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Oral Diseases (2002) 8, 1±2

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GUEST EDITORIAL
Disorders of the temporomandibular joint.
What comes next?
FJ Pereira Jr
1
Department of Occlusion and Temporomandibular Disorders, UNIGRANRIO and Department of Temporomandibular Disorders,
Universidade EstaÂcio de SaÂ, Rio de Janeiro, Brazil

Osteoarthrosis (OA), a primarily non-in¯ammatory raise the question whether or not disk displacement is a
joint disease, and internal derangement, an orthopedic pathologic entity or remains within the normal range of
term de®ned as a localized mechanical fault which anatomical or physiologic variation. As we approached
interferes with the smooth action of a joint, are the most the end of the last millenium and new information
frequent disorders a€ecting the temporomandibular became available, it was clear that the frequency of
joint (TMJ). Degenerative changes and disk displace- displaced disks in asymptomatic volunteers was much
ment are, by far, the most common morphologic lower when compared with the frequencies in patients
changes among TMJ patients. The presence of degener- with TMJ disorders (Tasaki et al, 1996; Ribeiro et al,
ative changes is a necessary sign for the diagnosis of 1997). Is disk displacement a coadjuvant factor that
osteoarthrosis while disk displacement is the main cause increases the chance of the development of TMJ pain in
of internal derangement. For decades, the associations some individuals? We still have little knowledge of the
between these disorders on one hand and the changes pathophysiologic mechanisms underlying the develop-
described on the other were highly investigated in several ment of TMJ pain. Signi®cant histological di€erences
studies and these morphologic changes were pointed out have been found between painful and asymptomatic
as being the most likely causes for pain in the TMJ. The TMJs with disk displacement, con®rming an association
recent experimental study by Imai et al (2001) in Oral between pain and histological changes of the retrodiskal
Diseases makes a further useful contribution. tissues (Pereira et al, 1996). There was an histological
As early as 1887 (Annandale, 1887) and 1918 (Pringle, indication of higher mechanical loads in the retrodiskal
1918), disk displacement was already mentioned as a tissues of painful TMJs. In spite of this, very little is
causative factor for TMJ pain and dysfunction. Yet, it known about the forces transmitted to the retrodiskal
was not until the late seventies that the association tissues. Moreover, it remains necessary to test each of
between this condition and disturbances of the TMJ the variables before these associations may be inter-
became available to a larger number of clinicians and preted in terms of cause-e€ect.
researchers (Wilkes, 1978). Since then, our understand- Another challenge for this century is the inconsistencies
ing of the dysfunctional mechanisms associated with regarding the presence of degenerative changes and its
disk displacement has shown a rapid and continued relation to diseases. Radiographic signs of degenerative
development, mainly because of the improvements in changes have been observed in the TMJ of patients with
the quality and resolution of imaging techniques such as OA (de Leeuw et al, 1995) and chronic in¯ammatory joint
arthrography and MRI. In 1987, disk displacement was diseases (Wenneberg et al, 1990), which implies that
also reported in asymptomatic volunteers (Kircos et al, degenerative changes may be a result of pathologic
1987). Later on, autopsy specimens belonging to a non- processes. Conversely, they have been present in TMJs
TMJ patient population revealed the presence of disk belonging to non-TMJ patients (Pereira et al, 1994b). In
displacement and gross degenerative changes (Pereira human autopsy material (Westesson and Rohlin, 1984)
et al, 1994b). Despite the high prevalence of morpho- and in rabbits (Ali and Sharawy, 1994), normal articular
logic changes observed, none of the individuals previ- surfaces have been associated with normal disk position
ously interviewed and examined had ever sought TMJ whereas joints with disk displacement had degenerative
treatment. They also reported few symptoms which changes. Another important issue in this regard is how the
never interfered with their normal lives. These results presence of degenerative changes relates to senescence. In
a large study comprising 2296 individuals, the prevalence
of radiographic degenerative changes in joints from the
Correspondence: Francisco J Pereira Jr, Rua Visconde de PirajaÂ, hands, feet and cervical spine was found to be 97% in
595/213 ± Ipanema, 22410-003 Rio de Janeiro, RJ, Brazil.
Fax: +55 21 2274-0189, E-mail: francp@attglobal.net
males and females over 64 years of age (Lawrence et al,
Received 24 January 2000; revised 28 February 2000; 1966), while in autopsy specimens the frequency of
accepted 16 October 2001 degenerative changes was higher in TMJs belonging to
Disorders of the temporomandibular joint
FJ Pereira Jr

2
elderly persons compared with TMJs from young persons model of degenerative joint disease. Am J Pathol 135:
(Pereira et al, 1994a). Strains of accelerated senescence 379±385.
prone mice developed condylar degenerative changes Imai H, Sakamoto I, Yoda T, Yamashita Y (2001). A model
earlier than did strains of accelerated resistant mice (Chen for internal derangement and osteoarthrosis of the tempo-
romandibular joint with experimental traction of the man-
et al, 1989). It is clear that the development of degener-
dibular ramus in rabbit. Oral Dis 7: 185±191.
ative changes in these animals is related not only to Kircos LT, Ortendahl DA, Mark AS et al (1987). Magnetic
chronological age but also to the accelerated senescence resonance imaging of the TMJ disc in asymptomatic
phenomenum. All these ®ndings support the assumption volunteers. J Oral Maxillofac Surg 45: 852±854.
that degenerative changes are probably a result of Lawrence JS, Bremner JM, Bier F (1966). Osteo-arthrosis.
di€erent processes a‚icting the TMJ. If this is true, how Prevalence in the population and relationship between
may each of these processes lead to the appearance of symptoms and x-ray changes. Ann Rheum Dis 25: 1±24.
these changes? How can we distinguish changes related to de Leeuw R, Boering G, Stegenga B et al (1995). Radio-
age from pathologic or adaptive changes? Further TMJ graphic signs of temporomandibular joint osteoarthrosis
studies at the cellular and molecular level are necessary to and internal derangement 30 years after nonsurgical treat-
ment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
shed light on these issues.
79: 382±392.
Biochemical synovial ¯uid analyses open new fron- Pereira FJ Jr, Lundh H, Eriksson L et al (1996). Micro-
tiers in TMJ pain research. Substances such as, calcito- scopic changes in the retrodiscal tissues of painful
nin gene-related peptide, neuropeptide Y and temporomandibular joints. J Oral Maxillofac Surg 54:
interleukin-1b have been identi®ed in the synovial ¯uid 461±468.
pertaining to pathologic TMJs (Appelgren et al, 1995; Pereira FJ Jr, Lundh H, Westesson P-L (1994a). Morphologic
Suzuki et al, 1999). These investigations have shown a changes in the temporomandibular joint in di€erent age
great potential to reveal new aspects on the pathogenesis groups. An autopsy investigation. Oral Surg Oral Med Oral
of TMJ disorders. They may provide explanations about Pathol 78: 279±287.
pain and destruction mechanisms in the TMJ during the Pereira FJ Jr, Lundh H, Westesson P-L et al (1994b). Clinical
®ndings related to morphologic changes in TMJ autopsy
in¯ammatory process and at the same time disclose why
specimens. Oral Surg Oral Med Oral Pathol 78: 288±295.
patients with OA and chronic in¯ammatory joint disease Pringle JH (1918). Displacement of the mandibular meniscus
have a higher degree of articular destruction when and its treatment. Br J Surg 6: 385±389.
compared with asymptomatic individuals. These ®nd- Ribeiro RF, Tallents RH, Katzberg RW et al (1997). The
ings might help the development of more speci®c prevalence of disc displacement in symptomatic and asymp-
diagnostic and treatment methods than the ones avail- tomatic volunteers aged 6±25 years. J Orofacial Pain 11:
able at present, through the identi®cation of markers of 37±47.
disease. As a result, these analyses may have a great Suzuki T, Segami N, Kaneyama K et al (1999). Speci®c
impact on to the development of antagonists to medi- expression of interleukin-1b in temporomandibular joints
ators of pain and in¯ammation. with internal derangements. Correlation with clinical ®nd-
ings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 88:
413±417.
References Tasaki MM, Westesson P-L, Isberg AM et al (1996). Classi-
®cation and prevalence of temporomandibular joint disc
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rabbit craniomandibular joint associated with experiment- Orthod Dentofac Orthop 109: 249±262.
ally induced anterior disk displacement (ADD). J Oral Wenneberg B, KoÈnoÈnen M, Kallenberg A (1990). Radio-
Pathol Med 23: 364±374. graphic changes in the temporomandibular joint of patients
Annandale T (1887). Displacement of the inter-articular with rheumatoid arthritis, psoriatic arthritis, and ankylosing
cartilage of the lower jaw, and its treatment by operation. spondylitis. J Craniomandib Disord Facial Oral Pain 4:
Lancet 1: 411. 35±39.
Appelgren A, Appelgren B, Kopp S et al (1995). Neuropep- Westesson P-L, Rohlin M (1984). Internal derangement
tides in the arthritic TMJ and symptoms and signs from the related to osteoarthrosis in temporomandibular joint
stomatognathic system with special consideration to rheu- autopsy specimens. Oral Surg 57: 17±22.
matoid arthritis. J Orofacial Pain 9: 215±225. Wilkes CH (1978). Arthrography of the temporomandibular
Chen W-H, Hosokawa M, Tsuboyama T et al (1989). Age- joint in patients with the TMJ pain-dysfunction syndrome.
related changes in the temporomandibular joint of the Minn Med 61: 645±652.
senescence accelerated mouse. SAM-P/3 as a new murine

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