INTRODUCTION I n humans, the temporomandibular joint (TMJ) is now generally considered to be load-bearing during masticatory function. Until 1980, however, this concept was controversial. Wilson (1920) reported that the fibrocartilage of the TMJ condyle was softer than hyaline cartilage, and therefore could not be load-bearing. Hylander and Bays (1979) indirectly measured TMJ condylar loading in the macaque with rosette strain gauges placed on the condylar neck, and found that the condylar bone surface was indeed loaded during function. Brehnan et al. (1981) and Boyd et al. (1990) directly measured the condylar loading in the macaque by means of a piezoelectric foil force transducer, and confirmed that the TMJ was indeed a load-bearing articulation. Other experimental and analytical studies (Smith et al., 1986; Koolstra et al., 1988; Korioth et al., 1992; Beek et al., 2000) have also demonstrated that the human TMJ was load-bearing under function. Although these studies are all simulations, partially performed on data from cadavers, they have shown that the fibrocartilaginous tissues, including the disc and articular cartilage, have important functions in stress distribution. TMJ disorders are characterized by intra-articular positional and/or structural abnormalities. Review studies published in the 1980s showed prevalence rates ranging from 16% to 59% for symptoms and from 33% to 86% for clinical signs (Carlsson and LeResche, 1995), although from 3% to 7% of the adult population has sought care for TMJ pain and dysfunction (Carlsson, 1999). It has been observed that up to 70% of persons with TMJ disorders suffer from displacement of the articular disc, coined 'internal derangement' of the TMJ (Farrar and McCarty, 1979). Meanwhile, the most common joint pathology affecting the TMJ is degenerative joint disease, also known as osteoarthrosis or osteoarthritis. Among individuals with TMJ disorders, 11% had symptoms of TMJ-osteoarthrosis (TMJ-OA) (Mejersjö and Hollender, 1984). An epidemiological study, meanwhile, showed that minimal flattening of the condyle and/or eminence was seen in 35% of TMJs in asymptomatic persons (Brooks et al., 1992). More advanced osseous changes were not seen; therefore, it was concluded that minimal flattening was probably of no clinical significance. However, once the breakdown in the joint starts, TMJ- OA can be crippling, leading to a variety of morphological and functional deformities (Zarb and Carlsson, 1999). This paper is divided into four parts. Part 1 will review the definition and etiology of TMJ disorders. A basic review of the TMJ disorders, their etiologies, and the biomechanical and biochemical factors associated with functional overloading of the joint will also be discussed. Part 2 will discuss the clinical, radiographic, and biochemical analytical findings important in the diagnosis of TMJ-osteoarthrosis. Part 3 will present the non- invasive and invasive modalities utilized in TMJ-osteoarthrosis management. Finally, in Part 4, the possibility of tissue-engineering for treatment of TMJ disorders with degenerative changes will be discussed. ABSTRACT Temporomandibular joint (TMJ) disorders have complex and sometimes controversial etiologies. Also, under similar circumstances, one person's TMJ may appear to deteriorate, while another's does not. However, once degenerative changes start in the TMJ, this pathology can be crippling, leading to a variety of morphological and functional deformities. Primarily, TMJ disorders have a non-inflammatory origin. The pathological process is characterized by deterioration and abrasion of articular cartilage and local thickening. These changes are accompanied by the superimposition of secondary inflammatory changes. Therefore, appreciating the pathophysiology of the TMJ degenerative disorders is important to an understanding of the etiology, diagnosis, and treatment of internal derangement and osteoarthrosis of the TMJ. The degenerative changes in the TMJ are believed to result from dysfunctional remodeling, due to a decreased host-adaptive capacity of the articulating surfaces and/or functional overloading of the joint that exceeds the normal adaptive capacity. This paper reviews etiologies that involve biomechanical and biochemical factors associated with functional overloading of the joint and the clinical, radiographic, and biochemical findings important in the diagnosis of TMJ-osteoarthrosis. In addition, non-invasive and invasive modalities utilized in TMJ-osteoarthrosis management, and the possibility of tissue engineering, are discussed. KEY WORDS: temporomandibular joint, degenerative disease, osteoarthrosis, tissue engineering. Received April 17, 2007; Last revision January 21, 2008; Accepted January 23, 2008 Degenerative Disorders of the Temporomandibular Joint: Etiology, Diagnosis, and Treatment E. Tanaka 1 *, M.S. Detamore 2 , and L.G. Mercuri 3 1 Department of Orthodontics and Dentofacial Orthopedics, The University of Tokushima Graduate School of Oral Sciences, 3-18-15 Kuramoto-cho, Tokushima 770-8504, Japan; 2 Department of Chemical and Petroleum Engineering, University of Kansas, Lawrence, KS, USA; and 3 Department of Surgery, Division of Oral and Maxillofacial Surgery, Stritch School of Medicine, Loyola University Medical Center, Maywood, IL, USA; *corresponding author, [email protected]J Dent Res 87(4):296-307, 2008 CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE 296
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INTRODUCTION
In humans, the temporomandibular joint (TMJ) is now generally
considered to be load-bearing during masticatory function. Until
1980, however, this concept was controversial. Wilson (1920)
reported that the fibrocartilage of the TMJ condyle was softer than
hyaline cartilage, and therefore could not be load-bearing. Hylander
and Bays (1979) indirectly measured TMJ condylar loading in the
macaque with rosette strain gauges placed on the condylar neck,
and found that the condylar bone surface was indeed loaded during
function. Brehnan et al. (1981) and Boyd et al. (1990) directly
measured the condylar loading in the macaque by means of a
piezoelectric foil force transducer, and confirmed that the TMJ was
indeed a load-bearing articulation. Other experimental and
analytical studies (Smith et al., 1986; Koolstra et al., 1988; Korioth
et al., 1992; Beek et al., 2000) have also demonstrated that the
human TMJ was load-bearing under function. Although these
studies are all simulations, partially performed on data from
cadavers, they have shown that the fibrocartilaginous tissues,
including the disc and articular cartilage, have important functions
in stress distribution.
TMJ disorders are characterized by intra-articular positional
and/or structural abnormalities. Review studies published in the
1980s showed prevalence rates ranging from 16% to 59% for
symptoms and from 33% to 86% for clinical signs (Carlsson and
LeResche, 1995), although from 3% to 7% of the adult population
has sought care for TMJ pain and dysfunction (Carlsson, 1999). It
has been observed that up to 70% of persons with TMJ disorders
suffer from displacement of the articular disc, coined 'internal
derangement' of the TMJ (Farrar and McCarty, 1979).
Meanwhile, the most common joint pathology affecting the
TMJ is degenerative joint disease, also known as osteoarthrosis or
osteoarthritis. Among individuals with TMJ disorders, 11% had
symptoms of TMJ-osteoarthrosis (TMJ-OA) (Mejersjö and
Hollender, 1984). An epidemiological study, meanwhile, showed
that minimal flattening of the condyle and/or eminence was seen in
35% of TMJs in asymptomatic persons (Brooks et al., 1992). More
advanced osseous changes were not seen; therefore, it was
concluded that minimal flattening was probably of no clinical
significance. However, once the breakdown in the joint starts, TMJ-
OA can be crippling, leading to a variety of morphological and
functional deformities (Zarb and Carlsson, 1999).
This paper is divided into four parts. Part 1 will review the
definition and etiology of TMJ disorders. A basic review of the
TMJ disorders, their etiologies, and the biomechanical and
biochemical factors associated with functional overloading of the
joint will also be discussed. Part 2 will discuss the clinical,
radiographic, and biochemical analytical findings important in the
diagnosis of TMJ-osteoarthrosis. Part 3 will present the non-
invasive and invasive modalities utilized in TMJ-osteoarthrosis
management. Finally, in Part 4, the possibility of tissue-engineering
for treatment of TMJ disorders with degenerative changes will be
discussed.
ABSTRACTTemporomandibular joint (TMJ) disorders have complex
and sometimes controversial etiologies. Also, under
similar circumstances, one person's TMJ may appear to
deteriorate, while another's does not. However, once
degenerative changes start in the TMJ, this pathology can
be crippling, leading to a variety of morphological and
functional deformities. Primarily, TMJ disorders have a
non-inflammatory origin. The pathological process is
characterized by deterioration and abrasion of articular
cartilage and local thickening. These changes are
accompanied by the superimposition of secondary
inflammatory changes. Therefore, appreciating the
pathophysiology of the TMJ degenerative disorders is
important to an understanding of the etiology, diagnosis,
and treatment of internal derangement and osteoarthrosis
of the TMJ. The degenerative changes in the TMJ are
believed to result from dysfunctional remodeling, due to a
decreased host-adaptive capacity of the articulating
surfaces and/or functional overloading of the joint that
exceeds the normal adaptive capacity. This paper reviews
etiologies that involve biomechanical and biochemical
factors associated with functional overloading of the joint
and the clinical, radiographic, and biochemical findings
important in the diagnosis of TMJ-osteoarthrosis. In
addition, non-invasive and invasive modalities utilized in
TMJ-osteoarthrosis management, and the possibility of
tissue engineering, are discussed.
KEY WORDS: temporomandibular joint, degenerative
disease, osteoarthrosis, tissue engineering.
Received April 17, 2007; Last revision January 21, 2008; Accepted
January 23, 2008
Degenerative Disorders of the Temporomandibular Joint:Etiology, Diagnosis, and Treatment
E. Tanaka1*, M.S. Detamore2, and L.G. Mercuri3
1Department of Orthodontics and Dentofacial Orthopedics, TheUniversity of Tokushima Graduate School of Oral Sciences, 3-18-15Kuramoto-cho, Tokushima 770-8504, Japan; 2Department ofChemical and Petroleum Engineering, University of Kansas,Lawrence, KS, USA; and 3Department of Surgery, Division of Oraland Maxillofacial Surgery, Stritch School of Medicine, LoyolaUniversity Medical Center, Maywood, IL, USA; *correspondingauthor, [email protected]
J Dent Res 87(4):296-307, 2008
CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE
296
J Dent Res 87(4) 2008 Degenerative Disorders of the TMJ 297
DEFINITION ANDETIOLOGY OF TMJDISORDERSClassification of TMJDegenerative DisordersUnlike rheumatoid arthritis, TMJ-
osteoarthrosis has a non-inflam -
matory origin. The pathological
process is characterized by
deterioration and abrasion of
articular cartilage and local
thickening and remodeling of the
underlying bone (Zarb and
Carlsson, 1999). These changes
are frequently accompanied by the
superimposition of secondary
inflammatory changes. Therefore,
mechanically induced osteo -
arthrosis may better reflect TMJ-
osteoarthrosis.
Internal derangement of the
TMJ is defined as an abnormal
positional relationship of the disc
relative to the mandibular condyle
and the articular eminence (Fig.
1). Wilkes (1989) established 5
stages based on clinical and
imaging criteria. In Stage I,
clinical observations include
painless clicking and unrestricted
mandibular motion. When imaged,
the disc is displaced slightly
forward on opening, although it is
reduced at the maximum mouth
opening ('reducing' refers to the
disc sliding back to a "normal"
anatomical position during mouth
opening, producing the audible
clicking sound), and the osseous
contours appear normal (Fig. 1A).
In Stage II, there are complaints of
occasional painful clicking,
intermittent locking, and
headaches. When imaged, the disc
appears slightly deformed and
displaced slightly forward at
maximum opening, but still
reduces at maximum opening (Fig.
1B). The osseous contours appear normal. In Stage III,
clinically, there is frequent joint pain and tenderness,
headaches, locking, and restricted range of mandibular motion,
as well as painful chewing. When imaged, anterior disc
displacement is seen, with moderate thickening (Fig. 1C). This
disc reduces early in Stage III, but progresses to non-reducing
(i.e., locking) on opening in the later stage. The bony contours
remain normal in appearance. At the maximum mouth opening,
the disc is subjected to deformity, because the condyle pushes
the disc forward and downward (Fig. 1C). Recent studies, using
individual oblique-axial magnetic resonance imaging, have
shown that most anteriorly displaced discs were laterally
displaced (YJ Chen et al., 2000, 2002). A series of
experimental studies with surgical induction of anterior disc
displacement in the rabbit showed that disc displacement led to
the degenerative changes in the condylar cartilage (Sharawy etal., 2000, 2003). In contrast, the apparent radiographic
association of articular degeneration with disc displacement has
led to the suggestion that the degenerative process may be a
predisposing factor for disc displacement (Dijkgraaf et al.,1995). However, cadaver (Rohlin et al., 1985), clinical
(Westesson et al., 1989), and magnetic resonance imaging
studies (Kircos et al., 1987) have demonstrated that disc
displacement is a common finding in asymptomatic
Figure 1. Magnetic resonance images of TMJ-internal derangement and -osteoarthrosis. Internalderangement of the TMJ is defined as an abnormal positional relationship of the disc relative to themandibular condyle and the articular eminence, while TMJ-osteoarthrosis is characterized by structuralfailure of articular cartilage in the early stage and by the deterioration of the cartilage and subchondralbone, resulting in shortening of the mandibular ramus and subsequent mandibular retrusion. Both internalderangement and osteoarthrosis of the TMJ are regarded as a frequent cause of pain and/or disturbedmandibular movement. The characteristic radiographic sign of TMJ-osteoarthrosis is dysfunctionalremodeling on the mandibular condyle and articular eminence surfaces with osteophyte formation. (A) Atthe initial stage, the disc reveals a slight anterior disc displacement but not complete displacement at theintercuspal position. At maximum mouth opening, the disc is located between the condylar and temporalbone surfaces, and the condyle and disc move harmoniously. Arrowheads indicate the anterior andposterior ends of the disc. (B) At the intercuspal position, the disc reveals anterior displacement, but notbony remodeling and deformation. On full opening, the disc reduces, usually resulting in 2 noises(reciprocal clicking). Arrowheads indicate the anterior and posterior ends of the disc. (C) Throughmandibular movements, the disc is displaced from its normal position, and on full opening, the discdeformity occurs because the condyles push the disc forward and downward. In this case, bony changeson the condylar surface are not detected. Arrowheads indicate the anterior and posterior ends of the disc.(D) The disc also reveals anterior displacement without reduction, in which the disc is severely deformed onfull opening. Arrowheads indicate the anterior and posterior ends of the disc. Furthermore, the osteophyteof the peripheral cortical bone, indicated by arrows, is clearly detected, indicating TMJ-osteoarthrosis. (E)The condyle shows severe bony deformation with flattening and erosion, indicating severe osteoarthrosis ofthe TMJ. Arrows indicate the deformed surface of the mandibular condyle. The disc also reveals anteriordisplacement without reduction. Arrowheads indicate the anterior and posterior ends of the disc. Theindividual at this stage is likely to have spontaneous joint pain and movement disability.
298 Tanaka et al. J Dent Res 87(4) 2008
individuals. In Stage IV, individuals complain of chronic pain,
headache, and restricted mandibular range of motion. When
imaged, a markedly thickened disc is anteriorly displaced and
does not reduce on opening, and abnormal contours to both the
condyle and articular eminence begin to become evident (Fig.
1D). In Stage V, clinically, individuals experience pain,
crepitus, and pain with mandibular function. When imaged, the
now grossly deformed disc is anteriorly displaced, without
reduction, and degenerative changes are present in the osseous
components of the articulation (Fig. 1E). The disease process is
characterized by deterioration and abrasion of articular
cartilage and disc surfaces, and occurrence of thickening and
remodeling of the underlying bone. Therefore, osteoarthrosis
may be a final common pathway for several joint conditions,
including inflammatory, endocrine, metabolic, developmental,
and biomechanical disorders (Zarb and Carlsson, 1999).
Etiology of TMJ Degenerative DisordersIncreased loading in the TMJ may stimulate remodeling,
involving increased synthesis of extracellular matrices
(Stegenga et al., 1989). Remodeling is an essential biological
response to normal functional demands, ensuring homeostasis
of joint form, and function and occlusal relationships (Smartt etal., 2005). Arnett et al. (1996a,b) proposed an explanation for
the pathophysiology of the degenerative changes as one that
results from dysfunctional articular remodeling due to (1) a
decreased adaptive capacity of the articulating structures of the
joint or (2) excessive or sustained physical stress to the TMJ
articular structures that exceeds the normal adaptive capacity.
The former is the host-adaptive capacity factor, which is
associated with the host's general condition. Advancing age,
systemic illness, and hormonal factors may define the host-
adaptive capacity of the TMJ. This factor may contribute to
dysfunctional remodeling of the TMJ, even when the
biomechanical stresses are within a normal physiologic range.
Age is clearly a predisposing factor, because both frequency
and severity of the disease appear to increase with aging. For
example, the calcium content of the human disc increases
progressively with aging (Takano et al., 1999). This increase in
calcification may be caused by aging as such, or by a changed
mechanical stress (Jibiki et al., 1999). Accordingly, the
material properties of the disc can also be expected to be
related to age (Tanaka et al., 2001). This implies that the disc
becomes more stiff and fragile in nature, reducing its capability
to handle overload. Articular cartilages can also change with
aging. The molecular weight of hyaluronic acid in human
articular cartilage decreases from 2000 to 300 kDa between the
ages of 2.5 and 86 yrs (Holmes et al., 1988). Hyaluronic acid in
articular cartilage is essential for it to maintain its viscosity, and
any decrease in molecular weight can lead to reduction of its
biorheological property in cartilage.
Systemic illness may also influence fibrocartilage
metabolism and could affect the adaptive capacity of the TMJ.
These illnesses may include autoimmune disorders, endocrine
disorders, nutritional disorders, metabolic diseases, and
infectious disease. Hormonal factors may also have a marked
influence on remodeling of the mandibular condyle. In these
cases, the TMJ degenerative disorders may be the result of
systemic disease.
Mechanical factors can also cause changes in the TMJ
structure. Despite host-adaptive capacity, excessive or
unbalanced mechanical loading in the TMJ can cause overload
of articular tissues, resulting in the onset and progression of
TMJ-osteoarthrosis. Furthermore, internal derangement of the
TMJ may be induced by excessive or unbalanced stress in the
TMJ. From a review of etiological mechanical events of TMJ-
and increased joint friction play a role (Stegenga et al., 1989;
Arnett et al., 1996a,b; Nitzan, 2001). These factors may occur
alone or may be interrelated, interdependent, and/or co-
existent.
Macrotrauma in the condylar area can cause degeneration
of the articular cartilage and production of inflammatory and
pain mediators. Trauma has been reported to alter the
mechanical properties of the disc (Nickel et al., 2001) and to
cause mechanical fatigue of the disc (Beatty et al., 2001, 2003).
Furthermore, it may cause cartilage degradation and production
of inflammatory and pain mediators. TMJ alterations occurred
over time after the macrotrauma, leading to progressive
condylar resorption and deformation (Arnett et al., 1996b).
However, only about one-third of the individuals with TMJ
degenerative changes reportedly suffered previous trauma to
the head and neck (Laskin, 1994). The mechanism of delayed
condylar resorption and deformation in secondary macrotrauma
is not understood, but the clinician should recognize the
etiologic importance of the macrotrauma and long-term
evaluation of the TMJ form and function after macrotrauma.
Parafunction may produce abnormal compression and
shear forces capable of initiating disc displacement and
condylar and articular eminence degenerative changes (Gallo etal., 2006). Parafunctional hyperactivity of the lateral pterygoid
muscle has been considered to lead to masticatory muscle pain
(Hiraba et al., 2000; Murray et al., 2001). Since the superior
head of the lateral pterygoid muscle attaches partly to the
articular capsule of the TMJ and directly or indirectly to its
articular disc (Murray et al., 2001), it has been hypothesized
that dysfunction of this muscle can lead to TMJ-internal
derangement and -osteoarthrosis (Hiraba et al., 2000).
Functional overloading and increased joint friction may
act together as etiological events for TMJ-internal derangement
and -osteoarthrosis. Growing evidence suggests that functional
overload with subsequent microtrauma is a crucial event for
TMJ-internal derangement and -osteoarthrosis. Milam et al.(1998) proposed the direct mechanical injury and
hypoxia/reperfusion injury model, suggesting that the oxidative
stress results in the accumulation of free radicals that damage
the articular tissues of the TMJ. Several studies have
demonstrated the presence of reactive oxidative radical species
in synovial fluid from diseased TMJs (Kawai et al., 2000;
Takahashi et al., 2003).
Mechanism of Functional Overloading for TMJ Degenerative Disorders (Fig. 2)In chondrocytes of articular cartilage, cyclic tensile loading up-
regulated the expression of matrix metalloproteinase (MMP)-
13 and vascular endothelial growth factor (VEGF) and down-
regulated the expression of tissue inhibitor of matrix
metalloproteinases (TIMP)-1, while cyclic hydrostatic pressure
induced opposite effects (Wong et al., 2003). VEGF expression
in osteoarthritic cartilage appeared to increase progressively
with the applied mechanical overload. Furthermore, VEGF
induction in chondrocytes by mechanical overload has been
linked to activation of hypoxia-induced transcription factor-1
J Dent Res 87(4) 2008 Degenerative Disorders of the TMJ 299
(Forsythe et al., 1996). Recently,
Tanaka et al. (2005a) showed that
mandibular condylar cartilage in
mechanically induced TMJ-
osteoarthrosis expressed abundant
VEGF. VEGF regulates the production
of MMPs and TIMPs, which are
among the effectors of extracellular
matrix remodeling (Pufe et al., 2004).
Reduction of TIMPs and induction of
MMPs result in an imbalance in the
turnover of extracellular matrix
components, collagens, and
proteoglycans, which are degraded
more rapidly than they are formed.
The loss of balance toward increased
extracellular matrix degradation
results in the destruction of cartilage
(Pufe et al., 2004).
The expression of VEGF is also
up-regulated in the synovial tissues
(Sato et al., 2003) and the TMJ disc
(Leonardi et al., 2003) in TMJ-internal
derangement. This suggests that
VEGF expression is involved in the
development of inflammatory changes
in the TMJ as a reaction to the
cytokine. The increased expression of
VEGF in the joint tissues might lead to
an increase of VEGF in the synovial
fluid of persons with symptomatic
TMJ-internal derangement (Sato et al.,2005). Consequently, mechanical
overload induces hypoxia-induced
transcription factor-1, and the
subsequently generated VEGF
activates the chondrocytes in an
autocrine manner to produce MMPs and reduces TIMPs (Pufe
et al., 2004). This implies that VEGF is probably induced in
chondrocytes by mechanical overload, facilitating hypoxia and
mediating the destructive processes associated with
osteoarthrosis as an autocrine factor.
Furthermore, in the condylar cartilage with TMJ-
osteoarthrosis, the number of blood vessels and osteoclasts is
markedly increased in the area subjacent to the hypertrophic
cell layer, where several VEGF-expressing chondrocytes are
detected (Tanaka et al., 2005a). Since VEGF plays an
important role not only in endothelial cell recruitment, but also
in osteoclast recruitment (Niida et al., 1999), VEGF has
overlapping function in the support of osteoclastic bone
resorption. Then, the increase in osteoclasts stimulated by
VEGF may induce destruction of cartilage, making vascular
invasion into the condylar cartilage easier.
Overloading also causes collapse of joint lubrication, as the
result of hyaluronan degradation by free radicals (Nitzan,
2001). With overloading, the increase in intra-articular
pressure, when it exceeds the capillary perfusion pressure, will
cause temporary hypoxia, which is corrected by re-oxygenation
on cessation of degradation by the overloading. Such a
hypoxia-reperfusion cycle has been reported to release reactive
oxidative radical species non-enzymatically (Grootveld et al.,
1991). Among other effects of reactive oxidative radical
species in synovial joints are inhibition of the biosynthesis and
degradation of hyaluronic acid, both causing marked reduction
in viscosity of synovial fluid (Grootveld et al., 1991).
In the healthy TMJ, the co-efficient of friction between the
cartilage surfaces can be assumed to be almost zero by the
presence of synovial fluid (Tanaka et al., 2004; Nickel et al.,2001, 2006). However, after an experimental abrasion of the
articular cartilage comparable with TMJ-osteoarthrosis, the co-
efficient of friction was 3.5 times greater than that in the intact
joint (Tanaka et al., 2005b). As the coefficient of friction
increases, the shear stresses between the articular surfaces,
within the disc, and articular cartilage become greater. Shear
stress can result in fatigue and damage and irreversibly deform
the TMJ tissues, initiating TMJ-internal derangement and -
osteoarthrosis (Beatty et al., 2003; Tanaka et al., 2003).
Hyaluronan degradation is likely to occur in pathologic
joints because of free-radical de-polymerization of the
hyaluronic acid chain (McNeil et al., 1985) or the abnormal
biosynthesis of hyaluronic acid by type B synovial cells
(Vuorio et al., 1982). Free radicals rapidly depolymerize
hyaluronic acid in vitro, which may implicate them in the
degradation of hyaluronic acid in vivo. Furthermore, the
degradation of hyaluronic acid may lead to cartilage destruction
Figure 2. The concept of the process of cartilage breakdown in the TMJ. A decreased adaptivecapacity of the articulating structures and/or excessive physical stress to the TMJ that exceeds thenormal adaptive capacity can induce dysfunctional remodeling. Functional overloading andincreased joint friction may act together as etiological events for TMJ degenerative changes.Functional overloading can facilitate hypoxia in the TMJ and mediate the destructive processesassociated with osteoarthrosis as an autocrine factor. Vascular endothelial growth factor (VEGF)induction in osteoarthritic cartilage by functional overloading is linked to activation of the hypoxia-induced transcription factor-1, leading to hypoxia in the joint tissue. Furthermore, VEGF regulatesthe production of matrix metalloproteinases and tissue-inhibitors of matrix metalloproteinases, whichare among the effectors of extracellular matrix remodeling. Overloading also causes collapse of jointlubrication as the result of the hyaluronic acid degradation by free radicals. The regulation ofhyaluronic acid production is controlled by various pro-inflammatory cytokines. Of these cytokines,tumor necrosis factor-� and interleukin-1 and -6 play crucial roles in the pathogenesis ofosteoarthrosis with respect to the acceleration and progression of cartilage degradation, becausethey promote bone resorption through the differentiation and activation of osteoclasts.
300 Tanaka et al. J Dent Res 87(4) 2008
in terms of the enhanced expression of MMPs (Ohno-Nakahara
et al., 2004). Since neither healthy nor inflammatory synovial
act as counter-irritants to reduce inflammation and pain.
Superficial warm and moist heat or localized cold may relieve
pain sufficiently to permit exercise. Therapeutic exercises are
designed to increase muscle strength, reduce joint
contractures, and maintain a functional range of motion.
Ultrasound, electrogalvanic stimulation, and massage
techniques are also helpful in reducing inflammation and pain
(De Laat et al., 2003).
Active and passive jaw movements, manual therapy
techniques, and relaxation techniques were used in the
management of 20 consecutive persons with TMJ-
osteoarthrosis. After treatment (mean, 46 days), pain at rest was
Table 2. Classification of Osteoarthrosis Based on Symptoms, Signs, and Imaging with Management Options.
Stage Symptoms Signs Imaging Management Options
I Joint/muscle pain Little or no Mild to moderate Non-InvasiveEarly Disease Limited function occlusal or facial erosive changes of or Minimally invasive
Crepitus esthetic changes condyle/fossa/eminence
II Little or no joint pain Class II malocclusion Flattened Bone and JointArrested Disease Muscle pain Apertognathia condyle/eminence Invasive or Salvage
Some joint dysfunctionCrepitus
III Joint/muscle pain High-angle Class II Gross erosive changes SalvageAdvanced Disease Loss of function malocclusion Loss of condyle and