- Email: [email protected]
An investigation into the mechanism of “locking” in the myofascial pain dysfunction syndrome (MPD)
lnt. J. Oral Sttrg. 1975: 4 : 6 9 - 7 2 (Key words: muscle tonus; temporomandibular joint)
An investigation into the mechanism of "locking" in the myofascial pain dysfunction syndrome (MPD) HESHAM E L - E S S A W Y
Department of Oral Sttrgery, King's College Hospital Dental School, London, U.K.
Locking of the temporomandibular joint is often attributed to uncoordinated muscle activity and muscle spasm. A simple experiment has been devised to test the hypothesis that locking occurs when uncoordinated elevator muscle tension (temporalis, masseter and medial pterygoid) precedes and interferes with the opening action of the lateral pterygoid muscle. By asking the patients with manifest locking to protrude prior to maximal opening (protrude-open maneuver, POM) a highly significant increase of mouth opening was found over that produced by s~mple maximal opening (MO). No significant difference was found in a group of patients with myofascial pain as tlteir only symptom, or in a group of healthy controls, suggesting that pain does not contribute to the mechanism of locking. ABSTRACT
-
(Received/or publication 25 September, accepted 16 December 1974)
The cardinal signs and symptoms of the myofascial pain dysfunction syndrome (MPD) are clicking, limitation of mandibular opening, masticatory muscle tenderness and pain in and around the temporomandibular joint region. It is often stated that these symptoms are due to incoordination of mastieatory muscle activity2,~, s,o,~o,15, 22. However, the question of the nature of this incoordination has received minimal attention as compared to perhaps the more important questions of etiology and treatment. The lateral pterygoid muscle is the prime mover in opening, protrusion and laterotru-
sion; it also serves either to stabilize movement or to guide the articular components of the temporomandibular joint1,1~. The elevators (masseters, temporales and medial pterygoids) act as antagonist-stabilizers that relax during the early phase of opening, and show some activity at the end of the movement, presumably to limit opening. Overactivity of the lateral pterygoid muscle has been blamed for the pathogenesis of the syndromeS, S,~1. However, in an electromyographie study of masticatory muscle forces, ~VIARKL'UND& MOLIN11 found in a group of subjects with manifest pain dysfunction syndrome that
70
EL-ESSAWY
during p r o t r u s i o n the m e a n force generated at m a x i m u m effort was only half the m e a n force similarly generated in a control group of non-afflicted subjects. T h e y interpreted the d i f f e r e n c e as being an effect of the p a i n experienced b y the m a n d i b u l a r dysfunction s y n d r o m e patients. However, this was cont r a d i c t e d b y a separate study is that showed p r a c t i c a l l y n o differences were found between t h e laterotrusive forces generated b y the patients towards a n d away from the p a i n f u l affected side or between the p a tients a n d the healthy subjects. On t h e other hand, most investigators agree that elevator muscle tension (i.e. masseter, temporalis ,and medial pterygoid) is significantly higher in patients with M P D c o m p a r e d with healthy controls~,Lv~,lL ~-3. T h e aim of this study is to investigate t h e role of the lateral pterygoid muscle in the limitation of mandibular opening, i.e. "locking". The working hypothesis is t h a t ill locking, the lateral pterygoid muscle is actually a "victim" rather than the cause. I n c r e a s e d elevator muscle tension upsets the coordination of the masticatory mechanism b y interfering with the lateral pterygoid muscle action during t h e opening movement, thus causing locking and ultimately pain, b u t if the lateral pterygoid is allowed to act uninterrupted during the opening m o v e m e n t , locking would be avoided and m o u t h opening could be increased.
Material and methods A simple experiment has been devised to test this hypothesis. By asking the patient to protrude the mandible prior to maximal opening (protrude-open maneuver, POM) the condyle is brought forwards and downwards, i.e. as close to its normal position in opening as possible, thus decreasing the time and distance in which interplay between the elevators and the lateral pterygoids occurs. This opening is compared with simple maximal opening (MO) (i.e. opening without prior protrusion). Measurements of interincisal distance were made using a Willis
bite gauge, taking the maximal reproducible reading between the same maxillary and mandibular incisal edges in every case. GROUPING Group A Thirty.five patients (5 males and 30 females) with manifest MPD are subdivided into the subgroups, A 1 and A 2 according to their symptoms. Subgroup A 1 Twenty patients (3 males and 17 females), mean age 27 + 8 years, with manifest clicking, locking and muscular pain. Subgroup A 2 Fifteen patients (2 males and 13 females), mean age 22 +__5 years, with manifest clicking and locking only. Care was taken to exclude cases of osteoarthrosis, traumatic arthritis and rheumatoid arthritis, since their signs and symptoms may mimic those described for Group A. The criteria for selection of patients in this group were the absence of radiographic changes (transpharyngeal technique and orthopantomograms were taken routinely), of joint disorders elsewhere, or crepitus, and history of direct joint trauma. Group B Fifteen patients (8 males and 7 females), mean age 27 -t- 7 years, in whom masticatory muscle pain was their only symptom (i.e. myofascial pain) were included to investigate whether muscle spasm and pain contributo to the mechanism of locking. None of the patients in this group had a history of joint noise, clicking or locking. Group C Thirty-five healthy subjects (8 males and 27 females), mean age 24 __+7 years, were used as controls. The results are summarized and tabulated in Table 1.
Discussion All patients with limitation of m o u t h opening "locking" (Groups A 1 a n d A 2) showed a significant increase in m o u t h opening following protrude-open m a n e u v e r
71
MYOFASCIAL PAIN DYSFUNCTION SYNDROME
Table 1.. The means and standard deviations in mm of maximal opening (MO), protrude-open maneuver (POM) and the difference (D) of each of the groups, A 1, A 2, B and controls. Group A 1 symptoms are clicking, locking and pain; Group A 2, clicking and locking only; and Group B is muscle pain only Group
A1
A2 $~$
B $g.'$
Controls $'0~
Maximal opening (MO)
35 _+ 7
25 +_ 9
38 _+ 8
44 _+ 5
Protrude-open maneuver (POM)
40 +_ 7
37 _+ 8
37 + 8
44 _. 5
$$~
***
Differences (D = P O M - M O )
5+ 1
12 +_ 5
-1
0
Percentage increase of mouth opening by POM
14 %
48 %
0%
0%
* Denotes a significant difference from controls (P < 0.05). ** Denotes a very significant difference from controls (P < 0.01). *** Denotes a highly significant difference from controls (P < 0.001).
(POM) over that produced by simple maximal opening (MO). This would appear to show t h a t conscious control of lateral pterygoid function suppresses the interference of the m o r e powerful elevators and so overcomes locking. N o significant increase was f o u n d in those patients with no manifest locking (Group B) or in controls (Group C). F o r patients with no pain (A 2) the percentage increase (48 %) was significantly higher than that produced by patients with manifest pain (A1) (14 %). The cause of this difference lies in their (MO) readings and n o t the (POM) readings. This is an interesting finding that could be interpreted as indicating that attempts by the patient to free his lock and perhaps "fight against it" m a y be a factor in pain production, especially in the lateral pterygoid muscle; hence, the higher M O readings in A l's. Such an interpretation is supported by the observation that clicking and locking comm o n l y precede the incidence of painLx~,~L However, as the age incidence for patients in pain (A 1) is significantly higher than for the patients with no pain (A2) (P <~ 0.001) there is also the possibility that
this group is heterogeneous and includes undisclosed cases of painful degenerative intraarticular changes due to dysfunction, as has been implied by the work of TOLenRis. This, o~ course, does not alter the concept of locking as described here. In Groups A a n d B the means of both MO and P O M were significantly less than those found in controls. This may be due to either elevator muscle spasm and/or depressor inhibition, which agrees with the electromyographic findings of MARI~I.rND & MOt IN1~ and MOLIN~8. In contrast to G r o u p A, the absence of any significant difference between M O and P O M in Group B indicates that muscle pain, caused by either spasm or fatigue, does not contribute to the locking mechanism (none of the patients in Group B described locking as one of their symptoms). It is the writer's view that, in spite of some similarity in the etiology and treatment of patients in Groups A and B, the difference in the nature of both disorders should be appreciated. A generalized increase in masticatory muscle tension alone may lead to muscular pain (myofascial
72
EL-ESSAWY
pain) while an uncoordinated increase in muscle tension m a y lead to Myofascial P a i n Dysfunction Syndrome. A c k n o w l e d g m e n t - I am greatly indebted to Mr. M. t-lAmtm, Consultant Oral Surgeon, King's College Hospital Dental School, for txis assistance and valuable criticism during preparation of this paper, also to Professor J. SoWm~Y, Head of the Department of Oral Surgery, Mr. G. FORMAN, Consultant Oral Surgeon, King's College Hospital, for granting me access to their patients in the Temporomandibular loint Clinic and their continuous encouragement, and to Mr. C. YATES for helpful comments during this investigation.
References I. CARLS56, S.: An eleetromyographic study of the function of the laterat pterygoid muscle. Swed. Dent. J. 1956: 66: 203-208. 2. F~NKS, A. S. T.: Masticatory muscle hyperactivity and TMJ dysfunction. Y. Prosthet. Dent. 1965: 15: 1122-1131. 3. GREENE, C. S., LERMAN, M. D., SUTCttER, H. D. & LASKIN, D. M.: The TMJ pain dysfunction syndrome: heterogeneity of the patient population. J. A m . Dent. Assoc. 1969: 79: 1168-1172. 4. GgwFrN, C. Y. & MUNRO, R. R.: Electromyography of the masseter and anterior temporalis muscles in patients with temporomandibular joint dysfunction. Arch. Oral Biol. 1971: 16: 929--949. 5. GROSS~hN, W. L, Gm~ENFr~LD, B. E. & "I'IMMS, D. T.: Electromyography as an aid in diagnosis and treatment analysis, Am. J. Orthodont. 1961: 47: 481-497. 6. IRELAND, V. E.: The problem of the clicking jaw. Proc. R. Soc. Med. 1951: 44: 363371. 7. Im~LAND, V. E.: Disorders of the mandibular joint, aetiology and differences of diagnosis and conservative treatment. Br. Dent. J. 1963: 115: 287-291. Address: D e p a r t m e n t o / Oral Surgery K i n g ' s College Hoepital Dental School D e n m a r k Hill London, S.E.5. U.K.
8. LERMAN,M. D.: A unifying concept of the TMJ pain dysfunction syndrome, g. Am. Dent. Assoc. 1973: 86: 833-841. 9. LASKIN, D. M.: Etiology of pain dysfunction syndrome. J. A m . Dent. Assoc, 1969: 79: 147-153. 10. MA~aeH, J. J.: Therapy for mandibular dysfunction in adolescents and adults. A m . J. Orthodont. I972: 62: 601-605. 11. MaRKLr~D, G. & MOL1N, C.: Horizontal isometric muscle forces of the mandible. A e t a Odontol. Scand. 1972: 30: 97-115. 12. M(3LLER, E.: The chewing apparatus. A c t a Physiol. Scand. 1966: Vol. 69: Suppl. 13, MOLIN, C.: An electromyographic study of the function of the lateral pterygoid muscle. Swed. Dent. J. 1973: 66: 203-208. 14. PERRY, H. T. JR.: Muscular changes associated with TMJ dysfunction. J. A m . D e n t . Assoc. 1957: 54: 644. 15. SCHWARTZ, L.: Pain associated with the TMJ. J. Am. Dent. Assoc. 3955: 51: 394397. 16. SCHWARTZ, L.: Conclusions of the T M J clinic at Colombia. J. Periodont. 1958: 29: 210-212. 17. TOLLER, P. A.: The synovial apparatus and temporomandibular joint function. Br. Dent. J. 1961: 111: 355-362. 18. TOLLER, P. A.: Temporomandibular joint arthrosis. Br. Dent. I. 1973: 134: 223-231. 19. T ~ o ~ s , L J., TruER, N. & SCmRESON, S.: The effect of anxiety and frustration o,f muscular tension related to the T M J syndrome. Oral Surg. 1973: 36: 763-768. 20. VXUOHt,N, H. D.: A study of the temporomandibular articulation. I. A m . D e n t . A s soc. 1943: 30: 1501-1507. 21. V~uor~aN, H. C.: Temporomandibular joint pain: a new diagnostic approach. 1. Prosthet. Dent. 1954: 4: 694. 22. YAVE~.OW, I., FORST~R, I. & WINNGER, M.: Mandibular relearning. J. Oral Surg. 1973: 36: 632-641. 23. YEMM, R.: A comparison of the activity of the left and right masseter muscles of mammals and patients with pain dysfunction syndrome during experimental stress. ]. Dent. Res. 1971: 50: 1320-1323.
An investigation into the mechanism of "locking" in the myofascial pain dysfunction syndrome (MPD) HESHAM E L - E S S A W Y
Department of Oral Sttrgery, King's College Hospital Dental School, London, U.K.
Locking of the temporomandibular joint is often attributed to uncoordinated muscle activity and muscle spasm. A simple experiment has been devised to test the hypothesis that locking occurs when uncoordinated elevator muscle tension (temporalis, masseter and medial pterygoid) precedes and interferes with the opening action of the lateral pterygoid muscle. By asking the patients with manifest locking to protrude prior to maximal opening (protrude-open maneuver, POM) a highly significant increase of mouth opening was found over that produced by s~mple maximal opening (MO). No significant difference was found in a group of patients with myofascial pain as tlteir only symptom, or in a group of healthy controls, suggesting that pain does not contribute to the mechanism of locking. ABSTRACT
-
(Received/or publication 25 September, accepted 16 December 1974)
The cardinal signs and symptoms of the myofascial pain dysfunction syndrome (MPD) are clicking, limitation of mandibular opening, masticatory muscle tenderness and pain in and around the temporomandibular joint region. It is often stated that these symptoms are due to incoordination of mastieatory muscle activity2,~, s,o,~o,15, 22. However, the question of the nature of this incoordination has received minimal attention as compared to perhaps the more important questions of etiology and treatment. The lateral pterygoid muscle is the prime mover in opening, protrusion and laterotru-
sion; it also serves either to stabilize movement or to guide the articular components of the temporomandibular joint1,1~. The elevators (masseters, temporales and medial pterygoids) act as antagonist-stabilizers that relax during the early phase of opening, and show some activity at the end of the movement, presumably to limit opening. Overactivity of the lateral pterygoid muscle has been blamed for the pathogenesis of the syndromeS, S,~1. However, in an electromyographie study of masticatory muscle forces, ~VIARKL'UND& MOLIN11 found in a group of subjects with manifest pain dysfunction syndrome that
70
EL-ESSAWY
during p r o t r u s i o n the m e a n force generated at m a x i m u m effort was only half the m e a n force similarly generated in a control group of non-afflicted subjects. T h e y interpreted the d i f f e r e n c e as being an effect of the p a i n experienced b y the m a n d i b u l a r dysfunction s y n d r o m e patients. However, this was cont r a d i c t e d b y a separate study is that showed p r a c t i c a l l y n o differences were found between t h e laterotrusive forces generated b y the patients towards a n d away from the p a i n f u l affected side or between the p a tients a n d the healthy subjects. On t h e other hand, most investigators agree that elevator muscle tension (i.e. masseter, temporalis ,and medial pterygoid) is significantly higher in patients with M P D c o m p a r e d with healthy controls~,Lv~,lL ~-3. T h e aim of this study is to investigate t h e role of the lateral pterygoid muscle in the limitation of mandibular opening, i.e. "locking". The working hypothesis is t h a t ill locking, the lateral pterygoid muscle is actually a "victim" rather than the cause. I n c r e a s e d elevator muscle tension upsets the coordination of the masticatory mechanism b y interfering with the lateral pterygoid muscle action during t h e opening movement, thus causing locking and ultimately pain, b u t if the lateral pterygoid is allowed to act uninterrupted during the opening m o v e m e n t , locking would be avoided and m o u t h opening could be increased.
Material and methods A simple experiment has been devised to test this hypothesis. By asking the patient to protrude the mandible prior to maximal opening (protrude-open maneuver, POM) the condyle is brought forwards and downwards, i.e. as close to its normal position in opening as possible, thus decreasing the time and distance in which interplay between the elevators and the lateral pterygoids occurs. This opening is compared with simple maximal opening (MO) (i.e. opening without prior protrusion). Measurements of interincisal distance were made using a Willis
bite gauge, taking the maximal reproducible reading between the same maxillary and mandibular incisal edges in every case. GROUPING Group A Thirty.five patients (5 males and 30 females) with manifest MPD are subdivided into the subgroups, A 1 and A 2 according to their symptoms. Subgroup A 1 Twenty patients (3 males and 17 females), mean age 27 + 8 years, with manifest clicking, locking and muscular pain. Subgroup A 2 Fifteen patients (2 males and 13 females), mean age 22 +__5 years, with manifest clicking and locking only. Care was taken to exclude cases of osteoarthrosis, traumatic arthritis and rheumatoid arthritis, since their signs and symptoms may mimic those described for Group A. The criteria for selection of patients in this group were the absence of radiographic changes (transpharyngeal technique and orthopantomograms were taken routinely), of joint disorders elsewhere, or crepitus, and history of direct joint trauma. Group B Fifteen patients (8 males and 7 females), mean age 27 -t- 7 years, in whom masticatory muscle pain was their only symptom (i.e. myofascial pain) were included to investigate whether muscle spasm and pain contributo to the mechanism of locking. None of the patients in this group had a history of joint noise, clicking or locking. Group C Thirty-five healthy subjects (8 males and 27 females), mean age 24 __+7 years, were used as controls. The results are summarized and tabulated in Table 1.
Discussion All patients with limitation of m o u t h opening "locking" (Groups A 1 a n d A 2) showed a significant increase in m o u t h opening following protrude-open m a n e u v e r
71
MYOFASCIAL PAIN DYSFUNCTION SYNDROME
Table 1.. The means and standard deviations in mm of maximal opening (MO), protrude-open maneuver (POM) and the difference (D) of each of the groups, A 1, A 2, B and controls. Group A 1 symptoms are clicking, locking and pain; Group A 2, clicking and locking only; and Group B is muscle pain only Group
A1
A2 $~$
B $g.'$
Controls $'0~
Maximal opening (MO)
35 _+ 7
25 +_ 9
38 _+ 8
44 _+ 5
Protrude-open maneuver (POM)
40 +_ 7
37 _+ 8
37 + 8
44 _. 5
$$~
***
Differences (D = P O M - M O )
5+ 1
12 +_ 5
-1
0
Percentage increase of mouth opening by POM
14 %
48 %
0%
0%
* Denotes a significant difference from controls (P < 0.05). ** Denotes a very significant difference from controls (P < 0.01). *** Denotes a highly significant difference from controls (P < 0.001).
(POM) over that produced by simple maximal opening (MO). This would appear to show t h a t conscious control of lateral pterygoid function suppresses the interference of the m o r e powerful elevators and so overcomes locking. N o significant increase was f o u n d in those patients with no manifest locking (Group B) or in controls (Group C). F o r patients with no pain (A 2) the percentage increase (48 %) was significantly higher than that produced by patients with manifest pain (A1) (14 %). The cause of this difference lies in their (MO) readings and n o t the (POM) readings. This is an interesting finding that could be interpreted as indicating that attempts by the patient to free his lock and perhaps "fight against it" m a y be a factor in pain production, especially in the lateral pterygoid muscle; hence, the higher M O readings in A l's. Such an interpretation is supported by the observation that clicking and locking comm o n l y precede the incidence of painLx~,~L However, as the age incidence for patients in pain (A 1) is significantly higher than for the patients with no pain (A2) (P <~ 0.001) there is also the possibility that
this group is heterogeneous and includes undisclosed cases of painful degenerative intraarticular changes due to dysfunction, as has been implied by the work of TOLenRis. This, o~ course, does not alter the concept of locking as described here. In Groups A a n d B the means of both MO and P O M were significantly less than those found in controls. This may be due to either elevator muscle spasm and/or depressor inhibition, which agrees with the electromyographic findings of MARI~I.rND & MOt IN1~ and MOLIN~8. In contrast to G r o u p A, the absence of any significant difference between M O and P O M in Group B indicates that muscle pain, caused by either spasm or fatigue, does not contribute to the locking mechanism (none of the patients in Group B described locking as one of their symptoms). It is the writer's view that, in spite of some similarity in the etiology and treatment of patients in Groups A and B, the difference in the nature of both disorders should be appreciated. A generalized increase in masticatory muscle tension alone may lead to muscular pain (myofascial
72
EL-ESSAWY
pain) while an uncoordinated increase in muscle tension m a y lead to Myofascial P a i n Dysfunction Syndrome. A c k n o w l e d g m e n t - I am greatly indebted to Mr. M. t-lAmtm, Consultant Oral Surgeon, King's College Hospital Dental School, for txis assistance and valuable criticism during preparation of this paper, also to Professor J. SoWm~Y, Head of the Department of Oral Surgery, Mr. G. FORMAN, Consultant Oral Surgeon, King's College Hospital, for granting me access to their patients in the Temporomandibular loint Clinic and their continuous encouragement, and to Mr. C. YATES for helpful comments during this investigation.
References I. CARLS56, S.: An eleetromyographic study of the function of the laterat pterygoid muscle. Swed. Dent. J. 1956: 66: 203-208. 2. F~NKS, A. S. T.: Masticatory muscle hyperactivity and TMJ dysfunction. Y. Prosthet. Dent. 1965: 15: 1122-1131. 3. GREENE, C. S., LERMAN, M. D., SUTCttER, H. D. & LASKIN, D. M.: The TMJ pain dysfunction syndrome: heterogeneity of the patient population. J. A m . Dent. Assoc. 1969: 79: 1168-1172. 4. GgwFrN, C. Y. & MUNRO, R. R.: Electromyography of the masseter and anterior temporalis muscles in patients with temporomandibular joint dysfunction. Arch. Oral Biol. 1971: 16: 929--949. 5. GROSS~hN, W. L, Gm~ENFr~LD, B. E. & "I'IMMS, D. T.: Electromyography as an aid in diagnosis and treatment analysis, Am. J. Orthodont. 1961: 47: 481-497. 6. IRELAND, V. E.: The problem of the clicking jaw. Proc. R. Soc. Med. 1951: 44: 363371. 7. Im~LAND, V. E.: Disorders of the mandibular joint, aetiology and differences of diagnosis and conservative treatment. Br. Dent. J. 1963: 115: 287-291. Address: D e p a r t m e n t o / Oral Surgery K i n g ' s College Hoepital Dental School D e n m a r k Hill London, S.E.5. U.K.
8. LERMAN,M. D.: A unifying concept of the TMJ pain dysfunction syndrome, g. Am. Dent. Assoc. 1973: 86: 833-841. 9. LASKIN, D. M.: Etiology of pain dysfunction syndrome. J. A m . Dent. Assoc, 1969: 79: 147-153. 10. MA~aeH, J. J.: Therapy for mandibular dysfunction in adolescents and adults. A m . J. Orthodont. I972: 62: 601-605. 11. MaRKLr~D, G. & MOL1N, C.: Horizontal isometric muscle forces of the mandible. A e t a Odontol. Scand. 1972: 30: 97-115. 12. M(3LLER, E.: The chewing apparatus. A c t a Physiol. Scand. 1966: Vol. 69: Suppl. 13, MOLIN, C.: An electromyographic study of the function of the lateral pterygoid muscle. Swed. Dent. J. 1973: 66: 203-208. 14. PERRY, H. T. JR.: Muscular changes associated with TMJ dysfunction. J. A m . D e n t . Assoc. 1957: 54: 644. 15. SCHWARTZ, L.: Pain associated with the TMJ. J. Am. Dent. Assoc. 3955: 51: 394397. 16. SCHWARTZ, L.: Conclusions of the T M J clinic at Colombia. J. Periodont. 1958: 29: 210-212. 17. TOLLER, P. A.: The synovial apparatus and temporomandibular joint function. Br. Dent. J. 1961: 111: 355-362. 18. TOLLER, P. A.: Temporomandibular joint arthrosis. Br. Dent. I. 1973: 134: 223-231. 19. T ~ o ~ s , L J., TruER, N. & SCmRESON, S.: The effect of anxiety and frustration o,f muscular tension related to the T M J syndrome. Oral Surg. 1973: 36: 763-768. 20. VXUOHt,N, H. D.: A study of the temporomandibular articulation. I. A m . D e n t . A s soc. 1943: 30: 1501-1507. 21. V~uor~aN, H. C.: Temporomandibular joint pain: a new diagnostic approach. 1. Prosthet. Dent. 1954: 4: 694. 22. YAVE~.OW, I., FORST~R, I. & WINNGER, M.: Mandibular relearning. J. Oral Surg. 1973: 36: 632-641. 23. YEMM, R.: A comparison of the activity of the left and right masseter muscles of mammals and patients with pain dysfunction syndrome during experimental stress. ]. Dent. Res. 1971: 50: 1320-1323.