes of this muscle.
3 Aims of the study
The aims of this study were to investigate pathological changes of the LPM by MRI in
patients with TMD.
Specific aims were:
1. To evaluate the visibility of the lateral pterygoid muscle in MRI of TMJ with
different projections.
2. To define MRI findings of the lateral pterygoid muscle in patients with TMD.
3. To compare MRI findings of the lateral pterygoid muscle with the clinical
symptoms of TMD.
4. To compare MRI findings of the lateral pterygoid muscle and disc position of
TMJ.
5. To analyze pathological changes of the lateral pterygoid muscle in different
types of TMD.
4 Materials and methods
4.1 Materials
4.1.1 General information on patients
The analysis of the visibility of the LPM in different projections of MR imaging was
based on 28 patients with TMD symptoms (10 males, 18 females, 20-60 years of age,
mean 33.5 years) and five volunteers defined by the clinical absence, in the past of
present, of any sign or symptoms of TMD (2 males and 3 females, mean age 27.8
years) (Paper I).
The patients in other studies were based on 325 patients examined by MRI (650
TMJs; 239 females; 86 males; range 15 to 72 years; mean 41.2 years), because of TMD
(1991 – 2002). The patients had been originally referred to the Oral and Maxillofacial
Surgery Department of Oulu University Central Hospital for diagnostic examination
and treatment of TMJ problems (Papers II-IV).
The relationship between pathological changes of the LPM and condyle mobility in
MRI and clinical symptoms was based on the 98 cases with TMJ hypermobility (75
females, 23 males; range 15 to 72 years; mean 42.5 years) (Paper II).
The MRI abnormalities of the LPM in patients in late stage of TMD were based on 142
patients with bilateral or unilateral anterior disc displacement without reduction in TMJ
in MRI (176 TMJs; 106 females; 36 males; range 19 to 72 years; mean 43.9
years)(Paper III).
Studies on disc positions, condyle mobility and clinical symptoms were based on
105 patients with bilateral or unilateral TMJ hypermobility in MRI (79 females; 26
males; range 15 to 72 years; mean 41.5 years)(Paper IV).
29
4.1.2 Information from patient files
For this retrospective study, information about clinical symptoms of the patients was
obtained from the patient files. A specially designed form for recording the clinical
symptoms of TMD was used with all the patients in this study. The same form was
used in clinical follow up of the patients. The form included the following aspects,
which related to this study:
Reason for seeking treatment was recorded as the chief complaint of the patient.
Stomatognathic anamneses included TMJ symptoms (clicking, tiredness, stiffness or
pain), jaw movements symptoms (difficulty in opening, pain on opening, pain on other
jaw movements, locking or subluxation), pain in other areas (headache, pain in neck,
shoulder or back) and other dysfunctional symptoms in head and neck.
Main location of symptoms: an illustration of head and neck showed the main
location of the symptoms.
Palpation pain of the masticatory muscles: palpation of temporal muscle, masseter
muscle, medial pterygoid muscle and lateral pterygoid muscle (intraoral palpation)
were performed. All pain symptoms were recoded on three scales: slight, mild or
strong.
Symptoms on clinical examinations of TMJ included palpation pain on lateral and
posterior TMJ, restricted movement, locking, subluxation, clicking and crepitation.
Symptoms on mandibular movement. Pain and clicking during these movements
were also recorded.
Patients with collagen vascular disease or rheumatoid arthritis or severe trauma
histories, i.e. mandibular or condyle fracture were excluded from this study.
4.2 Magnetic resonance imaging technique
4.2.1 MRI equipments and parameters
Before 1991 the studies were performed with a 0.3-T magnet (Fornor β-3000 Systemy);
1991-1996 with a 1.0-T magnet (Magnetom, Siemens), and after 1996, with a 1.5-T
magnet (Signa, GE.) T1- weighted (200-400/12-20/1or2) (TR range/TE
range/excitations), T2 - weighted (2000-3000/80-200/1) and Proton Density (PD)
(2000-3000/14-30/1), with nine 3-mm-thick imaging slices, a 10X10 field of view
(FOV) and a 256X192-256 or 128X128 (in 1.0-T) matrix were used for the images.
30
4.2.2 Imaging projections
All the patients underwent bilateral MRI examinations of the TMJ with TMJ surfacecoil. Sagittal, oblique sagittal, coronal, oblique coronal and/or condyle-lateral pterygoid
muscle (CLPM) projections were used in mouth-closed position. In maximally mouthopen position, only proton density (PD) oblique sagittal or CLPM and T1- weighted
sagittal images were taken.
Scout imaging. The location of condyle and scanning planes was determined on crosssection scout imaging of TMJ. Before 2000, scout imaging was only made in mouthclosed position (Fig. 1). Scout imaging has been done in both mouth-closed and mouthopen positions since 2000.
Sagittal and coronal imaging. The scanning planes were located in anatomical sagittal
(Fig.1A) and coronal direction (Katzberg et al. 1986).
Oblique sagittal and oblique coronal imaging. The scanning planes were perpendicular
(Fig.1B) or parallel to the long axis of the condyle (Musgrave et al. 1991, Gibbs et al.
1998).
Condyle-lateral pterygoid muscle (CLPM) imaging. The scanning plane was passing
through the condyle and parallel to the long axis of the main fiber direction LPM
(Fig.1C).
4.3 Grading of MRI findings
4.3.1 Lateral pterygoid muscle
4.3.1.1 Visibility of the LPM in MRI
In order to compare findings of the LPM with disc and condyle situations, the LPM
was observed in sagittal, oblique sagittal and CLPM imaging. Three levels were used
for evaluating whether the LPM could be detected clearly in these images (Fig.2):
If two bellies of the LPM were shown clearly in the images, visibility of the LPM
was referenced as V2 (Fig.2A).
If only one belly was shown clearly in the images, visibility of the LPM was
classified as V1 (Fig.2B).
If neither belly of the LPM could be clearly observed in the images, visibility of the
LPM was V0 (Fig.2C).
Diagnosis was made only on images in which two bellies of the LPM showed
clearly, and the same pathological finding was clearly observed on at least two slices of
the image.
31
4.3.1.2 Normal MRI findings of the LPM
The normal structure of the LPM in mouth-closed MRI was seen as a fan-like muscle
from the origins of the two bellies to the neck of the mandibular condyle or the disc
(Schellhas 1989b, Quemar et al. 1993)(Fig.3). The superior belly of the LPM and the
inferior belly of the LPM were separated by an evident gap with high signal layer in the
anterior one-third near the origin sides, with a high signal layer in between (Fig.3A).
The vessel may be found in the gap between the two bellies (Fig.3B). Two bellies were
fused near the insertion of the condyle and could not be separated from each other in
the imaging (Fig.3). The signal of normal muscle tissue was homogeneous intense on
all MRI sequences (Weinreb et al. 1985, Murphy et al. 1986). In mouth-closed
position, the upper and lower edges of the two bellies of the LPM were well identified.
4.3.1.3 Abnormal MRI findings of the LPM
Hypertrophy. Enlargement and increased size of muscles with homogeneous signal on
all MRI sequences was considered to be a sign of hypertrophy of the skeletal muscles
(Schellhas 1989b, Petersilge et al. 1995, Bertorini et al. 1994). Hypertrophy of the LPM
was manifested as an obvious enlargement in the middle part of the belly, because the
two ends of the belly were connected with the bony tissues. The hypertrophic belly of
the LPM showed that the upper and lower edges of the belly changed into convex
curves (Fig.4). Side-to-side comparing of each individual was noticed in diagnosis of
hypertrophy (Fig.4).
Atrophy. Atrophy of the LPM was characterized by fatty replacement with high signals
appearing in large areas in the muscles on short and long TR/short TE images with
non-increased, or reduced size of the LPM (Schellhas 1989b)(Fig.5 &6). Atrophy of the
LPM could be well identified in PD and T2-weighted imaging (Fig.7).
Contracture. Contracture of the LPM presented as size of the muscles increased, at the
same time fibrosis could be found as low signals in the muscles on PD and T2weighted images (Schellhas 1989b)(Fig.7 & 8). Side-to-side comparing was also made
in the diagnosis of contracture (Fig.7).
Diagnosis was made only when the same pathological finding was shown clearly on
at least two slices of the image.
32
4.3.2 Disc position
Disc position was diagnosed according to Katzberg et al. (1985). Normal disc position
was defined as the juncture of posterior band of the disc, and bilaminar zone was
located at the superior or 12 0’clock position relative to the condyle (Fig.9A&B).
Anterior disc displacement was diagnosed when this juncture was anteriorly located.
Anterior disc displacement with reduction (ADDr) was demonstrated if the anterior
displaced disc could return to the top of the condyle in mouth maximal opening
position (Fig.9C&D). If the anterior displaced disc remained in anterior position of the
condyle in the maximal mouth open position, it was classified as anterior disc
displacement with nonreducing (ADDnr) (Fig.9E&F).
4.3.3 Morphology of the disc
The morphology of the disc was assessed using the biconcave shape as the normal
point of reference. Disc deformity was defined when folded, thickening changes of the
disc, convex, or posterior band enlargement of the disc was found in the images
(Yoshida et al. 2000, Milano et al. 2000, Sato et al. 1999).
4.3.4 Effusion
Effusion of TMJ defined as a high fluid signal was found in T2-weighted MR images.
According to Schellhas (1989a), Effusion might be detected either in compartments of
TMJ or in the bilaminar zone of the disc, or both.
4.3.5 Osteoarthritis
Diagnosis of osteoarthritis was made when one or more of the following signs were
present on the condyle: flattening, osteophytes, erosions and sclerosis(Westesson
1985).
4.3.6 Condyle mobility
33
Condyle mobility was classified as hypomobility (limitation), normal mobility and
hypermobility by MRI findings. For this procedure, a horizontal tangential line of the
top of the articular fossa and a vertical line through the top of the articular eminence
were made on sagittal or oblique sagittal image of TMJ. The two lines met in point
“O”. From the point “O”, the articular eminence was divided by angles into three parts:
0º-90º, 90º-120º and 120º-180º. The top of the articular fossa was at 0º and the top of
the articular eminence was at 90º (Fig.10). The diagnosis of condylar mobility was
made by measuring the location of the top of the condyle in maximal mouth-open
images.
Hypomobility or limitation of the condyle. If the top of the condyle was located in 0º90º (<90º), hypomobility or limitation of the condyle was diagnosed. In this region, the
condyle did not translate or translated only slightly (<30º), or translated but did not
reach the top of the eminence (<90º) (Fig.10A).
Normal motion of the condyle. If the top of the condyle was located in 90º-120º of the
eminence, the mobility of the condyle was considered to be normal (Fig.10B).
Hypermobility of the condyle. When the condyle translated excessively, beyond and
superior to the level of the articular eminence (>120º) (moved more than 30º from the
top of the eminence), hypermobility of the condyle could be defined (Fig.10C).
This measurement was performed according to the principles of the standards of
Benito et al. (1998) and the standards of Boering, applied by Dijkstra et al. (1993).
4.4 Statistical methods
The SPSS software (10.0) was used in statistical analyses. Pearson’s chi-square test
was used to analyze the visibility of LPM in MRI with different projections (Paper I)
and to analyze the correlations between the pathological findings of the LPM with
clinical symptoms, disc displacements and other MRI abnormalities (Papers II, III, IV).
Fisher’s exact test (when the expected values were small) was applied in analysis of the
relationships between each subgroup of pathological changes of the LPM in patients
with TMD (Paper II, III, IV). Nonparametric goodness-of-fit Chi-square test was used
to compare frequent differences of the abnormal findings in different bellies of the
LPM (Paper II). A probability value (P) of less than 0.05 was considered a significance
difference.
5 Results
5.1 Visibility of LPM in MRI
The visible rate of the LPM on sagittal and CLPM imaging of TMJ is presented in
Paper I (Tables 1and 2 in Paper I). The results indicated that the visible rate of the LPM
on sagittal images was significantly affected by the degree of mouth opening and the
location of the imaging plane. CLPM images could show the LPM constantly. In 325
patients (650 TMJs), the visibility of the LPM on 580 oblique sagittal images, 274
sagittal images and 92 CLPM images of TMJ was compared (Table 1). In 102 patients
(204 TMJs) both sagittal and oblique sagittal images were taken. In 46 patients
(92TMJs) both CLPM and oblique sagittal images were taken. The clear visible rates of
the LPM in different projections, with the two bellies being clearly observed (Fig.2),
are presented in Table 2. It showed that the clear visible rate of the LPM was
significantly higher in CLPM images (100% 92/92) and oblique sagittal images
(74.5%, 432/580) than in sagittal images (27.8%, 76/274). The very significant
differences (P<0.001, Pearson Chi-square test) were found between each group (Table
2).
Table 1. Visibility of LPM in MRI with Different Projections
Projections
V2
V1
V0
Total
CLPM
92
0
0
92
Oblique Sagittal
432
98
50
580
Sagittal
76
39
159
274
Total
600
137
209
946
LPM= lateral pterygoid muscle; CLPM= condyle-LPM projection; V2= both bellies can be
observed on image; V1= only one belly can be seen in image; V0= non-belly can be seen in
image. P<0.001 Pearson Chi-square test (df=4).
35
Table 2. Clear Visible Rate of the LPM in MRI with Different Projections
X2
V2-Rate %
Sagittal
Oblique Sagittal
CLPM
100 (92/92)
144.835***
30.106***
Oblique Sagittal
74.5 (432/580)
254.806***
Sagittal
27.8 (76/274)
LPM= lateral pterygoid muscle; CLPM= condyle-LPM projection; V2= both bellies can be
observed on image; X2= Pearson Chi-square value. ***P<0.001.
Projections
5.2 MRI findings of the LPM in patients with TMD
In 650 TMJs of 325 patients in this study, the LPM was clearly observed in 470 TMJs.
Normal imaging of the LPM was found in 28.3% (133/470) TMJs. Abnormal imaging
of the LPM was found in 71.7% (337/470) TMJs (Table 3).
Abnormal findings of the LPM included hypertrophy (Fig.4 and 6), atrophy (Fig.5, 7
and 8) and contracture (Fig. 7 and 8). Pathological changes were found in either
superior belly or in inferior belly, or both. In 35.7% (168/470) TMJs, pathological
changes of the superior belly (hypertrophy, atrophy or contracture) was found.
Hypertrophy of the inferior belly combined with hypertrophy or atrophy of the superior
belly was observed in 26.0% (122/470) TMJs. Abnormal MRI findings only in inferior
belly (7%, 33/470) were relative rarely observed. The similar results were found in
patients either with symptomatic TMJ hypermobility (Paper II) or with ADDnr (Paper
III).
36
Table 3. MRI Findings of the LPM in 470 TMJs
Findings of LPM on MRI
N=470 (100%)
Normal
133 (28.3%)
SLP abnormal
SLP hypertrophy
SLP atrophy
SLP contracture
168 (35.7%)
93
57
18
ILP Abnormal
ILP Hypertrophy
ILP Contracture
33 (7.0%)
24
9
Two bellies abnormal
Hypertrophy of SLP and ILP
SLP atrophy with ILP hypertrophy
SLP contracture with ILP hypertrophy
SLP atrophy with ILP atrophy
SLP atrophy with ILP contracture
SLP contracture with ILP atrophy
SLP contracture with ILP contracture
136 (28.9%)
70
37
15
2
8
2
2
LPM = lateral pterygoid muscle; TMJ = Temporomandibular joint, SLP= Superior belly of
the LPM; ILP= Inferior belly of the LPM
The relationship between the imaging findings of the LPM in MRI and sex and age
of the patients was presented in Tables 4 and 5. Normal and different abnormal MRI
findings of the LPM had no significant association with sex (P=0.410>0.05, df=3,
Pearson Chi-square test, Table 4) or in different age groups (P=0.710>0.05, df=15,
Pearson Chi-square test, Table 5).
Table 4. The Relationship between Sex and Imaging finding of LPM
Female
Male
Total
Normal
Hypertrophy a
A,C & Hb
A ,C c
Total
92
41
133
139
48
187
41
11
52
67
31
98
339
131
470
LPM= lateral pterygoid muscle; Normal=LPM shows normal in image
a
Hypertrophy = hypertrophy of superior or inferior or both bellies.
b
A,C & Hb = atrophy or contracture of superior and hypertrophy of inferior belly
c
A, C = Atrophy or contracture of superior or inferior or both bellies ;
Pearson Chi-square test: P=0.410>0.05
37
Table 5. The Relationship between age and Imaging finding of LPM
<20yrs
20-30yrs
30-40yrs
40-50yrs
50-60yrs
>60yrs
Total
Normal
Hypertrophy a
A,C & Hb
A,C c
Total
4
15
28
35
30
21
133
5
21
45
55
32
29
187
2
4
12
20
12
2
52
1
8
20
29
24
16
98
12
48
105
139
98
68
470
LPM= lateral pterygoid muscle; Normal=LPM shows normal in image
a
Hypertrophy = hypertrophy of superior or inferior or both bellies.
b
A,C & Hb = atrophy or contracture of superior and hypertrophy of inferior belly
c
A, C = Atrophy or contracture of superior or inferior or both bellies ;Pearson Chi-square test:
P=0.710>0.05
5.3 MRI findings of the LPM and clinical symptoms
The relationships between MRI findings of the LPM and clinical symptoms in 470
TMJs are presented in Table 6. The abnormal findings of the LPM in MRI showed very
significant association with the main clinical symptoms of TMD, i.e. jaw restricted
movement, palpation pain on TMJ, palpation pain of the LPM and pain in jaw
movement (P<0.001, Pearson Chi-square test).
The close association between pathological changes of the LPM and clinical
symptoms were also found in patients with symptomatic condyle hypermobility (Paper
II) and in patients with ADDnr (Paper III).
38
Table 6. MRI Findings of LPM in and Clinical Symptoms of Patients with TMD
LPMan
(n = 337)
LPMn
(n =133)
Total
(N=470)
P
TMJ clicking
Non-clicking
178
159
62
71
240
230
0.226
TMJ locking
Non-locking
75
262
34
99
109
361
0.444
Jaw restricted movement
Non-restricted movement
130
207
20
113
150
320
0.001***
Pain in TMJ
Non-pain in TMJ
218
119
33
100
251
219
0.001***
Pain in LPM
Non-pain in LPM
230
107
34
99
264
206
0.001***
Pain in jaw moving
Non-pain in jaw moving
205
132
32
101
237
233
0.001***
Pain in other MM
Non-pain in other MM
151
186
55
78
206
264
0.497
LPM=Lateral pterygoid muscle; TMJ=Temporomandibular joint; TMD= Temporomandibular
disorders; LPMn=LPM shows normally in MRI; LPMan= LPM shows abnormally in MRI;
MM= masticatory muscles. Pearson Chi-square test: Significant level at P< 0.05.
*** Very significant level at P<0.001.
5.4 Imaging findings of the LPM, disc position and
condyle mobility in MRI
The relationship between LPM with normal or abnormal MRI findings and disc
positions is presented in Table 7. Normal and abnormal MRI findings of the LPM
exhibited no significant difference in TMJs with or without disc displacements
(P=0.082, Pearson’s Chi-square test, df=2). Abnormal imaging of the LPM could be
observed in TMJs with disc in normal position (66.7%, 142/213)(Fig.11A) as well as
in TMJs with ADDr (76.9%, 103/134) or ADDnr (74.8%, 92/123).
39
Table 7. MRI Findings of LPM and Disc Position in Patients with TMD
LPMn
LPMan
Total
NP
ADDr
ADDnr
Total
71
142
213
31
103
134
31
92
123
133
337
470
LPM = lateral pterygoid muscle, TMJ = Temporomandibular joint, NP=disc in normal position;
ADDr= Anterior disc displacement with reduction, ADDnr= Anterior disc displacement with
non-reduction, LPMn = the LPM shows normal in MRI, LPMan = the LPM shows abnormal in
MRI, Pearson’s Chi-Square test, P=0.082>0.05
Noticeable, normal imaging of the LPM could be found in 39.4% TMJs with disc
displacement, even in some TMJs with severe osteoarthritic changes (Fig.11B).
In order to analyze the possible reason which might lead to pathological changes of
the LPM in TMJs with disc in normal position,-the relationship between disc position
and condyle mobility in MRI was investigated. The results are presented in Table 8.
Condyle hypermobility was mostly found in TMJs with disc in normal position (57.2%,
91/159). Condyle hypomobility was significantly more observed in TMJs with ADDnr
(41.8%, 66/158)(P<0.001, Pearson’s Chi-square test).
Table 8. Disc Position and Condyle Mobility in MRI in Patients with TMD
NP
Hypomobility
Normal mobility
Hypermobility
Total
50
72
91***
213
ADDr
42
36
56
134
ADDnr
66***
45
12
123
Total
158
153
159
470
LPM = lateral pterygoid muscle; TMJ = Temporomandibular joint, NP=disc in normal position;
ADDr= Anterior disc displacement with reduction, ADDnr= Anterior disc displacement with
non-reduction, Pearson’s Chi-Square test, ***P<0.001
The clinical symptoms and disc position of the patients with symptomatic TMJ
hypermobility were studied in Paper IV. Clinical symptoms of TMD were found in
TMJs either with disc in normal position or with disc displacement (Table 1 in Paper
IV). Palpation pain of the LPM was significantly associated with the clinical
symptoms in the TMJs without disc displacements (52.2%, 48/92) (P<0.001, Pearson
Chi-square test, Table 2 in Paper IV).
40
5.5 Pathological changes of the LPM in different types of TMD
5.5.1 Pathological changes of the LPM in TMJ hypermobility
Similar to all TMD patients of this work (Table 3), the TMJ-hypermobility group
(Table 4 in Paper II) showed significantly more frequently MRI abnormalities in the
superior than in the inferior belly of the LPM (P<0.001, Nonparametric goodness-of-fit
Chi-square test). Comparing with other pathological findings, hypertrophy was
significantly more often observed in the superior belly (54.9%, 28/51) (P=0.012<0.05,
Fisher’s Exact test). In TMJs with MRI pathological findings in both bellies of the
LPM (Table5 in Paper II), hypertrophy of the inferior belly combined with various
pathological changes of the superior belly (89.4%, 42/47) was observed significantly
more often found in MRI than other abnormal findings (P=0.020, Fisher’s Exact test).
In patients with condyle hypermobility, abnormal MRI findings of the LPM were
very significantly more often observed in TMJs with normal-positioned disc than in
TMJs with ADDr or ADDnr (P=0.005, Fisher’s Exact test, Table 2 in Paper II).
Abnormalities of the LPM in MRI were significantly higher in the symptomatic group
of patients (P<0.001, Pearson Chi-square test, Table 3 in Paper II).
These results (Tables 2 and 3 in Paper II) indicated that pathological changes of the
LPM might act as a main factor leading to the clinical symptoms in the TMJs without
disc displacements in patients with condyle hypermobility
5.5.2 Pathological changes of the LPM in TMJs with ADDnr
The relationships among the MRI findings of the LPM with other imaging
abnormalities on MRI of TMJs with ADDnr are presented in Table 9. MRI findings of
the LPM in MRI showed no significant associations with condylar osteoarthritic
changes, TMJ effusions or disc deformities, but they did show a highly significant
association with condyle mobility (P=0.008, Fisher’s Exact test). The proportion of the
pathological findings of the LPM was significantly lower in TMJs with ADDnr in the
condylar hypomobility group (63.6%, 42/66) than in the condylar hypermobility
(83.3%, 10/12) and the condylar normal motion groups (88.9%, 40/45).
41
Table 9. The Relationship between Pathological Changes of the LPM and other MRI
Findings of 123 with ADDnr
LPMan
(n =
92)(74.8%)
LPMn
(n
=31)(25.2%)
Total
(N=123)(100
%)
Osteoarthritis
Osteoarthritis
Non-osteoarthritis
52 (76.5%)
40 (72.7%)
16
15
68
55
Condyle mobility
Hypomobility
Hypermobility
Normal
42 (63.6%)
10 (83.3%)
40 (88.9%)
24
2
5
66
12
45
Disc deformity
Disc deformity
Non- disc deformity
31 (79.5%)
61 (72.6%)
8
23
39
84
Effusion
TMJ compartment
Bilaminar zone
TMJ & bilaminar zone
Non-effusion
12 (70.6%)
25 (73.5%)
17 (85.0%)
38 (73.0%)
5
9
3
14
17
34
20
52
P
0.634
a
0.008***
0.414
a
0.711
LPM= Lateral pterygoid muscle, TMJ= Temporomandibular joint, ADDnr= Anterior disc
displacement with non-reduction, LPMn=LPM shows normally in MRI, LPMan= LPM shows
abnormally in MRI, % (Show proportion of the LPM abnormality in each imaging finding)
=LPMan/Total, Significant level base on Pearson Chi-square test or a Fisher’s Exact test.
***Very significant level at P<0.01.
As an etiological analysis for condylar hypomobility in TMJs with ADDnr, the
relationships among condyle mobility and other MRI findings were summarized (Table
4 in Paper III). The osteoarthritic changes of the condyle were found to be significantly
associated with the hypomobility of the condyle in TMJs with ADDnr (P=0.004,
Pearson Chi-square test).
6 Discussion
6.1 Methodological considerations
6.1.1 Subjects
The study was based on 353 patients with signs and symptoms of TMD diagnosed in
the Department of Prosthetic Dentistry and Stomatognathic Physiology and the
Department of Oral and Maxillofacial Surgery between 1989 and 2002. Information
concerning patients with TMD was recorded in the specially planned study form. Case
histories of the patients were reliable, written in the files by senior lectures and/or
specialists in prosthetic dentistry of oral and maxillofacial surgery.
Clinical examinations for all the patients and volunteers in Paper I were made by the
author and another experienced clinician (M.H.). A specialist in radiology (X.H. H.)
and the author made MRI diagnoses on the patients. All the information of the patients
and images was rechecked by another experienced clinician (A.D.) and final analysis of
the materials was finished in the Departments of Head & Neck Surgery, University of
Leuven, Belgium.
The analyses in Papers II, III and IV were based on retrospective material and the
information concerning TMD was collected from patient files at the Department of
Prosthetic Dentistry and Stomatognathic Physiology, Institute of Dentistry, University
of Oulu. The author has collected and analyzed all patient files and MR images with
experienced clinicians (A.M.R. and P.T.).
The weakness of the material part of the study was the small number of normal
volunteers and asymptomatic cases (Papers I and II). Asymptomatic TMJs in the study
were selected from the asymptomatic side of the patients (Paper II). However, the focus
of the study was to analyze the MRI findings of the LPM in patients with TMD. All the
patients had evident clinical symptoms of TMD. The normal imaging of the LPM
43
found in volunteers was used as the standard to evaluate the normal MRI finding of the
LPM in patients with TMD (Paper I, Paper II). For further evaluation of MRI findings
of the LPM in normal or asymptomatic TMJs larger samples are needed, selected from
asymptomatic populations.
Several TMJ problems could be found in patients with collagen vascular disease or
rheumatoid arthritis (Koh et al. 1999) or severe trauma histories, i.e. mandibular or
condyle fracture (Thoren et al. 2001). These patients have been excluded from the
study. Collagen vascular disease, rheumatoid arthritis or severe trauma might also lead
to pathological changes of the masticatory muscles (Schellhas 1989b, Koh et al. 1999).
The main aim of the study was to define MRI findings of the LPM in patients with
TMD and to analyze the correlations between these imaging findings and clinical
symptoms, not to discuss the etiological factors behind pathological changes in the
LPM. For etiological analysis of masticatory muscle disease more factors should be
taken into consideration, e.g. general health (Schellhas 1989b, Koh et al. 1999),
maxillofacial trauma (Hu et al. 1998), parafunctional oral habits (Sari & Sonmez 2002,
Wanman & Agerberg 1986, Mahan et al. 1983), malocclusion (Ai & Yamashita 1992,
Liu et al. 2000) and mandibular retrognathia deformity (Harper et al. 1997).
6.1.2 Methods
Many studies have shown that MRI is the best method of imaging both the hard and the
soft tissues of the TMJ (Harms et al. 1985, Katzberg et al. 1986, Schellhas et al. 1986,
Raustia et al. 1995, Brooks et al. 1997, Gibbs et al. 1998). The studies have been well
documented in comparing MRI of TMJ with arthrography and CT (Schellhas et al.
1988, Liedberg et al. 1996, Trumpy et al. 1997) and in comparing the MRI findings
with anatomical and histological observations (Westesson et al. 1987a,b, Larheim et al.
1999). MR imaging diagnoses concerning disc position, effusion and osteoarthritic
changes of TMJ were made at the Diagnostic Radiology Department by radiologists.
The author rechecked all the images. The variation between the diagnoses was found to
be low.
Normal MRI findings of the LPM (Paper I and II) were based on six volunteers
defined by the clinical absence, past or present, of any signs or symptoms of TMD who
were examined by the author and other experienced clinicians (H.M. and A.M.R.).
Diagnosis of atrophy and contracture of the LPM was based on signal changes of fatty
replacement, which can be well identified in MRI (Schellhas 1989b, Benito et al. 1998,
Paper II). Hypertrophy of the LPM was diagnosed according to the size and
morphological changes of the muscle (Schellhas 1989b, van Spronsen et al. 1989).
Variations in size of the muscle between individuals might relate to many factors,
including skeletal size, age, sex and general health (Schellhas 1989b, van Spronsen et
al. 1991). Side-to-side size and morphological comparing in the same individual has
been used in the diagnosis of hypertrophy in the LPM, which can reduce and control
the individual differences (Schellhas 1989b, Paper II, Paper III). Normal and abnormal
MRI findings of the LPM were detected several times in different sessions by the
44
author. For some parts of the images normal and abnormal MRI findings of the LPM
were examined by other clinicians (J.P., A.M.R., and H.P.). Inter-and intra-observer
errors were not calculated, but the results indicate that these errors were rather small.
TMJ hypermobility is over-movement of the condyle during jaw opening (Katzberg
et al. 1982, Dijkstra et al. 1993). In previous studies, TMJ hypermobility was
diagnosed according to measurement of maximal mouth opening range (Winocur et al.
2000, Westling et al. 1992), plain film radiography (Dijkstra et al. 1993), tomography
(Katzberg et al. 1982) and MRI (Benito et al. 1998). Axiography and sonography have
also been reported in diagnosis of TMJ hypermobility (Piehslinger et al. 1995,
Bernhardt et al. 1999, Landes et al. 2000). MRI is considered to be an accurate method
for diagnosing condyle mobility and it has been used as an evaluating standard for
other methods (Benito et al. 1998, Piehslinger et al. 1995, Bernhardt et al. 1999,
Landes et al. 2000). All the patients of this study had undergone MRI for diagnosis of
TMD. Condyle mobility can be well identified in MR images of these patients, i.e.
hypomobility, normal motion and hypermobility (Fig.3) (Paper II and III). In order to
diagnose condyle mobility correctly, the patients were asked to open their mouths as
wide as possible when mouth-open images were taken. A mouth-opener was used to fix
mouth in maximal open position.
The studies in Paper II, III and IV were based on retrospective material traced back
to 1991. Intraoral palpation of the inferior belly of the LPM was still the method used
to evaluate palpation pain of the LPM. This method has been applied in many studies
(Schwartz & Chayes 1966, Campell et al. 1982, Wanman & Agerberg 1986, SindetPedersen 1988, Ai & Yamashita 1992, Molina et al. 2000, Liu et al. 2000), although
some authors suspect that this method might give an unreliable evaluation (Johnstone
& Templeton 1980, Stratmann et al. 2000, Turp & Minagi 2001). Functional
manipulation or provocation of the LMP has been suggested to replace the intraoral
palpation method (Thomas et al. 1987, Stratmann et al. 2000). Functional manipulation
of the LPM was a method to estimate the pain symptoms, which might be related to the
LPM by functional provocation rather than direct palpation (Thomas et al. 1987). The
result of the study found that the MRI abnormal findings of the LPM showed a close
association with palpation pain of the muscle (Paper II, III and IV). Whether functional
provocation could be a better method in evaluating pathological situations of the LPM
than palpation of the muscle could not be discussed in this study. However, MRI
findings of the LPM might provide further useful imaging evidence for comparing
these two methods in the future.
6.2 Visibility of the LPM in MRI
The main aim of the study reported here was to explore MRI findings of the LPM in
patients with TMD. For this purpose, the first thing was to find out whether the LPM
could be shown clearly and constantly on the images. Previous studies had discussed
some normal and abnormal imaging findings of the LPM in sagittal or oblique sagittal
MR images (Katzberg et al. 1985, Schellhas 1989a,b, Benito et al. 1998), but another
45
study reported that the findings of the LPM were not constant on the images (Schellhas
1989a). The present study found that the visibility of the LPM was evidently affected
by different imaging projections, location of imaging layers and different jaw positions
(Table 1 and 2 in Paper I).
In order to diagnose pathological changes in the superior or inferior belly of the
LPM, it was necessary to observe both bellies clearly on the images. Anatomical
studies of the LPM have reported that the anterior part of the two bellies are separated
by a space, or gap, which is filled by fibrous and adipose tissue and usually contains
the maxillary artery, but the two bellies blend, or fuse, together near the insertion
(Sicher 1965, Wilkinson 1988, Schmolke 1994, Bittar et al. 1994, Fujita et al. 2001).
Imaging of the LPM in present study agreed with these anatomical findings (Fig.2A,
Fig.4). The two bellies could be well identified on the image with the anterior gap
between the two bellies. This gap between was near the origin side of the LPM
(Fig.2A, Fig.4). When this gap was observed, it indicated that the most part of the LPM
had been shown on the image and the image was suitable for diagnosis of
morphological and signal intensity changes for each belly (Fig.2A). Oppositely, if only
the insertion part of the LPM was shown on the images, the two bellies could not be
separately identified. The evaluation of the LPM could not be made according to these
images (Fig.2 B and C).
Clear visible rate of the LPM with two bellies observed in MRI was significantly
higher in CLPM (100%, 92/92) and oblique sagittal images (74.5%, 432/580) than in
sagittal images (27.8%, 76/274)(Table 2). The long axis of the LPM running angularly
to the sagittal plane was considered to be the main reason behind these differences
(Quemar et al. 1993, Paper I). The angle between the long axis of the LPM and sagittal
or oblique sagittal plane could be observed clearly on cross-section imaging (Fig.1 A
and B). When the angle became smaller, the trend of scanning plane was towards
parallel to the long axis of the LPM, and more parts of the muscle could be scanned
(Fig. 1), the better the visibility of the muscle on the images that might be obtained.
The oblique sagittal scanning plane was nearer to the parallel sections of the long axis
of LPM than the true sagittal plane (Fig.1 A and B). In CLPM projection the angle
between the long axis of the LPM and scanning became zero (Fig.1C). It seemed that
the CLPM and oblique sagittal images of TMJ was suitable for evaluating the LPM.
In some studies axial cross-section and coronal planes have been applied in MRI to
investigate the masticatory muscles, including the LPM (Kahl-Nieke & Fischbach
1999, van Spronsen et al. 1989, van Spronsen et al. 1991).
The axial cross-sectional and coronal plane are nearly perpendicular or parallel to the
long axis of the masseter muscle, temporal muscle and medial pterygoid muscle, but
the LPM runs angular to these planes. On axial cross-sectional imaging, the location
and the running direction of the main fibers of the LPM can be observed (Paper I,
Quemar et al. 1993). However, only the upper part of the superior belly was shown on
the image (Fig.1). For this reason, the axial cross-section image may be not suitable for
detecting the imaging abnormalities in both bellies of the LPM. The LPM runs from the
origins to the insertion with a fan shape (Paper I, Quemar et al. 1993, van Spronsen et
al. 1989).
Coronal or oblique coronal imaging planes are near to the cross-section plane of the
LPM (van Spronsen et al 1989, Gibbs et al. 1998). van Spronsen et al. pointed out that
46
for a fan-shaped muscle, such as the temporal muscle and the LPM, a small shift of the
scanning plane might result in a considerable changes in areas, or size, of the muscle in
cross-section imaging, so these muscles are more susceptible to scan or patientpositioning errors in cross-section scanning (van Spronsen et al. 1989). Other authors
have excluded the cross-section imaging of the temporal muscle and the LPM from
their study, because it is possible to make false evaluations (Hannam & Wood 1989).
Neither coronal nor axial cross-sectional imaging of TMJ can show the relationship
between the LPM and the disc. However, CLPM and oblique sagittal images of TMJ
can show the condyle, disc and the LPM in the same image.
The imaging diagnoses of the LPM in this study were based on images with the two
bellies clearly and in mouth-closed position. In mouth opening images, the length and
width of the LPM is altered, which may affect the morphological evaluation of the
muscle (Paper I, Quemar et al. 1993). The morphological characteristics of the LPM in
mouth-open imaging need further researches in future.
6.3 Pathological changes of the LPM and clinical symptoms of TMD
In the studies reported here, different types of imaging pathological changes in LPM
were found in patients with TMD, i.e. hypertrophy (Fig.5), atrophy (Fig.6,7,8) and
contracture (Fig.8,9). These pathological changes were found in the superior belly,
inferior belly or both (Table 3). The MRI abnormal imaging of the LPM might be
found in either male or female or in different ages groups of the patients with TMD
(Tables 4 and 5).
In studies of other skeletal muscles, the MR imaging abnormalities of the muscles
have been reported associated with chronic pain symptoms in the leg, back and
shoulder, possibly leading to abnormal and dysfunctional movements of the related
joints (Bertorini et al. 1994, Jacobs et al. 1994, Chen et al. 1998, Thyagarajan et al.
1998, Katz & Ropper 2000, Kader et al. 2000). These pathological changes and clinical
symptoms are in some way similar to TMD.
In an anatomical study on autopsy specimens, Schmidt et al. (1998) observed that
the single trunk of the auriculotemporal nerve was evident along the medial aspect of
the condylar neck and was in direct contact with the condylar neck at the posterior
border of the LPM. The anteriorly dislocated disc and displaced capsular tissue were
considered to produce nerve irritation and to cause painful symptoms. In addition, the
authors proposed that hypertrophy of the LPM might also lead to entrapment or
compression of the nerve. However, in their study hypertrophy of the LPM was only
expected, but not being proved (Schmidt et al. 1998). In the studies reported here,
hypertrophy of the LPM was observed in MRI in patients with TMD (Fig.5,7)(Table
3).
When analyzing the relationship between atrophy and contracture of the LPM in
MRI and clinical symptoms of TMD, Schellhas (1989b) reported that atrophy and
contracture of the muscle might lead to painful symptoms in the muscles, abnormal
47
joint movements and pain on TMJ movement, which might be considered pain-induced
reflex sympathetic dystrophy.
The results of these earlier studies (Schellhas 1989b, Schmidt et al. 1998) agreed
with the present findings that pathological changes of the LPM in MRI were associated
with main symptoms of TMD (Table 6). It indicates that patients might complain of
these symptoms when pathological changes of the LPM are observed in MRI.
6.4 Pathological changes of the LPM in different types of TMD
6.4.1 Pathological changes of the LPM and disc displacements
Excessive exercise, overloading, abnormal stretching (Bertorini et al. 1994), minor
trauma (Thyagarajan et al. 1998), and denervation disease (Petersilge et al. 1995) have
been mentioned as possible factors contributing to muscle hypertrophy. Atrophy and
contracture of the muscles have generally been considered to be caused by disuse and
denervation (Thyagarajan et al. 1998). Collagen vascular disease or rheumatoid
arthritis may also affect masticatory muscles (Koh et al. 1999). If patients have no
history of severe trauma, collagen vascular disease, debilitating diseases or denervation
disease, atrophy or contracture of muscles are considered to be the secondary changes
of excessive muscle activity, stretching and work overload (Thyagarajan et al. 1998,
Kader et al. 2000). This was most likely the situation of the patients with TMD in this
study.
The pathological changes of the LPM in TMD need to be discussed on the basis of
the function of LPM. The functional activity of LPM is not fully understood, but most
EMG studies support the notion that the superior belly of the LPM is active during jaw
closing and clenching movements to act against biting force and to stabilize the
relationship between the condyle and the disc. The inferior belly of the LPM is active
during mouth opening, protrusion of the mandible, and movement of the mandible to
the contralateral side (Mahan et al. 1983, Lafreniere et al. 1997, Hiraba et al. 2000). In
case of excessive exercise, overloading or minor trauma in functional activities of the
LPM, pathological changes of the muscle may occur.
Farrar and McCarty described micro- and macrotrauma in internal derangement of
TMJ (Farrar and McCarty 1979). The abnormal disc-condyle relationship was regarded
as the factor leading to traumas and damage of TMJ structures (Farrar and McCarty
1979, Farrar 1971). Many studies have found abnormal positions of the disc to be
associated with disc deformities (Yoshida et al. 2000, Taskaya-Yilmaz & OgutcenToller 2001), disc degenerative changes (Widmalm et al. 1992, Kondoh et al. 1998)
and osseous changes of the condyle (Westesson 1985, Kurita et al. 2000, Bertram et al.
2001). The abnormal relationship between disc and condyle is considered to be
associated with pain symptoms in TMD (Emshoff et al. 2001). The results of these
studies indicate that disc displacement may lead to abnormal and unstable condyle-disc
relationships in jaw movements. Under this situation, the superior belly of the LPM has
to work excessively to keep the relationship between condyle and disc stable
48
(Lafreniere et al. 1997). Excessive work or overloading may lead to hypertrophy and
secondary atrophy or contracture of the muscle. It can explain the findings of this study
that imaging abnormalities of the LPM were found in 76.8% (103/134) TMJs with
ADDr and 74.8% (92/123) TMJs with ADDnr (Table 7). It may also explain the
finding of this study that pathological changes of the superior belly of the LPM were
more often observed than other imaging abnormalities in MRI in the patients with disc
displacements (Table 1 in Paper III).
However, imaging abnormalities of the LPM were not only found in TMJs with disc
displacements but also in 66.7% (142/213) TMJs with disc in normal position in the
material of this study (Fig.11A). There is no significant difference between the
distribution of pathological changes of the LPM in TMJs with or without disc
displacements (Table 7). Obviously, disc displacements cannot explain pathological
changes of the LPM and possible related symptoms in TMJs with the disc in normal
position.
6.4.2 Symptoms of the LPM in TMJs with disc in normal position
TMD symptoms in TMJs with disc in normal position have been noticed in some other
studies (Muller-Leisse et al. 1996, Benito et al. 1998, Bernhardt et al. 1999, Emshoff et
al. 2001). The prevalence of TMJs with clinical symptoms but with normally
positioned disc was 10.2% to 19% in these studies. Benito et al. (1998) have analyzed
the relationships between the clinical symptoms of TMD, disc movement and condyle
translation by MRI. The study found that pain symptoms of TMJ with or without disc
displacements might relate to static disc during the jaw movements. However, normal
positioned discs with static in movement were rare (Benito et al. 1998).
Abnormal translations of the condyle, either hypomobility or hypermobility, have
been discussed as the important factor that may be related to the symptoms of TMD in
many studies (Katzberg et al. 1982, Westling 1989, Bernhardt et al. 1999, Landes et al.
2000). TMJ hypermobility is regarded as a subgroup diagnosis in early stage of TMD
(Wilkes 1989, McNeill et al. 1990). Katzberg et al. (1982) investigated 102 TMJs with
internal derangements by arthrotomography and found that in 28 patients who had
ADDr with painful clicking they were combined with condyle hypermobility. Other
reports have also considered TMJ hypermobility to be associated with disc
displacements, because the patients experienced clicking or painful clicking (Westling
1989, Westling et al. 1992, Holmlund et al. 1999). The study carried out by Katzberg
et al in 1982 was based on patients with internal derangements. TMJs with the disc in
normal position might have been excluded from the study. Clicking may not be a
reliable sign to determine disc displacements. Some studies have found that the
clicking in TMJs with hypermobility might not be associated with disc displacements
(Solberg 1986b, Buckingham et al. 1991, Khan & Pedlar 1996). These reports consider
that condyle hypermobility may be caused by laxity of capsular structures, and joint
laxity may lead to joint clicking even without disc displacements (Solberg 1986b, Khan
& Pedlar 1996). It seems that more detailed information is needed in comparing disc
49
positions and related symptoms in TMJs with condyle hypermobility with a reliable
method, such as MRI.
Disc positions and condyle mobility were analyzed in this study (Table 8). In 57.2%
(91/159) of TMJs with condyle hypermobility the disc was in normal position, which
was observed significantly more frequently than ADDr and ADDnr. The clinical
symptoms of TMJs with condyle hypermobility have no significant difference in TMJs
with or without disc displacements (Table 1 in Paper IV). It seems that TMJs with disc
in normal position may have clinical symptoms as well as the joints with the disc
displacements when condyle hypermobility has occurred. Painful clicking was the main
symptom of these joints (Table 1 in Paper IV). It was found that in TMJs with disc in
normal position the painful symptoms were originated mainly from the LPM (Table 2
in Paper IV). This indicates that hypermobility of the condyle and related pathological
changes of the LPM may play important roles leading to clinical symptoms in TMJs
with the disc in normal position.
6.4.3 Pathological changes of the LPM in TMJ hypermobility
Clinically, different terms have been used to denote TMJ hypermobility, such as
recurrent luxation of TMJ (Holmlund et al. 1999), recurrent mandibular dislocation
(Undt et al. 1997) or recurrent subluxation of TMJ (Sacks et al. 1990). The most
common clinical complaint of symptomatic condyle hypermobility is clicking with
painful symptoms related to TMJ and masticatory muscles (Katzberg et al. 1982,
Dijkstra et al. 1993, Holmlund et al. 1999). Similar clinical symptoms of TMJs with
condylar hypermobility were also found in present study (Papers II and IV).
MRI abnormal findings of the LPM were significantly more often observed in TMJs
with disc in normal position (Table 2 in Paper II). The abnormalities of the LPM were
also significantly more often found in the TMJs with symptomatic hypermobility
(Paper II, Table 3). These findings show that pathological changes of the LPM and
condyle hypermobility may play important roles in giving rise to the symptoms in the
TMJs with the disc in normal position.
From the etiological point of view, the loose connective tissues and ligaments around
joints are considered to lead to TMJ hypermobility as well as generalized joint laxity
(Westling 1989, Westling et al. 1990, Sacks et al. 1990, Buckingham et al. 1991,
Westling et al. 1992, Winocur et al. 2000). Laxity of the joint structures may
destabilize the condyle-disc relationship in TMJ (Dijkstra 1993, Westling et al. 1992).
Under this condition, as a possible explanation for the findings of this study, the
superior belly of LPM might have an abnormal over-loading in order to keep the
structures stable, which might cause excessive exercised hypertrophy of the belly. In an
anatomical study of the TMJ, Grunert et al. (2000) noticed that the evident hypertrophy
in the superior belly of LPM was observed in some TMJs with normal-positioned disc.
He also suspected that hypertrophic changes of the superior belly of LPM might be
caused by chronic overloading.
50
Minor trauma may also cause local muscle hypertrophy, chronic pain and chronic
spasms (Thyagarajan et al. 1998). Condyle hypermobility may lead to microtrauma of
TMJ (Farrar 1971, Bernhardt et al. 1999). Westling et al. (1990) pointed out that lax
joints provide less protection against microtrauma and macrotrauma. The results of
anatomical studies show the superior belly of LPM inserting into condyle and the
capsule (Wilkinson 1988, Heylings et al. 1995, Naidoo 1996). When the condyle is
hypermobilized on mouth opening, the condyle may press the anterior part of the
capsule where the insertion of the superior belly of LPM is located (Fig.3c). This
pressure might cause a microtrauma directly to the superior belly. From the anatomical
point of view, it could be hypothesized that the microtrauma caused by the
hypermobilized condyle may also be a possible factor causing hypertrophy of the
superior belly of the LPM and associated clinical symptoms.
Prolonged chronic overloading or microtrauma might act as factors causing atrophic
changes of the muscle as observed in this study. Atrophy or contracture of muscles is
regarded as secondary changes of excessive muscle activity, stretching and work
overload when there is no history of disuse after trauma, immobility, debilitating
disease or denervation disease involved (Bertorini et al. 1994).
It could be assumed that laxity of the joint structures and possible minor trauma
caused by a hypermobile condyle might lead to pathological changes of the LPM, even
in TMJs with the disc in normal position (Table 2 in Paper II).
6.4.4 Pathological changes in the two bellies of the LPM
Another characteristic feature of pathological changes in the LPM observed in this
study was that hypertrophy of the inferior belly combined with various pathological
changes of the superior belly of LPM affected both bellies significantly more often than
other imaging abnormalities (Table 3). This finding might agree with the result of the
EMG study of LPM by Lafreniere et al (1997). They found that EMG activity of the
inferior belly was significantly higher when the superior belly of LPM seemed to have
lost its disc-stabilizing function. The inferior belly was considered to adapt its function
to instead of the hypo-functional superior belly. The excessive work of the inferior
belly might occur after the superior belly becomes hypo-functional under chronic
overloading and might result in secondary hypertrophy of the inferior belly. This is
supported by the present results which show that atrophy or contracture of the superior
belly combined with hypertrophy of the inferior belly was found in 38.2% (52/136) of
the TMJs with MRI abnormal findings in the two bellies (Table 3).
Unstable movement between condyle and disc, which may be caused by disc
displacement or laxity structures, might also directly affect the inferior belly of the
LPM. Some histological and anatomical studies on autopsy specimens have found not
only the superior belly but also some fibers of the inferior belly inserting into the
capsular tissues near the disc (Schmolke 1994, Bittar et al. 1994, Fujita et al. 2001). It
has been suggested that both bellies of the LPM may influence, or be influenced by, the
stable position of the disc on jaw movements (Schmolke 1994). This means that
51
unstable relationship between disc and condyle might lead to excessive work of both
bellies. In MRI, hypertrophy in both bellies of the LPM has been observed in 51.5%
(70/138) TMJs with pathological changes in bellies in this study (Table 3) (Fig.6 in
Paper II and Fig.7 in Paper III).
6.4.5 Pathological changes of the LPM in late stage of TMD
In this study, it was found that the pathological MRI changes of the LPM show a close
association with symptomatic condyle hypermobility (Table 3 in Paper II). As a
comparative analysis, it was worthwhile to investigate the LPM in TMJs with condyle
hypomobility. Many studies have reported that hypomobility of the condyle occurs
more often in TMJs with ADDnr (Katzberg et al. 1982, Wilkes 1989, Schellhas 1989a,
Westesson 1993). This was found in present study also (Table 8).
Many studies have considered ADDnr to be the advanced stage, or late stage of
TMD (Katzberg et al. 1982, Wilkes 1989, Schellhas 1989a, Westesson 1993).
Condylar osteoarthritic changes, hypomobility of condyle, TMJ effusion and disc
deformities were reported as main MR imaging abnormalities in the joints with ADDnr
(Westesson et al. 1984, Westesson et al 1985, Kurita et al. 2000, Emshoff et al. 2001,
Taskaya-Yilmaz and Ogutcen-Toller 2001). Hypomobility of the condyle has been
regarded as a progressive symptom of TMD (Wilkes 1989, Benito et al. 1998, Yoshida
et al. 2000). In this study, MRI abnormal findings of the LPM were found in 74,8 %
(92/123) of TMJs with ADDnr. The present TMJs with ADDnr showed a close
association with condyle hypomobility. Interestingly, statistical analysis of this study
showed, however, that the proportion of the LPM abnormality was significantly lower
in the condylar hypomobility group (Table 9). Moreover, in some cases, although
evident osteoarthritic changes and limitation of the condyle were observed, the LPMs
showed as normal (Fig. 11B and Figs. 10-12 in Paper III).
Osteoarthritic changes were suspected as a closely associated factor for condyle
hypermobility in the study (Table 4 in Paper III). Benito et al. (1998) reported that the
movement of disc was poor in TMJ with osteoarthritis. They found that hypomobility
of the condyle was significantly associated with the static disc. Adhesion of the disc
was suspected. When the possibility of condyle movement becomes poor due to a fixed
disc (Benito et al. 1998) or because adhesion has occurred between osteoarthritic bony
tissues and disc (Schellhas 1989a, Eberhard et al. 2000), the relationship between the
disc and the condyle might become relatively stable. The overloading of the LPM
might be reduced because of condylar hypomobility. That may lead to pathological
changes of the LPM reduced in TMJs with ADDnr as observed in this study (Table 9).
Understandable, the symptoms associated with the LPM could be released. Condylar
hypomobility was considered to be a pathway for ADDnr (Wilkes 1989, Westesson
1993), the symptom, especially the symptom concerned with the LPM, probably is
possible to be released in the later stage of TMD. This finding may explain the results
of other reports that the clinical symptoms may be released in some TMJs with ADDnr
52
even without treatment (Lundh et al. 1992, Kurita et al. 1998, Sato et al. 1998, Sato et
al. 1999).
In this study the MRI abnormal findings of the LPM seemed independent of joint
effusion, osteoarthritic changes on the condyle and disc deformities (Table 9). This
suggests that osteoarthritic changes, joint effusion and disc deformities may not be
improved even if pathological changes and the related symptoms of the LPM had been
relieved. These findings provide imaging evidence to verify the results of other studies,
which found that the clinical symptoms of TMJs with ADDnr may trend to be relieved
with or without treatment, but that disc displacement, disc deformity and osseous
changes of the joint do not change (Montgomery et al. 1992, Kurita et al. 1998, Sato et
al. 1999, Nishimura et al. 2001). The alteration of the pathological situations in the
LPM found in this study may also explain why internal derangement and degenerative
changes inside of TMJ shows as a progressive damaging procedure, oppositely, clinical
symptoms might show as a chronic, gradually released procedure (Wilkes 1989).
7 General discussion
Since the time Costen (1934) reported this syndrome until now, many aspects in the
diagnosis and treatment of TMD have been controversial and continue to be an area for
debate. Etiology of TMD is still poorly understood (Sherman and Turk 2001).
Although several defined terms are based on different etiology (Costen 1934, Laskin
1969, Thompson 1971, McNeill 1990) similar signs and symptoms are presented,
comprising a number of clinical problems that mainly involves two aspects: the
masticatory muscles and/or the temporomandibular joint (Westesson 1993).
Within the last 20 years, improvements of imaging methods in TMJ using
arthrography and MRI have led to increasingly accurate diagnosis of disc position
(Wilkes 1978a, Katzberg et al. 1979, Westesson et al. 1980, Harms et al. 1985,
Schellhas et al. 1986). Studies on TMD are in many aspects profound. Disc
displacements in TMJ are considered to be factors which may lead to disc deformities,
osseous changes and clinical symptoms of TMD (Westesson 1985, Farrar & McCarty
1979, Katzberg et al. 1996, Yoshida et al. 2000, Bertram et al. 2001). These imaging
findings have been proved right by surgical observations (Wilkes 1978 a, b, Schellhas
1989a) as well as histological and anatomical studies in autopsy specimens (Westesson
& Rohlin 1984, Larheim et al. 1999, Leonardi 2001). All these studies have provided
more and more evidence in the diagnosis of TMD. It should be noticed that these
studies focus mainly on disc displacements.
In comparison, research on the masticatory muscles concerning TMD is still under
development (Helkimo 1974a, b, Solberg 1986a, De Laat 1998, Greene 2001). Among
the masticatory muscles, the LPM is considered to play an important role in TMD
procedures (Juniper 1984, Lafreniere et al.1997, Raustia et al. 1998). However, the
LPM is a deep located muscle and it is difficult to detect by either clinical examination
or EMG (Stratmann et al. 2000, Hiraba et al. 2000). Normal and abnormal functions of
the LPM have been discussed in EMG studies, but they still remain unclear (Hiraba et
al. 2000). More visible evidence is needed to diagnose pathological changes of the
muscle.
Clinical studies concerning the skeletal muscles have shown that MRI is a reliable
imaging method for diagnosing muscle diseases (Weinreb et al. 1985, Schellhas 1989b,
54
Shellock & Fleckenstein 2000). The main questions explored in the study reported here
areas follows: whether MRI can detect pathological changes of the LPM; what kinds of
pathological changes of the LPM may appear in TMD; the characteristics of these
pathological changes and associated clinical symptoms. No reports on these appear in
previous studies.
The results of this study show that the visibility of the LPM in MRI is influenced by
imaging projections (Paper I). Imaging diagnosis of pathological changes of the LPM
should be based on images that can show both bellies clearly and be less affected by
shifting of the scanning plane. According to the anatomic characteristics of the LPM,
the more nearly parallel the scanning plane is to the long axis of the LPM, the clearer
the observation of the muscle that can be obtained (Paper I, Quemar et al. 1993). A
new imaging projection-CLPM projection for TMJ and the LPM is reported in this
study, going through the condyle and parallel to the long axis of the LPM (Paper I). It
is able to show the LPM constantly in either mouth closed or mouth opening images
(Paper I). It appears that most of the CLPM and oblique sagittal images of TMJ can
show the LPM and joint structures clearly. The characteristics of CLPM images need to
be discussed with a more extensive patient material in further studies (Paper I, Quemar
et al. 1993).
Normal imaging of the LPM, hypertrophy, atrophy and contracture of the muscle in
patients with have been described in the studies reported here (Papers I-III). It appears
that pathological changes of the superior belly and hypertrophy of the inferior belly
combined with various abnormalities of the superior belly are the most frequently
findings in the LPM of the patients with TMD (Papers II and III). These findings may
provide imaging evidences for diagnosis of pathological changes of the LPM in TMD.
Muscular diseases may lead to pain symptoms, and abnormal functional movements
of the related joints have been confirmed in studies concerning the leg, shoulder and
back (Bertorini et al. 1994, Jacobs et al. 1994, Chen et al. 1998, Thyagarajan et al.
1998, Katz & Ropper 2000, Kader et al. 2000). Similarly, close associations are found
between the imaging abnormalities of the LPM and the clinical symptoms of TMD in
the studies reported here (Papers II and III). This indicates that the imaging findings of
the LPM may explain the clinical symptoms of TMD and their alterations.
There are two other important findings in this study. One is that condyle
hypermobility and related pathological changes of the LPM may play an important role
in giving rise to the clinical symptoms in TMJs with disc in normal position (Papers II
and IV). The other is that imaging abnormalities of the LPM are significantly reduced
in condyle hypomobility cases in TMJs with ADDnr even osteoarthritis and disc
deformities may occur in these cases (Paper III). Imaging abnormalities may be found
in TMJs with disc in normal position, but normal imaging of the LPM may be observed
in TMJs with severe disc displacement, osteoarthritic changes and disc deformity
(Fig.11). These findings may give some imaging evidence for understanding clinical
symptoms that cannot be totally explained by disc displacements. The recognition of
muscle alterations may lead to a correct diagnosis and improved understanding of the
clinical symptomatology and disease pathophysiology under investigation (Schellhas
1989b). MRI findings of the LPM may provide more evidence for etiological study of
pain symptoms in TMD.
55
Many treatments have been reported to release muscle pain in TMD, e.g. splint
treatment (Dao & Lavigne 1998, Williamson & Rosenzweig 1998), manual therapy
(Nicolakis et al. 2001), biofeedback and cognitive-behavioural therapy (Sherman &
Turk 2001). However, proof of pathological changes of the masticatory muscles still
seem to be lacking in these studies (Nicolakis et al. 2001, Williamson & Rosenzweig
1998). MRI findings of the LPM may offer a useful tool for diagnosis and give
important information to evaluate the clinical efficacy of these different treatment
procedures.
Obviously, histological confirmation of the imaging pathological findings in the
LPM is very important and further research is needed in future.
8 Conclusions
1.
2.
3.
4.
5.
CLPM images and most oblique sagittal images of TMJ are able to show two
bellies of the LPM more clearly than straight sagittal images and they are
recommended to be used in the evaluation of the LPM.
In MRI, hypertrophy, atrophy and contracture are found in the LPM of the
patients with TMD. Pathological changes of the superior belly and
hypertrophy of the inferior belly combined with various pathological changes
of the superior belly are the most frequently observed abnormal MRI findings
of the LPM in TMD.
MRI abnormalities of the LPM show close associations with the main
symptoms of TMD, i.e. jaw movement pain, palpation pain in the LPM,
restricted jaw movement and palpation pain in TMJ.
In patients with TMD, pathological changes of the LPM may be found in
TMJs with or without disc displacements. Abnormal MRI findings may be
observed in TMJs with disc in normal position. Normal imaging of the LPM
can be found in TMJs with disc displacement and severe osteoarthritic
changes.
In different types of TMD, condyle hypermobility and related pathological
changes of the LPM may play an important role in giving rise to the clinical
symptoms in TMJs with disc in normal position. Imaging abnormalities of the
LPM are significantly reduced in condyle hypomobility related to TMJs with
ADDnr, which may explain the improvement of clinical symptoms in these
cases.
9 References
Agerberg G, Carlsson GE. (1975) Symptoms of functional disturbances of the masticatory
system. A comparison of frequencies in a population sample and in a group of patients. Acta
Odontol Scand. 33(4):183-90.
Ai M, Yamashita S. (1992) Tenderness on palpation and occlusal abnormalities in
temporomandibular dysfunction. J Prosthet Dent. 67(6):839-45.
Aquilino SA, Matteson SR, Holland GA, Phillips C. (1985) Evaluation of condylar position
from temporomandibular joint radiographs. J Prosthet Dent. 53(1):88-97.
Arat ZM, Gokalp H, Erdem D, Erden I. (2001) Changes in the TMJ disc-condyle-fossa
relationship following functional treatment of skeletal Class II Division 1 malocclusion: a
magnetic resonance imaging study. Am J Orthod Dentofacial Orthop. 119(3):316-9.
Avrahami E, Horowitz I, Cohn DF. (1984) Computed tomography of the temporo-mandibular
joint. Comput Radiol. 8(4):211-6.
Aziz MA, Cowie RJ, Skinner CE, Abdi TS, Orzame G. (1998) Are the two heads of the human
lateral pterygoid separate muscles? A perspective based on their nerve supply. J Orofac
Pain. 12(3):226-39.
Barkin S, Weinberg S.(2000) Internal derangements of the temporomandibular joint: the role of
arthroscopic surgery and arthrocentesis. J Can Dent Assoc. 66(4):199-203. Review.
Benito C, Casares G, Benito C. (1998) TMJ static disk: correlation between clinical findings
and pseudodynamic magnetic resonance images. Cranio. 16(4):242-51.
Bernhardt O, Schwahn B, Meyer G. (1999) Craniomandibular disorders--comparative
investigations with clinical examination and electronic axiography. Anat Anz. 181(1):51-3.
Berrett A. (1983) Radiology of the temporomandibular joint. Dent Clin North Am. 27(3):52740.
Bertilsson O, Strom D. (1995) A literature survey of a hundred years of anatomic and functional
lateral pterygoid muscle research. J Orofac Pain. 9(1):17-23.
Bertorini T, Woodhouse C, Horner L. (1994) Muscle hypertrophy secondary to the tethered
cord syndrome. Muscle Nerve. 17(3):331-5.
Bertram S, Rudisch A, Innerhofer K, Pumpel E, Grubwieser G, Emshoff R. (2001) Diagnosing
TMJ internal derangement and osteoarthritis with magnetic resonance imaging. J Am Dent
Assoc. 132(6):753-61
58
Bittar GT, Bibb CA, Pullinger AG. (1994) Histologic characteristics of the lateral pterygoid
muscle insertion to the temporomandibular joint. J Orofac Pain. 8(3):243-9.
Blaschke DD, Blaschke TJ. (1981) Normal TMJ bony relationships in centric occlusion. J Dent
Res. 60(2):98-104.
Bonilla-Aragon H, Tallents RH, Katzberg RW, Kyrkanides S, Moss ME. (1999) Condyle
position as a predictor of temporomandibular joint internal derangement. J Prosthet Dent.
82(2):205-8.
Brand JW, Whinery JG Jr, Anderson QN, Keenan KM. (1989) The effects of
temporomandibular joint internal derangement and degenerative joint disease on
tomographic and arthrotomographic images. Oral Surg Oral Med Oral Pathol. 67(2):220-3
Brand JW. (1990) Temporomandibular joint arthrography. In: DelBalso AM, ed. Maxillofacial
imaging. Philadelphia: WB Saunders Co. 635-52.
Brooks SL, Westesson PL, Eriksson L, Hansson LG, Barsotti JB. (1992) Prevalence of osseous
changes in the temporomandibular joint of asymptomatic persons without internal
derangement. Oral Surg Oral Med Oral Pathol. 73(1):118-22.
Brooks SL, Brand JW, Gibbs SJ, Hollender L, Lurie AG, Omnell KA, Westesson PL, White
SC.(1997) Imaging of the temporomandibular joint: a position paper of the American
Academy of Oral and Maxillofacial Radiology. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 83(5):609-18.
Buckingham RB, Braun T, Harinstein DA, Oral K, Bauman D, Bartynski W, Killian PJ, Bidula
LP. (1991) Temporomandibular joint dysfunction syndrome: a close association with
systemic joint laxity (the hypermobile joint syndrome) Oral Surg Oral Med Oral Pathol.
72(5):514-9.
Campbell CD, Loft GH, Davis H, Hart DL. (1982) TMJ symptoms and referred pain patterns. J
Prosthet Dent. 47(4):430-3.
Carraro JJ, Caffesse RG, Albano EA. (1969) Temporomandibular joint syndrome. A clinical
evaluation. Oral Surg Oral Med Oral Pathol. 28(1):54-62
Chen CK, Yeh L, Chen CT, Pan HB, Yang CF, Resnick D. (1998) Contracture of the deltoid
muscle: imaging findings in 17 patients. AJR Am J Roentgenol. 170(2):449-53.
Chen YJ, Gallo LM, Meier D, Palla S. (2000) Individualized oblique-axial magnetic resonance
imaging for improved visualization of mediolateral TMJ disc displacement. J Orofac Pain.
14(2):128-39.
Cholitgul W, Petersson A, Rohlin M, Tanimoto K, Akerman S. (1990) Diagnostic outcome and
observer performance in sagittal tomography of the temporomandibular joint.
Dentomaxillofac Radiol. 19(1):1-6.
Cohen H, Ross S, Gordon R. (1985) Computerized tomography as a guide in the diagnosis of
temporomandibular joint disease.J Am Dent Assoc. 110(1):57-60
Costen JB. (1997) A syndrome of ear and sinus symptoms dependent upon disturbed function
of the temporomandibular joint. 1934. Ann Otol Rhinol Laryngol. 106(10 Pt 1):805-19.
Dao TT, Lavigne GJ. (1998) Oral splints: the crutches for temporomandibular disorders and
bruxism? Crit Rev Oral Biol Med. 9(3):345-61.
De Laat A. (1998) Scientific basis of masticatory disorders. In: Linden RWA, ed. The scientific
basis of eating. Front Oral Biol. Basel, Karger, (9);122-134.
De Laat A. (2000) Temporomandibular disorders as a source of orofacial pain. Acta Neurol
Belg. 101(1):26-31.
DelBalso AM. (1990) Radiography of the temporomandibular joint. In: DelBalso AM, ed.
Maxillofacial imaging. Philadelphia: WB Saunders Co. 607-634.
Dijkstra PU, de Bont LG, de Leeuw R, Stegenga B, Boering G (1993) Temporomandibular joint
osteoarthrosis and temporomandibular joint hypermobility. Cranio. 11(4):268-75.
Eberhard D, Bantleon HP, Steger W. (2000) Functional magnetic resonance imaging of
temporomandibular joint disorders. Eur J Orthod. 22(5):489-97.
59
Eckerdal O, Lundberg M. (1979) The structural situation in temporomandibular joints. A
comparison between conventional oblique transcranial radiographs, tomograms and
histologic sections. Dentomaxillofac Radiol. 8(1):42-9.
Emshoff R, Innerhofer K, Rudisch A, Bertram S. (2001) Relationship between
temporomandibular joint pain and magnetic resonance imaging findings of internal
derangement. Int J Oral Maxillofac Surg. 30(2):118-22.
Farman TT, Farman AG. (1999) Temporomandibular joint pantomography using chargecoupled device, photostimulable phosphor, and film receptors: a comparison. J Digit
Imaging. 12(2 Suppl 1):9-13.
Farrar WB. (1971) Diagnosis and treatment of anterior dislocation of the articular disc. N Y J
Dent. 41(10):348-51.
Farrar WB. (1978) Characteristics of the condylar path in internal derangements of the TMJ. J
Prosthet Dent. 39(3):319-23.
Farrar WB, McCarty WL Jr.(1979) Inferior joint space arthrography and characteristics of
condylar paths in internal derangements of the TMJ. J Prosthet Dent. 41(5):548-55.
Friedman MH. (1997) The hypomobile temporomandibular joint. Gen Dent. 45(3):282-5.
Fujita S, Iizuka T, Dauber W. (2001) Variation of heads of lateral pterygoid muscle and
morphology of articular disc of human temporomandibular joint--anatomical and
histological analysis. J Oral Rehabil. 28(6):560-71.
Fyfe EC, Kabala J, Guest PG. (1999) Magnetic resonance imaging in the diagnosis of
asymmetrical bilateral masseteric hypertrophy. Dentomaxillofac Radiol. 28(1):52-4.
Gibbs CH, Mahan PE, Wilkinson TM, Mauderli A. (1984) EMG activity of the superior belly of
the lateral pterygoid muscle in relation to other jaw muscles. J Prosthet Dent. 51(5):691702.
Gibbs SJ, Simmons HC 3rd. (1998) A protocol for magnetic resonance imaging of the
temporomandibular joints. Cranio. 16(4):236-41.
Gniadecka M, Weismann K, Herning M. (1997) Swelling of the temporal region: a case of
benign masticatory muscle hypertrophy. Br J Dermatol. 136(2):242-4.
Greene CS, Laskin DM. (1988) Long-term status of TMJ clicking in patients with myofascial
pain and dysfunction. J Am Dent Assoc. 117(3):461-5.
Greene CS. (2001) The etiology of temporomandibular disorders: implications for treatment. J
Orofac Pain. 15(2):93-105; discussion 106-16.
Gross A, Gale EN. (1983) A prevalence study of the clinical signs associated with mandibular
dysfunction. J Am Dent Assoc. 107(6):932-6.
Grunert I, Grubwieser GJ, Ulmer H. (2000) Bilateral investigation of the temporomandibular
joint. An autopsy study of edentulous individuals. J Oral Rehabil. 27(8):671-81.
Habets LL, Bezuur JN, Jimenez Lopez V, Hansson TL. (1989) The OPG: an aid in TMJ
diagnostics. III. A comparison between lateral tomography and dental rotational panoramic
radiography (Orthopantomography). J Oral Rehabil. 16(4):401-6.
Haley DP, Schiffman EL, Lindgren BR, Anderson Q, Andreasen K. (2001) The relationship
between clinical and MRI findings in patients with unilateral temporomandibular joint pain.
J Am Dent Assoc. 132(4):476-81.
Hannam AG, Wood WW. (1989) Relationships between the size and spatial morphology of
human masseter and medial pterygoid muscles, the craniofacial skeleton, and jaw
biomechanics. Am J Phys Anthropol. 80(4):429-45.
Hansson LG, Westesson PL, Katzberg RW, Tallents RH, Kurita K, Holtas S, Svensson SA,
Eriksson L, Johansen CC. (1989) MR imaging of the temporomandibular joint: comparison
of images of autopsy specimens made at 0.3 T and 1.5 T with anatomic cryosections. AJR
Am J Roentgenol. 152 (6): 1241-4.
Harms SE, Wilk RM, Wolford LM, Chiles DG, Milam SB. (1985) The temporomandibular
joint: magnetic resonance imaging using surface coils. Radiology. 157(1):133-6.
60
Harper RP, de Bruin H, Burcea I. (1997) Muscle activity during mandibular movements in
normal and mandibular retrognathic subjects. J Oral Maxillofac Surg. Mar;55(3):225-33.
Helkimo M. (1974a) Studies on function and dysfunction of the masticatory system. I. An
epidemiological investigation of symptoms of dysfunction in Lapps in the north of Finland.
Proc Finn Dent Soc. 70(2):37-49.
Helkimo M. (1974b) Studies on function and dysfunction of the masticatory system. 3. Analyses
of anamnestic and clinical recordings of dysfunction with the aid of indices. Sven Tandlak
Tidskr. 67(3):165-81.
Helms CA, Katzberg RW, Dolwick MF, Bales DJ. (1980) Arthrotomographic diagnosis of
meniscus perforations in the temporomandibular joint. Br J Radiol. 53(628):283-5.
Helms CA, Morrish RB Jr, Kircos LT, Katzberg RW, Dolwick MF. (1982) Computed
tomography of the meniscus of the temporomandibular joint: preliminary observations.
Radiology. 145(3):719-22
Helms CA, Kaplan P. (1990) Diagnostic imaging of the temporomandibular joint:
recommendations for use of the various techniques. AJR Am J Roentgenol. 154(2):319-22.
Heylings DJ, Nielsen IL, McNeill C. (1995) Lateral pterygoid muscle and the
temporomandibular disc. J Orofac Pain. 9(1):9-16.
Hiraba K, Hibino K, Hiranuma K, Negoro T. (2000) EMG activities of two heads of the human
lateral pterygoid muscle in relation to mandibular condyle movement and biting force. J
Neurophysiol. 83 (4): 2120-37.
Holmlund AB, Gynther GW, Kardel R, Axelsson SE. (1999) Surgical treatment of
temporomandibular joint luxation. Swed Dent J.;23(4):127-32.
Holmlund AB, Axelsson S, Gynther GW. (2001) A comparison of discectomy and arthroscopic
lysis and lavage for the treatment of chronic closed lock of the temporomandibular joint: a
randomized outcome study. J Oral Maxillofac Surg. 59(9):972-7; discussion 977-8.
Honee G. (1972) The anatomy of the lateral pterygoid muscle. Acta Morphol Neerl-Scand
10:331-40.
Howard JA. (1990) Imaging techniques for the diagnosis and prognosis of TMD. J Calif Dent
Assoc. 18(3):61-71.
Hu K, Zhou JL, Liu HC, Hu M, Wang DS, Rong QG, Fang J. (1998) Stress distribution in the
mandible with unilateral condylar fracture. Chin J Dent Res. 1(2):26-36.
Isselee H, De Laat A, Bogaerts K, Lysens R. (2001) Long-term fluctuations of pressure pain
thresholds in healthy men, normally menstruating women and oral contraceptive users. Eur
J Pain. 5(1):27-37.
Jacobs JW, Griep EN, Lems WF, Witkamp TD, Weber J. (1994) Local muscle hypertrophy due
to an arterio-venous malformation. Br J Rheumatol. 33(2):173-4.
Jarenwattananon A, Gentry LR. (1990) Magnetic resonance imaging of the upper Maxillofacial
region. In: DelBalso AM, ed. Maxillofacial imaging. Philadelphia: WB Saunders Co. 521563.
Johnstone DR, Templeton M. (1980) The feasibility of palpating the lateral pterygoid muscle. J
Prosthet Dent. 44(3):318-23.
Jonsson B. and Bagge UE. (1968) Displacement deformity and fracture of wire electrodes for
electromyography. Electromyography 8:329-347.
Juniper RP.(1981) The superior pterygoid muscle? Br J Oral Surg. 19(2):121-8.
Juniper RP. (1984 ) Temporomandibular joint dysfunction: a theory based upon
electromyographic studies of the lateral pterygoid muscle. Br J Oral Maxillofac Surg.
22(1):1-8.
Kaban LB, Bertolami CN. (1981) The role of CT scan in diagnosis of TMJ ankylosis: report of
case. J Oral Surg. 39(5):370-2.
Kader DF, Wardlaw D, Smith FW. (2000) Correlation between the MRI changes in the lumbar
multifidus muscles and leg pain. Clin Radiol. 55(2):145-9.
61
Kaplan PA, Helms CA. (1989) Current status of temporomandibular joint imaging for the
diagnosis of internal derangements. AJR Am J Roentgenol. 152(4):697-705.
Katz JD, Ropper AH. (2000) Progressive necrotic myelopathy: clinical course in 9 patients.
Arch Neurol. 57(3):355-61.
Katzberg RW, Dolwick MF, Bales DJ, Helms CA. (1979) Arthrotomography of the
temporomandibular joint: new technique and preliminary observations. AJR Am J
Roentgenol. 132(6):949-55
Katzberg RW, Keith DA, Guralnick WC, ten Eick WR. (1982) Correlation of condylar
mobility and arthrotomography in patients with internal derangements of the
temporomandibular joint. Oral Surg Oral Med Oral Pathol. 54(6):622-7.
Katzberg RW, Keith DA, Ten Eick WR, Guralnick WC. (1983) Internal derangements of the
temporomandibular joint: an assessment of condylar position in centric occlusion. J Prosthet
Dent. 49(2):250-4.
Katzberg RW, O'Mara RE, Tallents RH, Weber DA. (1984) Radionuclide skeletal imaging and
single photon emission computed tomography in suspected internal derangements of the
temporomandibular joint. J Oral Maxillofac Surg. 42(12):782-7
Katzberg RW, Schenck J, Roberts D, Tallents RH, Manzione JV, Hart HR, Foster TH, Wayne
WS, Bessette RW. (1985) Magnetic resonance imaging of the temporomandibular joint
meniscus. Oral Surg Oral Med Oral Pathol. 59(4):332-5.
Katzberg RW, Bessette RW, Tallents RH, Plewes DB, Manzione JV, Schenck JF, Foster TH,
Hart HR. (1986) Normal and abnormal temporomandibular joint: MR imaging with surface
coil. Radiology. 158(1):183-9.
Katzberg RW. (1989) Temporomandibular joint imaging. Radiology. 170(2):297-307.
Katzberg RW, Westesson PL, Tallents RH, Drake CM. (1996) Anatomic disorders of the
temporomandibular joint disc in asymptomatic subjects. J Oral Maxillofac Surg. 54(2):14753; discussion 153-5.
Khan FA, Pedlar J. (1996) Generalized joint hypermobility as a factor in clicking of the
temporomandibular joint. Int J Oral Maxillofac Surg. 25(2):101-4.
Kim HJ, Jeon BS, Lee KW. (2000) Hemimasticatory spasm associated with localized
scleroderma and facial hemiatrophy. Arch Neurol. 57(4):576-80.
Kircos LT, (1990) Ortehdahl. Magnetic resonance imaging of the temporomandibular joint. In:
DelBalso AM, ed. Maxillofacial imaging. Philadelphia: WB Saunders Co., 675-695.
Knoernschild KL, Aquilino SA, Ruprecht A. (1991) Transcranial radiography and linear
tomography: a comparative study. J Prosthet Dent. 66(2):239-50
Koh ET, Yap AU, Koh CK, Chee TS, Chan SP, Boudville IC. (1999) Temporomandibular
disorders in rheumatoid arthritis.J Rheumatol. 26(9):1918-22.
Kondoh T, Westesson PL, Takahashi T, Seto K. (1998) Prevalence of morphological changes in
the surfaces of the temporomandibular joint disc associated with internal derangement. J
Oral Maxillofac Surg. 56(3):339-43; discussion 343-4
Kononen M, Kilpinen E. (1990) Comparison of three radiographic methods in screening of
temporomandibular joint involvement in patients with psoriatic arthritis. Acta Odontol
Scand. 48(4):271-7.
Koole P, Beenhakker F, de Jongh HJ, Boering G. (1990) A standardized technique for the
placement of electrodes in the two heads of the lateral pterygoid muscle. Cranio. 8(2):15462.
Kopp S, Rockler B. (1978) Variation in interpretation of radiographs of temporomandibular and
hand joints. Dentomaxillofac Radiol. 7(2):95-102
Kopp S, Rockler B. (1979) Relationship between radiographic signs in the temporomandibular
joint and hand joints. Acta Odontol Scand. 37(3):169-75.
62
Kuboki T, Takenami Y, Orsini MG, Maekawa K, Yamashita A, Azuma Y, Clark GT. (1999)
Effect of occlusal appliances and clenching on the internally deranged TMJ space. J Orofac
Pain. 13(1):38-48
Kurita K, Westesson PL, Yuasa H, Toyama M, Machida J, Ogi N. (1998) Natural course of
untreated symptomatic temporomandibular joint disc displacement without reduction. J
Dent Res. 77(2):361-5.
Kurita H, Ohtsuka A, Kobayashi H, Kurashina K. (2000) Flattening of the articular eminence
correlates with progressive internal derangement of the temporomandibular joint.
Dentomaxillofac Radiol. 29(5):277-9
Kurita H, Ohtsuka A, Kobayashi H, Kurashina K. (2001) A study of the relationship between
the position of the condylar head and displacement of the temporomandibular joint disk.
Dentomaxillofac Radiol. 30(3):162-5.
Lafreniere CM, Lamontagne M, el-Sawy R. (1997) The role of the lateral pterygoid muscles in
TMJ disorders during static conditions. Cranio. 15(1):38-52
Landes C, Walendzik H, Klein C. (2000) Sonography of the temporomandibular joint from 60
examinations and comparison with MRI and axiography. J Maxillofac Surg. 28(6):352-361.
Larheim TA, Kolbenstvedt A. (1984) High-resolution computed tomography of the osseous
temporomandibular joint. Some normal and abnormal appearances. Acta Radiol Diagn
(Stockh). 25(6):465-9.
Larheim TA, Westesson PL, Hicks DG, Eriksson L, Brown DA. (1999) Osteonecrosis of the
temporomandibular joint: correlation of magnetic resonance imaging and histology. J Oral
Maxillofac Surg. 57(8):888-98.
Laskin DM. (1969) Etiology of the pain-dysfunction syndrome. J Am Dent Assoc. 79(1):14753.
Laurell KA, Tootle R, Cunningham R, Beltran J, Simon D. (1987) Magnetic resonance imaging
of the temporomandibular joint. Part II: Comparison with laminographic, autopsy, and
histologic findings. J Prosthet Dent. 58(2):211-8.
Lehr RP Jr, Owens SE Jr. (1980) An electromyographic study of the human lateral pterygoid
muscles. Anat Rec. 196(4):441-8.
Leonardi R, Villari L, Bernasconi G, Caltabiano M. (2001) Histochemical study of the elastic
fibers in pathologic human temporomandibular joint discs. J Oral Maxillofac Surg.
59(10):1186-92.
Liedberg J, Panmekiate S, Petersson A, Rohlin M. (1996) Evidence-based evaluation of three
imaging methods for the temporomandibular disc. Dentomaxillofac Radiol. 25(5):234-41.
Lindqvist C, Jokinen J, Paukku P, Tasanen A. (1988) Adaptation of autogenous costochondral
grafts used for temporomandibular joint reconstruction: a long-term clinical and radiologic
follow-up. J Oral Maxillofac Surg. 46(6):465-70.
Lindvall AM, Helkimo E, Hollender L, Carlsson GE. (1976) Radiographic examination of the
temporomandibular joint. A comparison between radiographic findings and gross and
microscopic morphologic observations. Dentomaxillofac Radiol. 5(1-2):24-32.
Liu ZJ, Yamagata K, Kuroe K, Suenaga S, Noikura T, Ito G.(2000) Morphological and
positional assessments of TMJ components and lateral pterygoid muscle in relation to
symptoms and occlusion of patients with temporomandibular disorders. J Oral Rehabil.
27(10):860-74.
Ludlow JB, Davies KL, Tyndall DA. (1995) Temporomandibular joint imaging: a comparative
study of diagnostic accuracy for the detection of bone change with biplanar multidirectional
tomography and panoramic images. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
80(6):735-43
Lundh H, Westesson PL, Eriksson L, Brooks SL. (1992) Temporomandibular joint disk
displacement without reduction. Treatment with flat occlusal splint versus no treatment.
Oral Surg Oral Med Oral Pathol. 73(6):655-8.
63
Ma XC. (1987) [Double-contrast arthrography in temporomandibular joint derangement
syndrome]. In Chinese Zhonghua Fang She Xue Za Zhi. 21(3):160-1.
Mahan PE, Wilkinson TM, Gibbs CH, Mauderli A, Brannon LS. (1983) Superior and inferior
bellies of the lateral pterygoid muscle EMG activity at basic jaw positions. J Prosthet Dent.
50(5):710-8.
Major P, Kamelchuk L, Nebbe B, Petrikowski G, Glover K. (1997) Condyle displacement
associated with premolar extraction and nonextraction orthodontic treatment of Class I
malocclusion. Am J Orthod Dentofacial Orthop. 112(4):435-40.
Matin P. (1983) Bone scintigraphy in the diagnosis and management of traumatic injury. Semin
Nucl Med. 13(2):104-22. Review
McNamara JA Jr. (1973) The independent functions of the two heads of the lateral pterygoid
muscle. Am J Anat. 138(2):197-205.
McNeill C (1990) Craniomandibular disorders. Guidelines for evaluation, diagnosis, and
management. Chicago (IL):Quintessence Publishing Co.
McNeill C, Mohl ND, Rugh JD, Tanaka TT. (1990) Temporomandibular disorders: diagnosis,
management, education, and research. J Am Dent Assoc. 120(3):253-263.
Milano V, Desiate A, Bellino R, Garofalo T. (2000) Magnetic resonance imaging of
temporomandibular disorders: classification, prevalence and interpretation of disc
displacement and deformation. Dentomaxillofac Radiol. 29(6):352-61.
Molina OF, dos Santos Junior J, Nelson SJ, Nowlin T. (2000) Profile of TMD and Bruxer
compared to TMD and nonbruxer patients regarding chief complaint, previous
consultations, modes of therapy, and chronicity. Cranio. 18(3):205-19.
Montgomery MT, Gordon SM, Van Sickels JE, Harms SE. (1992) Changes in signs and
symptoms following temporomandibular joint disc repositioning surgery. J Oral Maxillofac
Surg. 50(4):320-8.
Muller-Leisse C, Augthun M, Bauer W, Roth A, Gunther R. (1996) Anterior disc displacement
without reduction in the temporomandibular joint: MRI and associated clinical findings. J
Magn Reson Imaging. 6(5):769-74.
Murakami K, Yokoe Y, Yasuda S, Tsuboi Y, Iizuka T. (2000) Prolonged mandibular
hypomobility patient with a "square mandible" configuration with coronoid process and
angle hyperplasia. Cranio. 18(2):113-9.
Murphy WA, Totty WG, Carroll JE. (1986) MRI of normal and pathologic skeletal muscle. AJR
Am J Roentgenol. 146(3):565-74.
Murray GM, Orfanos T, Chan JY, Wanigaratne K, Klineberg IJ. (1999) Electromyographic
activity of the human lateral pterygoid muscle during contralateral and protrusive jaw
movements. Arch Oral Biol. 44(3):269-85.
Musgrave MT, Westesson PL, Tallents RH, Manzione JV, Katzberg RW. (1991) Improved
magnetic resonance imaging of the temporomandibular joint by oblique scanning planes.
Oral Surg Oral Med Oral Pathol. 71(5):525-8.
Naidoo LC. (1996) Lateral pterygoid muscle and its relationship to the meniscus of the
temporomandibular joint. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 82(1):4-9.
Nicolakis P, Burak EC, Kollmitzer J, Kopf A, Piehslinger E, Wiesinger GF, Fialka-Moser V.
(2001) An investigation of the effectiveness of exercise and manual therapy in treating
symptoms of TMJ osteoarthritis. Cranio. 19(1):26-32.
Nishimura M, Segami N, Kaneyama K, Suzuki T. (2001) Prognostic factors in arthrocentesis of
the temporomandibular joint: evaluation of 100 patients with internal derangement. J Oral
Maxillofac Surg. 59(8):874-7; discussion 878
Nørgaard F (1947). Temporomandibular srthrography (thesis). Copenhagen: Munksgaard.
Omnell KA, Petersson A. (1976) Radiography of the temporomandibular joint utilizing oblique
lateral transcranial projections. Comparison of information obtained with standardized
technique and individualized technique. Odontol Revy. 27(2):77-92.
64
Orfanos T, Sarinnaphakorn L, Murray GM, Klineberg IJ. (1996) Placement and verification of
recording electrodes in the superior head of the human lateral pterygoid muscle. Arch Oral
Biol. 41(5):493-503.
Osborn JW. (1985) The disc of the human temporomandibular joint: design, function and
failure. J Oral Rehabil. 12(4):279-93.
Ozawa S, Boering G, Kawata T, Tanimoto K, Tanne K. (1999) Reconsideration of the TMJ
condylar position during internal derangement: comparison between condylar position on
tomogram and degree of disk displacement on MRI. Cranio. 17(2):93-100.
Petersilge CA, Pathria MN, Gentili A, Recht MP, Resnick D. (1995) Denervation hypertrophy
of muscle: MR features. J Comput Assist Tomogr. 19(4):596-600.
Petersson A, Rohlin M. (1988) Rheumatoid arthritis of the temporomandibular joint. Evaluation
of three different radiographic techniques by assessment of observer performance.
Dentomaxillofac Radiol. 17(2):115-20
Phanachet I, Wanigaratne K, Whittle T, Uchida S, Peeceeyen S, Murray GM. (2001) A method
for standardizing jaw displacements in the horizontal plane while recording single motor
unit activity in the human lateral pterygoid muscle. J Neurosci Methods. 15;105(2):201-10.
Piehslinger E, Schimmerl S, Celar A, Crowley C, Imhof H. (1995) Comparison of magnetic
resonance tomography with computerized axiography in diagnosis of temporomandibular
joint disorders. Int J Oral Maxillofac Surg. Feb;24(1 Pt 1):13-9.
Porter MR. (1970) The attachment of the lateral pterygoid muscle to the meniscus. J Prosthet
Dent. 24(5):555-62.
Pullinger A, Hollender L. (1985) Assessment of mandibular condyle position: a comparison of
transcranial radiographs and linear tomograms. Oral Surg Oral Med Oral Pathol. 60(3):32934.
Pullinger AG, Hollender L, Solberg WK, Petersson A. (1985) A tomographic study of
mandibular condyle position in an asymptomatic population. J Prosthet Dent. 53(5):706-13.
Pullinger AG, Solberg WK, Hollender L, Guichet D. (1986) Tomographic analysis of
mandibular condyle position in diagnostic subgroups of temporomandibular disorders. J
Prosthet Dent55(6):723-9.
Quemar JC, Ravalec X, Akoka S. (1993) Parasagittal magnetic resonance imaging of the lateral
pterygoid muscle: a preliminary study. J Orofac Pain. 7(2):169-74.
Raadsheer MC, Van Eijden TM, Van Spronsen PH, Van Ginkel FC, Kiliaridis S, PrahlAndersen B. (1994) A comparison of human masseter muscle thickness measured by
ultrasonography and magnetic resonance imaging. Arch Oral Biol. 39(12):1079-84.
Ramfjord SP (1961) Dysfunctional temporomandibular joint and muscle pain. J Prosthet Dent
11:353-374.
Rammelsberg P, Pospiech PR, Jager L, Pho Duc JM, Bohm AO, Gernet W. (1997) Variability
of disk position in asymptomatic volunteers and patients with internal derangements of the
TMJ. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 83(3):393-9.
Rauhala K, Oikarinen KS, Raustia AM. (1999) Role of temporomandibular disorders (TMD) in
facial pain: occlusion, muscle and TMJ pain. Cranio. 17(4):254-61
Raustia AM, Pyhtinen J, Virtanen KK. (1986) Densities and sizes of the main masticatory
muscles in computed tomography compared with clinical findings related to
temporomandibular joint (TMJ) dysfunction. ROFO Fortschr Geb Rontgenstr Nuklearmed.
144(3):327-31.
Raustia AM, Pyhtinen J, Pernu H. (1994) Clinical, magnetic-resonance imaging and surgical
findings in patients with temporomandibular joint disorder--a survey of 47 patients. Rofo
Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr. 160(5):406-11.
Raustia AM, Pyhtinen J, Tervonen O. (1995) Clinical and MRI findings of the
temporomandibular joint in relation to occlusion in young adults. Cranio. Apr;13(2):99-104.
65
Raustia AM, Oikarinen KS, Pyhtinen J. (1998) Densities and sizes of main masticatory muscles
in patients with internal derangements of temporomandibular joint obtained by computed
tomography. J Oral Rehabil. 25(1):59-63.
Rohlin M, Petersson A. (1989) Rheumatoid arthritis of the temporomandibular joint: radiologic
evaluation based on standard reference films. Oral Surg Oral Med Oral Pathol. 67(5):594-9.
Rosenberg HM, Graczyk RJ. (1986) Temporomandibular articulation tomography: a corrected
anteroposterior and lateral cephalometric technique. Oral Surg Oral Med Oral Pathol.
62(2):198-204.
Ryan D, Ahmed S, Harris M. (1990) Arthrotomography and the surgical correction of
temporomandibular joint disorders. Br J Oral Maxillofac Surg. 28(4):228-33.
Sacks H, Zelig D, Schabes G. (1990) Recurrent temporomandibular joint subluxation and facial
ecchymosis leading to diagnosis of Ehlers-Danlos syndrome: report of surgical management
and review of the literature. J Oral Maxillofac Surg. 48(6):641-7.
Sahm G, Witt E. (1989) Long-term results after childhood condylar fractures. A computertomographic study. Eur J Orthod. 11(2):154-60.
Sari S, Sonmez H.(2002) Investigation of the relationship between oral parafunctions and
temporomandibular joint dysfunction in Turkish children with mixed and permanent
dentition. J Oral Rehabil. 29(1):108-112.
Sato S, Sakamoto M, Kawamura H, Motegi K. (1999) Long-term changes in clinical signs and
symptoms and disc position and morphology in patients with nonreducing disc displacement
in the temporomandibular joint. J Oral Maxillofac Surg. 57(1):23-9; discussion 29-30
Sato S, Takahashi K, Kawamura H, Motegi K. (1998) The natural course of nonreducing disk
displacement of the temporomandibular joint: changes in condylar mobility and
radiographic alterations at one-year follow up. Int J Oral Maxillofac Surg. 27(3):173-7.
Schellhas KP, Wilkes CH, Heithoff KB, Omlie MR, Block JC. (1986) Temporomandibular
joint: diagnosis of internal derangements using magnetic resonance imaging. Minn Med.
69(9):516-9.
Schellhas KP, Wilkes CH, Omlie MR, Peterson CM, Johnson SD, Keck RJ, Block JC, Fritts
HM, Heithoff KB. (1988) The diagnosis of temporomandibular joint disease: twocompartment arthrography and MR. AJR Am J Roentgenol. 151(2):341-50.
Schellhas KP, Wilkes CH, Baker CC. (1989) Facial pain, headache, and temporomandibular
joint inflammation. Headache. 29(4):229-32.
Schellhas KP, Wilkes CH. (1989) Temporomandibular joint inflammation: comparison of MR
fast scanning with T1- and T2-weighted imaging techniques. AJR Am J Roentgenol.
153(1):93-8.
Schellhas KP. (1989a) Internal derangement of the temporomandibular joint: radiologic staging
with clinical, surgical, and pathologic correlation. Magn Reson Imaging. 7(5):495-515.
Schellhas KP. (1989b) MR imaging of muscles of mastication. AJR Am J Roentgenol.
153(4):847-55.
Schmidt BL, Pogrel MA, Necoechea M, Kearns G. (1998) The distribution of the
auriculotemporal nerve around the temporomandibular joint. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 86(2):165-8.
Schmolke C. (1994) The relationship between the temporomandibular joint capsule, articular
disc and jaw muscles. J Anat. 184 ( Pt 2):335-45.
Schwaighofer BW, Tanaka TT, Klein MV, Sartoris DJ, Resnick D. (1990) MR imaging of the
temporomandibular joint: a cadaver study of the value of coronal images. AJR Am J
Roentgenol. 154(6):1245-9.
Schwartz L, Chayes CM. (1966) The examination of the patient with facial pain and/or with
mandibular dysfunction. Dent Clin North Am. 537-44.
66
Shellock FG, Pressman BD. (1989) Dual-surface-coil MR imaging of bilateral
temporomandibular joints: improvements in the imaging protocol. AJNR Am J Neuroradiol.
10(3):595-8.
Shellock FG, Fleckenstein JL. (2000) Muscle physiology and pathophysiology: magnetic
resonance imaging evaluation. Semin Musculoskelet Radiol. 4(4):459-79.
Sherman JJ, Turk DC. (2001) Nonpharmacologic approaches to the management of myofascial
temporomandibular disorders. Curr Pain Headache Rep. 5(5):421-31.
Sicher H. (1965) Chapter II: The muscles of head and neck. In: Sicher M, ed. Oral anatomy.
Saint Louis: CV Mosby Co. 4th ed, 141-168.
Siegelman ES, Outwater EK. (1999) Tissue characterization in the female pelvis by means of
MR imaging. Radiology. 212(1):5-18.
Silvennoinen U, Raustia AM, Lindqvist C, Oikarinen K. (1998) Occlusal and
temporomandibular joint disorders in patients with unilateral condylar fracture. A
prospective one-year study. Int J Oral Maxillofac Surg. Aug;27(4):280-5.
Sindet-Pedersen S. (1988) Intraoral myotomy of the lateral pterygoid muscle for treatment of
recurrent dislocation of the mandibular condyle. J Oral Maxillofac Surg. 46(6):445-9.
Smith HJ. (1988) A non-mathematical approach to basic MRI. Madison, Wisc, Medical Physics
Publishing,.
Solberg WK. (1986a ) Temporomandibular disorders: masticatory myalgia and its management.
Br Dent J. 24;160(10):351-6.
Solberg WK. (1986b) Temporomandibular disorders: clinical significance of TMJ changes. Br
Dent J. 5;160(7):231-6
Steed PA, Wexler GB. (2001) Temporomandibular disorders--traumatic etiology vs.
nontraumatic etiology: a clinical and methodological inquiry into symptomatology and
treatment outcomes. Cranio. 19(3):188-94.
Stratmann U, Mokrys K, Meyer U, Kleinheinz J, Joos U, Dirksen D, Bollmann F. (2000)
Clinical anatomy and palpability of the inferior lateral pterygoid muscle. J Prosthet Dent.
83(5):548-54.
Stratmann U, Mokrys K, Meyer U, Kleinheinz J, Joos U, Dirksen D, Bollmann F. (2000)
Clinical anatomy and palpability of the inferior lateral pterygoid muscle. J Prosthet Dent.
83(5):548-54.
Tanimoto K, Hansson LG, Petersson A, Rohlin M, Johansen CC. (1989) Computed tomography
versus single-contrast arthrotomography in evaluation of the temporomandibular joint disc.
A study of autopsy specimens. Int J Oral Maxillofac Surg. 18(6):354-8
Tanimoto K, Petersson A, Rohlin M, Hansson LG, Johansen CC. (1990) Comparison of
computed with conventional tomography in the evaluation of temporomandibular joint
disease: a study of autopsy specimens. Dentomaxillofac Radiol. 19(1):21-7.
Tasaki MM, Westesson PL. (1993) Temporomandibular joint: diagnostic accuracy with sagittal
and coronal MR imaging. Radiology. 186(3):723-9.
Taskaya-Yilmaz N, Ogutcen-Toller M. (2001) Magnetic resonance imaging evaluation of
temporomandibular joint disc deformities in relation to type of disc displacement. J Oral
Maxillofac Surg. 59(8):860-5; discussion 865-6
Thilander B. (1964) The structure of the collagen of the temporomandibular disc in man. Acta
Odontol Scand 22:135-49.
Thomas CA, Okeson JP. (1987) Evaluation of lateral pterygoid muscle symptoms using a
common palpation technique and a method of functional manipulation. Cranio. 5(2):125-9.
Thompson H (1971) Mandibular dysfunction syndrome. Br Dent J 130:187-193.
Thompson JR, Christiansen E, Hasso AN, Hinshaw DB Jr. (1984) Temporomandibular joints:
high-resolution computed tomographic evaluation. Radiology. 150(1):105-10.
67
Thoren H, Hallikainen D, Iizuka T, Lindqvist C. (2001) Condylar process fractures in children:
a follow-up study of fractures with total dislocation of the condyle from the glenoid fossa. J
Oral Maxillofac Surg. 59(7):768-73; discussion 773-4.
Thyagarajan D, Kompoliti K, Ford B. (1998) Post-traumatic shoulder 'dystonia': persistent
abnormal postures of the shoulder after minor trauma. Neurology. 51(4):1205-7.
Toyama M, Kurita K, Koga K, Rivera G. (2000) Magnetic resonance arthrography of the
temporomandibular joint. J Oral Maxillofac Surg. 58(9):978-83; discussion 984.
Trumpy IG, Eriksson J, Lyberg T. (1997) Internal derangement of the temporomandibular joint:
correlation of arthrographic imaging with surgical findings. Int J Oral Maxillofac Surg.
26(5):327-30.
Turp JC, Minagi S. (2001) Palpation of the lateral pterygoid region in TMD-where is the
evidence? J Dent. 29(7):475-83.
Undt G, Kermer C, Rasse M. (1997) Treatment of recurrent mandibular dislocation, Part II:
Eminectomy. Int J Oral Maxillofac Surg. 26(2):98-102
Van Sickels JE, Bianco HJ Jr, Pifer RG. (1983 ) Transcranial radiographs in the evaluation of
craniomandibular (TMJ) disorders. J Prosthet Dent. 49(2):244-9.
van Spronsen PH, Weijs WA, Valk J, Prahl-Andersen B, van Ginkel FC. (1989) Comparison of
jaw-muscle bite-force cross-sections obtained by means of magnetic resonance imaging and
high-resolution CT scanning. J Dent Res. 68(12):1765-70.
van Spronsen PH, Weijs WA, Valk J, Prahl-Andersen B, van Ginkel FC. (1991) Relationships
between jaw muscle cross-sections and craniofacial morphology in normal adults, studied
with magnetic resonance imaging. Eur J Orthod. 13(5):351-61.
Wang MQ, Yan CY, Yuan YP. (2001) Is the superior belly of the lateral pterygoid primarily a
stabilizer? An EMG study. J Oral Rehabil. 28(6):507-10.
Wanman A, Agerberg G. (1986) Relationship between signs and symptoms of mandibular
dysfunction in adolescents. Community Dent Oral Epidemiol. 14(4):225-30.
Weijs WA, Hillen B. (1984) Relationship between the physiological cross-section of the human
jaw muscles and their cross-sectional area in computer tomograms. Acta Anat (Basel).
118(3):129-38.
Weinberg LA. (1979) Role of condylar position in TMJ dysfunction-pain syndrome. J Prosthet
Dent. 41(6):636-43.
Weinreb JC, Cohen JM, Maravilla KR. (1985) Iliopsoas muscles: MR study of normal anatomy
and disease. Radiology. 156(2):435-40.
Westesson PL, Omnell KA, Rohlin M. (1980) Double-contrast tomography of the
temporomandibular joint. A new technique based on autopsy specimen examinations.Acta
Radiol Diagn (Stockh). 21(6):777-84.
Westesson PL. (1982) Double-contrast arthrography and internal derangement of the
temporomandibular joint. Swed Dent J Suppl. 13 Suppl:1-57.
Westesson PL, Rohlin M. (1984)a Internal derangement related to osteoarthrosis in
temporomandibular joint autopsy specimens. Oral Surg Oral Med Oral Pathol. Jan;57(1):1722
Westesson PL, Rohlin M. (1984)b Diagnostic accuracy of double-contrast arthrotomography of
the temporomandibular joint: correlation with postmortem morphology. AJR Am J
Roentgenol. 143(3):655-60.
Westesson PL. (1985) Structural hard-tissue changes in temporomandibular joints with internal
derangement. Oral Surg Oral Med Oral Pathol. 59(2):220-4
Westesson PL, Bronstein SL, Liedberg J. (1986) Temporomandibular joint: correlation between
single-contrast videoarthrography and postmortem morphology. Radiology. 160(3):767-71.
Westesson PL, Bronstein SL. (1987) Temporomandibular joint: comparison of single- and
double-contrast arthrography. Radiology. 164(1):65-70.
68
Westesson PL, Katzberg RW, Tallents RH, Sanchez-Woodworth RE, Svensson SA. (1987a) CT
and MR of the temporomandibular joint: comparison with autopsy specimens. AJR Am J
Roentgenol. 148(6):1165-71.
Westesson PL, Katzberg RW, Tallents RH, Sanchez-Woodworth RE, Svensson SA, Espeland
MA. (1987b) Temporomandibular joint: comparison of MR images with cryosectional
anatomy. Radiology. 164(1):59-64.
Westesson PL. (1993) Reliability and validity of imaging diagnosis of temporomandibular joint
disorder. Adv Dent Res. 7(2):137-51.
Westling L. (1989) Craniomandibular disorders and general joint mobility. Acta Odontol
Scand. 47(5):293-9.
Westling L, Carlsson GE, Helkimo M. (1990) Background factors in craniomandibular
disorders with special reference to general joint hypermobility, parafunction, and trauma. J
Craniomandib Disord. 4(2):89-98
Westling L, Holm S, Wallentin I. (1992) Temporomandibular joint dysfunction. Connective
tissue variations in skin biopsy and mitral valve function. Oral Surg Oral Med Oral Pathol.
74(6):709-18.
Widmalm SE, Lillie JH, Ash MM Jr. (1987) Anatomical and electromyographic studies of the
lateral pterygoid muscle. J Oral Rehabil. 14(5):429-46.
Widmalm SE, Westesson PL, Brooks SL, Hatala MP, Paesani D. (1992) Temporomandibular
joint sounds: correlation to joint structure in fresh autopsy specimens. Am J Orthod
Dentofacial Orthop. 101(1):60-9.
Wilkes CH. (1978a) Arthrography of the temporomandibular joint in patients with the TMJ
pain-dysfunction syndrome. Minn Med. 61(11):645-52.
Wilkes CH. (1978b) Structural and functional alterations of the temporomandibular joint.
Northwest Dent. 57(5):287-94.
Wilkes CH. (1989) Internal derangements of the temporomandibular joint. Pathological
variations. Arch Otolaryngol Head Neck Surg. 115(4):469-77
Wilkinson TM. (1988) The relationship between the disk and the lateral pterygoid muscle in the
human temporomandibular joint. J Prosthet Dent. 60(6):715-24.
Williamson EH, Rosenzweig BJ. (1998) The treatment of temporomandibular disorders through
repositioning splint therapy: a follow-up study. Cranio. 16(4):222-5.
Williamson PC, Major PW, Nebbe B, Glover KE, Prasad NG. (1999) Horizontal condylar
angulation and condyle position associated with adolescent TMJ disk status. Cranio.
17(2):101-8.
Winocur E, Gavish A, Halachmi M, Bloom A, Gazit E. (2000) Generalized joint laxity and its
relation with oral habits and temporomandibular disorders in adolescent girls. J Oral
Rehabil. 27(7):614-22.
Wood WW, Takada K, Hannam AG. (1986)The electromyographic activity of the inferior part
of the human lateral pterygoid muscle during clenching and chewing. Arch Oral Biol.
31(4):245-53.
Yoshida H, Hirohata H, Onizawa K, Niitsu M, Itai Y. (2000) Flexure deformation of the
temporomandibular joint disk in pseudodynamic magnetic resonance images. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 89(1):104-11.
Yoshida K, Kaji R, Takagi A, Iizuka T. (1999) Customized EMG needle insertion guide for the
muscle afferent block of jaw-deviation and jaw-opening dystonias. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod. 88(6):664-9.
Zhou D, Hu M, Liang D, Zhao G, Liu A. (1999) Relationship between fossa-condylar position,
meniscus position, and morphologic change in patients with Class II and III malocclusion.
Chin J Dent Res. 2(1):45-9.
69
10 Appendix: Figures
70
Fig.1 MRI projections of TMJ are oriented on axial imaging. The upper part of the superior belly and running
direction of the lateral pterygoid muscle (LPM) can be observed.
(A) Axial MR images show orientation of orthogonal sagittal MRI scanning planes. Angle “α”
indicates the LPM runs angularly with the scanning plane.
(B) Axial MR images show orientation of oblique sagittal MRI scanning planes. Scanning plane is
perpendicular to the long axis of the condyle. Angle “β” shows the angle between the main fibers’
running direction of the LPM and the scanning plane. Comparing (A) and (B), note that β<α.
Oblique sagittal scanning planes are nearer to parallel to the long axis of the LPM than orthogonal
sagittal scanning.
(C) Axial MR images show orientation of condyle-lateral pterygoid muscle (CLPM) MRI scanning
planes. The scanning planes are parallel to the main fibers’ running direction of the LPM. In
CLPM projection the angle between the long axis of the LPM and scanning became zero
Note that when the angle between the long axis of the LPM and scanning plane becomes smaller, the trend of
scanning plane is towards parallel to the long axis of the LPM, and more parts of the muscle can be scanned.
Fig.2 Visibility of the LPM in MRI.
(A) Both bellies of the LPM can be observed clearly in MRI, classified as V2. Anterior gap (arrow)
between the superior belly (SB) and inferior belly (IB) can be seen. (C=condyle)
(B) Only one belly of the LPM can be observed in MRI, classified as V1. In image B, only superior
belly of the LPM (SB) is shown. (C=condyle)
(C) Non-belly or only insertion part of the LPM can be observed in MRI, classified as V0. In image C,
anterior displaced disc with deformity is found (arrow), but the LPM cannot be observed.
(C=condyle).
71
Fig.3 Normal imaging of the LPM obtained from volunteer and asymptomatic TMJs.
(A) Mouth-closed, oblique sagittal, Proton Density (2000/20) (1.5-T magnet) left TMJ image of a 28year-old male volunteer who had no suspicious clinical signs and symptoms of TMD. The normal
LPM structures show as a fan-like muscle from the origins to the neck of the mandibular condyle
or disc. A high signal layer of fat tissue separates the superior belly of the LPM (SB) form the
inferior belly of the LPM (IB). A high-signal fat layer can be observed between the two bellies
(arrow). Near the insertion part of the LPM the two bellies are fused with each other (C=condyle;
D=disc).
(B) Normal LPM find in mouth-closed oblique sagittal PD (3000/14) MRI image of left TMJ of a 65year-old female who has experienced pain on jaw movement and clicking of right but no clinical
symptoms on left side. On this image of the left TMJ, the disc is seen in normal position. The
superior belly (SB) and inferior belly (IB) of the LPM appear normal. Vessels and fat layer can be
observed between the two bellies (arrow) (C=condyle).
72
Fig.4 Hypertrophy of superior belly of the LMP shows in images of a 52-year-old female with chronic facial
pain, jaw movement pain and TMJ pain on right side for nine years, symptoms released after splint treatment.
Left TMJ recurrently painful and restricted in 3 months. Palpation pain of LPM and locking were detected on
the left. Palpation pain of temporal muscles was found on both sides. Anterior disc displacement with nonreduction was found in TMJ on both sides in MRI (SB= the superior belly; IB=inferior belly of the LPM;
C=condyle).
(A) In mouth-closed image (oblique sagittal, 3000/14, 1.5T, 3-mm-thick) of left TMJ, hypertrophy of
the superior belly (SB) of the LPM is suggested by the evidently enlarged size of the belly
(compare with the superior belly of the LPM of right TMJ in image B). Disc is anteriorly
displaced and deformed (black arrow). Effusion can be found at bilaminar zone (white arrow).
(B) The LPM shows as normal on mouth-closed image of right TMJ (oblique sagittal, 3000/14, 1.5T,
3-mm-thick). The disc shows anterior displacement (arrow). Osteoarthritic change of the condyle
can be observed.
73
Fig.5 Atrophy of the superior belly of the LPM is found in TMJs either with disc in normal position or with
disc displacement (C=condyle; D=disc; IB=inferior belly of the LPM).
(A) Atrophy of the LPM superior belly (arrow) in a 42-year-old female who has had progressing pain
in the TMJ, facial and temporal pain on the right side for five years. Palpation pain in the LPM
and movement pain in both TMJs associate with painful clicking. The mouth-closed oblique
sagittal PD (3000/15) (1,5-T magnet) MRI image of the right TMJ reveals atrophy and fatty
replacement in superior belly of the LPM (arrow). Disc (D) appears in normal position. Condyle
hypermobility was found in maximal mouth-open imaging of this joint.
(B) Atrophy of the superior belly of the LPM (arrow) is revealed in a 35-year-old female who suffered
pain on jaw movement, had difficult in mouth opening as well as facial pain on left TMJ for the
past two years. The symptoms could not be improved by splint treatment. Painful locking and
severe palpation pain on the LPM are detected on the left side. In mouth-closed, oblique sagittal
image of the left TMJ (3000/14, 1.5-T magnet), atrophy of the superior belly of the LPM with
large area high signal fatty replacement (arrow) is noted. The inferior belly appears normal.
Anterior disc displacement (D) and osteophyte of the condyle (C) are found. The displaced disc
cannot reduce in maximal mouth-open image.
74
Fig.6 Hypertrophy of the inferior belly combined with atrophy of the superior belly of the LPM has been
diagnosed by side-to-side comparing in a 41-year-old female with long-term chronic pain on right TMJ for
five years with recurrent subluxation. Movement pain, palpation pain of TMJ and masticatory muscles
(temporal muscle and LPM) are found on the right side. The mandible is towards the left during mouth
opening. No symptoms were found on the left side. Hypermobility of the condyle is found on both sides in
maximal mouth open MRI (C= condyle; SB=superior belly; IB = inferior belly).
(A) Normal LPM reveals on mouth-closed image of the left TMJ (oblique sagittal, 3000/20).
Anterior gap between the two bellies can be clearly observed (arrow). Disc is in normal position.
(B) Mouth-closed image of the right TMJ (oblique sagittal, 3000/20) shows hypertrophy of inferior
belly combined with atrophy of superior belly (arrow) of the LPM. Atrophy shows as high signal
fatty replacement in superior belly of the LPM (arrow). Hypertrophy of the inferior belly (IB) is
shown as increased size of the belly (compare with the inferior belly of the LPM on the left side
in image A). Note the anterior gap between the two bellies might have been occupied by
hypertrophic muscular tissue of the inferior belly. The upper edges of the inferior belly become
convex curves. Disc is in normal position.
75
Fig.7 Atrophy and contracture of the LPM is suspected in a 36-year-old female with occasional locking and
chronic pain on both TMJs for 5 years, painful on the left side and restricted in jaw movements for 9 months.
Symptoms show no evident improvement after splint and muscle exercising treatment. Severe palpation pain
of the lateral pterygoid muscle (LPM) is found on both sides, painful on the left. In MRIs, the anterior
displacements of disc are found on both sides. The displaced disc shows reducing on the left TMJ and nonreducing on the right.
(A) Atrophy of the superior belly of the LPM is shown in the mouth-closed, oblique sagittal, proton
dense image of the right TMJ (3000/14, 1.5-T magnet). High signal fatty replacement tissue can
be observed inside the superior belly (white arrow). The inferior belly of the LPM (IB) shows as
normal. Disc is anteriorly displaced (black arrow). (C= condyle).
(B) In T2-weighted (3000/125, 1.5-T magnet) image mouth-closed oblique sagittal of right TMJ, the
high signal fatty replacement in the superior belly of the LPM is observed more clearly (white
arrow). The normal inferior belly shows isointense signals in either proton dense or T2-weighted
image (compare image A and B). (C= condyle).
(C) Atrophy of the superior belly combined with contracture of the inferior belly of the LPM is
noticed in the mouth-closed, oblique sagittal, proton dense image of left TMJ (3000/14, 1.5-T
magnet). The size of the inferior belly of the left LPM is evidently enlarged comparing to the
right side (comparing with image A). Fatty replacement and fibrosis are found in both bellies
(small arrows). Anterior disc displacement can be observed (big arrow).
(D) T2-weighted (3000/125, 1.5-T magnet) mouth-closed oblique sagittal image of left TMJ, fatty
replacement in both belly of the left LPM are evident (arrows).
76
Fig.8 Contracture and atrophy of the LMP find in a 46-year-old female with a long history of chronic facial
pain and movement pain on both sides and occasional locking of left TMJ. Anterior disc displacement with
non-reduction is found in the left TMJ in MRI (C= condyle).
(A) Mouth-closed, oblique sagittal image of left TMJ (3000/14, 3-mm-thick), the atrophy of superior belly
in the LPM shows as high-signal fatty replacement (white arrow). The contracture of the inferior belly
shows fibrosis with lower signals (black arrow). The thickened disc is anteriorly displaced (white
arrow head).
(B) T2-weighted image (3000/125,3-mm-thick) of the TMJ in image A, the fatty replacement of the
superior belly of the LPM (big white arrow) and the contracture of the inferior belly with lower
signals fibrosis (black arrow) are more clearly observed. Effusion of the bilaminar zone (small white
arrow) is suspected.
77
Fig. 9 Disc position of temporomandibular joint (TMJ) is demonstrated by MRI (C=condyle, E=articular
eminence)
(A) Disc appears in normal position on mouth closed oblique sagittal PD (3000/14) (1,5-T magnet)
MR image (arrow). The junction of bilaminar zone and posterior band of disc can be observed at
12 o’clock on the top of the condyle.
(B) In the same TMJ of (A), reduction of the disc (arrow) is seen in maximal mouth open direct
sagittal T1-weighted (400/12) (1,5-T magnet) MR image.
(C) Anterior disc displacement (arrow) is seen in the mouth closed oblique sagittal PD (3000/15) (1,5T magnet) MR image.
(D) Maximal mouth open direct sagittal T1-weighted (400/12) (1,5-T magnet) MR image of TMJ in
Fig. C shows reduction of the disc (arrow). Fig. C and D presents anterior disc displacement with
reduction (ADDr).
(E) Disc anterior displacement (arrow) with deformity is found in mouth-closed oblique sagittal (1,5T magnet) MR image. Osteoarthritic change of the condyle can be noticed.
(F) In the same TMJ of Fig. E, maximal mouth open direct sagittal T1-weighted (400/12) (1,5-T
magnet) MR image shows that the disc is still blocked in front of the condyle (arrow) and anterior
disc displacement with non-reduction (ADDnr) is considered.
78
Fig.10 Classifications of the condylar mobility: a horizontal tangential line of the top of the articular fossa
and a vertical line through the top of articular eminence are made on sagittal or oblique sagittal image of
TMJ. Two lines meet in point “O”. From the point “O”, making angles divide the articular eminence. The top
of the articular fossa (TF) is on 0º and the top of the articular eminence (TE) on 90º. (C=condyle, E=articular
eminence, TC=top of the condyle)
(A) Hypomobility (limitation) of the condyle shows in maximal mouth open imaging.
(B) Schematic representation of figure A, hypomobility of the condyle shows as the top of the
condyle locates in 0º-90º (<90º).
(C) Normal mobility of the condyle shows in maximal mouth-open imaging.
(D) Schematic representation of figure C, normal motion shows as the top of the condyle located in
90º-120º of the eminence in maximal mouth opening.
(E) Hypermobility of the condyle is found. Note that the hypermobilized condyle may put pressure on
the anterior part of the disc (arrow).
(F) Schematic representation of figure E, the condyle translates excessively, beyond and superior to
the level of the articular eminence (>120º) in the images of mouth maximal opening.
79
Fig.11 Imaging abnormalities of the LPM can be found in TMJs with disc in normal position. The normal
LPM may be observed in TMJs with severe osteoarthritic changes (C=condyle).
(A) Atrophy of the LPM superior belly in a 36-year-old female who has had progressing pain in the
TMJ, facial and temporal pain on the right side for five years. Palpation pain in the LPM and
movement pain in both TMJs. The mouth-closed oblique sagittal PD (3000/15) (1,5-T magnet)
MRI image of the right TMJ reveals atrophy and fatty replacement in superior belly of the LPM
(arrow). Disc appears in normal position. In maximal mouth-open images bilateral TMJ
hypermobility is found.
(B) Normal image of the LPM is found in a 35-year-old male with painful locking, crepitating and
movement pain in right TMJ, palpation pain of LPM and head-neck pain on both sides for three
years. Pain symptoms have been released evidently after splint and psychical therapies, but
mouth-opening limitation became worse. No palpation pain of the LPM and movement pain on
both TMJs, slight palpated pain on right TMJ. The width of mouth opening is only 15mm. Mouthclosed oblique sagittal, PD image (3000/20, 3-mm-thick) of right TMJ shows severe erosion on
the condyle (C). Disc becomes thinning (arrow). The LPM appears normal.