| Magnetic resonance imaging of the lateral pterygoid muscle in temporomandibular disorders | ||
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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 & Ogutcen-Toller 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 (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.
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 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.
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.
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).
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 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).
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 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).