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The effect of pain from orthodontic arch wire adjustment on masseter muscle electromyographic activity
The effect of pain from orthodontic arch wire adjustment on masseter muscle electromyographic activity Hilton Goidreich, DDS," Esther Gazit, DMD, b Myron A. Lieberman, DDS, MS, ~ and John D. Rugh, PhD d
Dailas and San Antonio, Texas, and Tel Aviv, Israel Pain has been shown to have an effect on muscle activity even when it does not originate in the muscle itself or in the related joint. The effect of pain from arch wire adjustment on jaw muscle activity is unclear. This study systematically evaluated the effects of orthodontic arch wire adjustment pain on masseter electromyographic (EMG) activity and on the swallowing threshold. The EMG recordings were made on 22 subjects (ages 11 to 15) under three conditions: chewing five peanuts (10 seconds), watching TV chewing gum (15 minutes), and watching -rv with no gum (15 minutes). An arch wire adjustment or placebo adjustment was then made. Subjects returned after 48 h0urs, and the EMG measurements were made under the same conditions. After 3 weeks, subjects received arch wire or placebo treatment in a crossover design with identical recording procedures. The EMG levels while chewing peanuts decreased in 18 of 22 subjects after treatment, compared with 9 of 22 subjects after the placebo. While watching TV with gum, the EMG levels of 20 of 22 subjects decreased after treatment, compared with 9 of 22 subjects after the placebo. The number of chewing strokes before swallowing increased significantly after treatment compared with after placebo. The results suggest that orthodontic pain on teeth tend to reduce muscle activity during function. (AM J ORTHODDENTOFACORTHOP1994;106:365-70.)
A
common clinical observation is that after the application or adjustment of orthodontic arch wires, a patient will avoid chewing hard foods for a few days? This avoidance could be the result of conditioned, and/or nociceptive reflexes in re: sponse to the pain associated with the initial tooth movement after orthodontic arch wire activation. Ngan et aI? found a significant increase in the levels of discomfort after insertion of either separators or arch wires at 4- and24-hour intervals but n6t at 7 days. Pain receptors exist in the periodontal ligament: Pain is believed to be a result Of the effects of compression or tension of these endings? It has been shown that pain has an effect on muscle activity even When it does not originate in the muscle itself Or in the related joint. High et al. 3 measured maximum biting force and subjective pain levels before and after the extraction of third
Supported by grants from Alpha Omega and by NIH/NIDR training grant DEO7160. "Orthodontic Resident, Baylor College of Dentistry, Dallas, Texas. bProressor and Chair, Department of Occlusion, Tel Aviv University. CProfessor and Chair, Department of Orthodontics, Tel Aviv University. aProfessor, Department of Orthodontics; Director of Research, UTHSCSan Antonio Dental School. Copyright 9 1994 by the American Association of Orthodontists. 0889-5406/94/$3.00 + 0 811/45393
molars. They found that the maximum biting force of almost all subjects was much less after surgery. In a study by Stohler 4 and quoted by Lund et al., s pain was associated with a decrease in electromyographic (EMG) activity of a muscle acting as an agonist and an increase when the muscle acts as an antagonist. Lund and others 5 have described a theoretical model to explain the changes in muscle activity caused by chronic pain. They suggest "that motor programs control the premotor nociceptive interneuron to agonist and antagonist motoneurons in a reciprocal way. To account for the lowering of agonist output in the presence of pain, the motor command includes excitation (or facilitation) Of the inhibitory group and the inhibition (or disfacilitation) of the excitatory group supplying agonist motoneurons. The increase of antagonist muscle EMG activity is explained by facilitation of the excitatory pathway and reduction of transmission through the inhibitory interneurons." In other words, agonist and antagonist muscles are controlled by two pathways. One that excites the muscle when stimulated and another that inhibits the muscle when stimulated. The effects of these pathways on agonist and antagonis~ muscles is reciprocal (if the agonist is excited, the antagonist 365
Goldreich el al.
366
AmericanJournalof Orthodonticsand DentofacialOrthopedics October 1994
Table I. Raw data for all conditions
EMG muscle activity hi uV*seconds Chewingpeanuts Patient No. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22
lVatching re,vision relaxed -
-
IVatching television with gum
Treatment
Placebo
Treaonent
Placebo
Treatment
Placebo
Before [After
Before [After
Before latter
Before latter
Before [After
Before I After
1608 7319 9121 4296 660 1265 8107 547 1178 5621 152 22 2881 i377 2871 975 66 20,200 1971 3108 20 52
4268 1033 1658 3219 1537 946 1900 550 3473 4999 120 116 127 901 846 294 15 10,640 12,119 1468 343 344
186 413 259 889 189 42 177 171 419 331 188 55 380 325 246 424 95 709 541 188 144 303
104 195 99 380 138 7 230 0 239 265 11 99 289 373 1 111 16 568 741 20 33 168
256 430 230 865 131 129 134 132 283 303 146 92 207 281 257 426 92 865 1456 262 195 259
204 306 249 660 287 150 209 141 400 258 i88 11 352 300 148 437 155 836 1158 322 187 318
1104 81 24 0 41 25 0 35 11 0 10 0 60 26 0 89 27 862 1485 529 94 0
67 12 22 0 0 4 0 0 18 0 38 0 0 30 0 0 42 85 1820 0 1 0
583 206 69 16 8 15 0 20 6 6 0 0 2 2 1 10 0 0 6180 110 '19 0
562 138 51 3 6 C/O* 2 30 17 2 10 0 C/O* 0 4 104 0 9 3128 102 0 0
284 2425 2972 336 94 374 2022 2 25 5241 15 5 3187 2602 70 97 4 5631 1378 5 6 1
499 1453 2265 5617 2409 777 4273 1114 2765 2514 152 0 57 1210 1312 1089 473* 8706 14,978 1685 178 74
*Faulty or loose electrodes.
will be inhibited). In the presence of pain, the agonist muscles' activity is lowered because of the inhibitory pathway being stimulated and the excitatory pathway being inhibited. The opposite is true for the antagonist muscle. This model is proposed "to explain why pain arising from joints, teeth, and other nonmuscular tissues can sometimes cause the same signs of dysfunction as muscle pain; because the interneurons receive convergent excitatory inputs from different tissues." 9 of the pain iassociated with the constant forces on the fibers'of the periodontal ligament during orthodontictreatment, one would expect agonist muscle activity to decrease after the activation of orthodontic arch wires. If pain and muscle activity (chewing) are affected by the activation of arch wires, it is possible that the swallow could be affected as well. There is still debate over the determination of the swallowing threshold, i.e., the numbei" o f chews before swallowing. The purpose of this investigation was to test the model proposed by Lund et al.5 in the context of orthodontic treatment. The study evaluates the
effects of orthodontic forces and its associated pain on the muscles of the maxillofacial region. The specific aims were to determine the effects of orthodontic force application on masseter muscle EMG activity, to test the effect of arch wire activation on the number of chewing strokes before swallowing and :to determine whether perceived pain is 9 with changes in EMG activity. METHODS AND MATERIALS The overall study design was a within-subject comparison of masseteric EMG levels before and after an
arch wire Change; Each subject received an active adjustment and a placebo adjustment. Twenty-two subjects were selected from an orthodontic practice in Tel-Aviv, Israel. Informed subject consent was obtained from each subject and the parent or guardian before entry into the study. Subjects ranged in age from 11 to 15 years. Each subject Wag screened by one of the investigators (E.G.) for evidence of TMD and/or dental pain and eliminated if either of these conditions were present. All subjects were receiving comprehensive orthodontic treatment in: volving the beginningstages of tooth alignment, withoiat altering jaw position. Integrated EMG data were collected under the following conditions before and after
Goldreich et al. 367
American Journal of Orthodontics and Dentofacial Orthopedics Volume 106, No. 4
Number of chew strokes before swallow
Treatment Before 31 29 52 38 25 25 22 26 25 17 26 19 30 14 22 33 33 45 19 23 28 22
I
Subjective pabz 1 to I00 mm scale
Placebo After
Before
27 33 62 35 21 35 17 31 28 16 57 17 27 22 140" 33 45 43 16 40 37 18
23 29 30 38 40 25 16 30 28 26 30 20 25 ll 41 40 30 42 16 32 28 21
[
Treatment After
Before
31 25 33 34 28 30 14 22 24 20 26 20 34 15 32 34 38 47 18 28 25 21
5 1 I 2 .3 1 10 3 2 3 1 3 15 2 27 3 3 0 2 0 0 2
active and placebo treatments: (1) EMG muscle activity while chewing five peanuts for 10 seconds, (2) watching a videotape for 15 minutes while relaxed, and (3) watching a videotape for 15 minutes while chewing gum. Integrated EMG levels were recorded with a portable EMG unit (AL-200, Aaron Laboratories, San Antonio, Texas). 6 The area over the right masseter muscle was cleansed with alcohol, and an acetate template was used to ensure repeatable placement of a tripod electrode (J & J model SE-45, J & J Engineering, Poulsbo, Wash.). The threshold of the EMG unit was set at 25 uV. The subjects were asked to count from 1 to 10 to ensure that muscle activity related to talking and swallowing would not be recorded. The same brand of gum was used during each visit, and the same videotape was shown with the patient starting the video tape at the position where the last appointment ended. Assessments were also made of the number of chewing strokes before swallowing the peanuts, and the subjective pain rating during chewing on a 0 to 100 mm scale. The subjects were asked to raise their hands when the bolus was swallowed so that the number of chewing strokes could be counted. See Table I. During the first visit, subjects were randomly assigned either to receive an active arch wire treatment or to receive a placebo treatment, in which case the orth-
Placebo
[After 33 49 68 48 3 67 58 56 46 75 70 17 58 87 89 27 68 28 12 51 100 13
Before 1 3 3 1 l 3 4 1 0 1 1 0 1 1 3 2 11 0 0 25 0 1
[After 2 2 3 l l 20 5 1 I l 1 0 20 2 4 2 7 3 l 0 0 1
odontist would remove the arch wire and replace the identical wire. The subjects returned after a 48-hour period and the measurements were repeated. Each subject returned after 3 weeks and the same procedure was followed except in the reverse order; i.e., subjects who received a placebo adjustment at the first visit received the true adjustment and those who received the true adjustment at the first visit received a placebo adjustment. This counterbalance procedure was to control for order effects. A 3-week time lapse between arch wire changes was required to assure complete patient comfort with the appliance at the time the baseline was established.
RESULTS T h e d a t a for i n d i v i d u a l subjects are p r o v i d e d in T a b l e I. A s s h o w n in T a b l e I, m u s c l e activity while c h e w i n g p e a n u t s d e c r e a s e d i n 18 of the 22 subjects after t r e a t m e n t a n d in 9 of t h e 22 subjects with n o t r e a t m e n t . T h e E M G while chewing g u m a n d w a t c h i n g T V d e c r e a s e d in 20 subjects after treatm e n t a n d in 9 subjects with n o t r e a t m e n t . O n the subjective p a i n scale, 21 subjects r e p o r t e d a n increase o f p a i n after arch wire a d j u s t m e n t , w h e r e a s
368 Goldreich et aL
American Journal of Orthodontics and Dentofacial Orthopedics October 1994
EMG PERCENT DIFFERENCE EMQ % Difference
T R E A T M E N T VS. P L A C E B O CHEWING PEANUTS
9
I
i,oot
'i
150
_._
. . . . . .
i J i i i i 1 2 3 4 5 6
i i i i i i i i i i i i i t i i i I 7 8 9 10 It 12 13 14 15 16 17 18 19 20 21 22 AVERAGE t-3.41, pc.05 PATIENT # TREATMENT
~
PLACEBO
Fig. 1. Eating peanuts.
EMG PERCENT DIFFERENCE
EMG % Difference 300-
_~
T R E A T M E N T VS. P L A C E B O CHEWING
GUM/WATCHING
T.V.
i l 200 100 -
0-
-100 -o -
2 t
0 2 3 4 5 6
m 9k
0 ~ 7 8 9 10 11 12.13 14 15 16 17 18 19 20 21 22 AVERAGE PATIENT # t-3.89, p,.05 TREATMENT
[~
PLACEBO
patient deleted due to f a u l t y electrode
F i g . 2. C h e w i n g
gum/watching
9 of the 22 subjects reported very small increases in pain after the placebo. The avei'age pain increase after treatment was 46 mm compared with 7 mm after placebo on a 100 mm scale. No correlation was found between EMG change scores and subjective pain scales. The percent differences in EMG and chewing strokes were calculated between the treatment and placebo condition for all but one parameter. Watching television while relaxed was excluded because of the frequent number of zero EMG readings. This was due to the muscle activity being below the instrumental threshold. The percent dif-
television.
ferences and the average of the percent differences are shown in Figs. 1, 2, and 3. A single tailed paired t test was used to compare the treatment and nontreatment outcomes for the three of the four conditions. A single tailed test was used because the direction of the expected differences were predicted by the hypotheses being tested~ Statistically significant differences were found in all three parameters. While chewing peanuts after treatment, the EMG decreased significantly compared with the EMG after the placebo. (t21 = 3.41, p < 0.05). The same was true after chewing gum (t19 = 3.89, p < 0.05). The number-of chewing strokes before
Goldreich et aL
American Journal of Orthodontics and Dentofacial Orthopedics Volume 106, No. 4
369
# OF CHEWING STROKES PERCENT DIFFERENCE % dlfferencq In r
TREATMENT VS. PLACEBO
strokes
140 120
,o
~
~o $0
~ -o
0
~ tg
zo -40 2
3
4
5
6
7
8
9
10 11 12 13 14 15 16 17 18 19 2 0 21 2 2
PATIENT # m *
TREATMENT
~
Average
t.-l.77,pr PLACEBO
patient deleted due to faulty electrode
Fig. 3. Chewing strokes percent difference.
swallowing increased significantly after treatment compared with after placebo (t20 = -1.77, p < 0.046). The t test could not be applied for subjects not chewing gum while watching television because of the frequent number of zero EMG readings. The number of subjects used in calculating these statistics varied because of exclusion of subjects in whom electrodes were faulty (two subjects) or electrodes came loose (two subjects) identified by asterisks in Table I. Unpaired t tests,were also used to test for differences in sex and age. No differences were detected. Order effects of treatment were tested with a nonpaired two-tailed test. No significant order effects were found. The mean and standard deviation of the EMG percent differences for subjects receiving treatment first (x = -56.5, SD = 54.2) were not significantly different than those who received treatment after the placebo treatment (x = -73.1, SD = 37.9). DISCUSSION
Masseter EMG activity decreased while subjects watched TV (chewing gum) and while eating peanuts after arch wire treatment. In this study a true arch wire treatment was compared with a placebo arch wire treatment. These results are consistent with the results of the study by Smith et a17 who reported a significant decrease in masseter EMG levels integrated over 11 hour periods in three of five subjects after arch wire changes. In the
study by Smith, masseter EMG was recorded in the patients' natural environment during wakefulness and during sleep. The decrease in EMG after arch wire adjustment suggests a reluctance of the subjects to use as much force while chewing. It should be noted that the total EMG activity was recorded, therefore one cannot separate agonist (jaw closing) from antagonist (jaw opening) activity. However, even if antagonist activity increases in pain, it is unlikely to pass the threshold used in this study, and therefore all the changes seen are probably occurring in the closing phase. These results are consistent with the model proposed by Lund et al. 5 in the introduction. This model proposed that, "pain arising from nonmuscular tissues can sometimes cause the same signs of dysfunction as muscle pain, because the interneurons receive convergent excitatory inputs from different tissues." In our study, the perceived pain did not arise from the masseter muscle but rather from the paradental tissues in subjects receiving the treatment. Other explanations for the reduction in EMG could be that the noxious input arising from teeth, periodontal membrane, and perioral structures produce a protective reflex with inhibition of the jaw closing muscles, s Also, in addition to the role of the cortex in the voluntary act of mastication, evidence indicates that the cortex may be receiving peripheral feedback from intraoral receptors during the masticatory act and be implicated in our ability to make' contact with the food bolus and crush it. An obvious source of
370
Goldreich et al.
the information would be the periodontal receptors, providing a form of positive feedback on jaw closing muscle activity. And at the level of the brain stem, periodontal receptors are capable of inducing both facilitatory and inhibitory effects on jaw closing motoneurone activity.9"~~ A significant difference was also found between treatment and placebo for the number of chewing strokes before swallowing. A net increase was found after treatment, whereas no change was found after the placebo. The fact that the subject takes more strokes to prepare the food in the presence of pain and the EMG activity decreases suggests that particles of constant size are being swallowed. The results of this study are limited by a few general concerns. Although an attempt was made to blind the subjects to their treatment condition, it is possible that they were aware of the true treatment. However, there is no reason to believe that this knowledge would bias the study, as the subjects were not aware of the anticipated direction of change. Another potential limitation is that this study assessed pain at 48 hours after treatment. Although it has been found that there is a significant increase in pain at 24 hours, 2 completing the study in a private practice setting required that we assess pain at 48 hours. Our subjective level of pain after 48 hours was found to be elevated. However, our results may have been more dramatic at 24 hours. A last limitation is that this study did not provide a naeasure of arch wire forces. In summary, our findings confirm the clinical observation that adjustment of orthodontic arch wires reduces muscle activity in chewing 48 hours after activation of arch wires. This reduction of muscle activity during function is possibly due to the noxious stimulation of the periodontal membrane and paradental receptors triggering a reflex mechanism and thus causing inhibition of the jaw closing muscles, or to the Painarising in nonmuscular tissues causing the same signs of dysfunction as muscle pa!n because the interneurons receive
American Journal of Orthodontics and Dentofacial Orthopedics October 1994
convergent excitatory signals from different tissues. These findings also suggest that the periodontal receptors could play an important role in the triggering of a swallow. We thank Drs. Arthur Storey and James Lund for their critical comments and advice. REFERENCES
1. Gianelly AA, Goldman ttM. Tooth movement. In: Gainclly AA, Goldman HM, eds. Biologic basis of orthodontics. Philadelphia: Lea & Febiger, 1971:116-204. 2. Ngan P, Kess B, Wilson S. Perception of discomfort by patients undergoing orthodontic treatment. AM J ORTtIOD DENTOFAC ORTttOP 1989;96:47-53. 3. High AS, Macgregor AJ, Tomlinson GE. A gnathodynamometer as an objective means of pain assessment following wisdom tooth removal. Br J Oral Maxillofac Surg 1988;26: 284-91. 4. Stohler CS, Ashton-Miller, Carlson DS. The effects of pain from the mandibular joint and muscles on masticatory motor behavior in man. Arch Oral Biol 1988;33:175-82. 5. Lund JP, Donga R, Widmer CG, Stohler CS. The painadaptation model: a discussion of the relationship between chronic musculoskeletal pain and motor activity. Can J Phys Pharm 1991;69:683-94. 6. Burgar CG, Rugh JD. An EMG integrator for muscle activity studies in ambulatory subjects. IEEE Trans Biomed Eng 1983;30:66-9. 7. Smith BR, Flanary CM, Hui'st CL, Rugh JD. Effects of orthodontic archwire changes on masseter muscle activity. J Dent Res 1984;63:258. 8. Dubner R. Chairman's introduction. In: Sessle BJ, Hannam A, eds. Mastication and swallowing: biologic and chemical correlates. Toronto: University of Toronto Press, 1976:81-2. 9. Lund JP, Lamarre Y. The importance of positive feedback from periodontal pressoreceptors during voluntary isometric contraction of jaw closing muscle in man. J Biol Bucc 1973;1:345-51. 10. Lund JP, Sessle BJ. Oral-facial and jaw muscle afferent projections to neurones in cat frontal cortex. Exp Neurol 1974;45:314-31. Reprint requests to:
Dr. John D. Rugh Department of Orthodontics UTHSC-San Antonio 7703 Floyd Curl Dr. San Antonio, TX 78284-7910
Dailas and San Antonio, Texas, and Tel Aviv, Israel Pain has been shown to have an effect on muscle activity even when it does not originate in the muscle itself or in the related joint. The effect of pain from arch wire adjustment on jaw muscle activity is unclear. This study systematically evaluated the effects of orthodontic arch wire adjustment pain on masseter electromyographic (EMG) activity and on the swallowing threshold. The EMG recordings were made on 22 subjects (ages 11 to 15) under three conditions: chewing five peanuts (10 seconds), watching TV chewing gum (15 minutes), and watching -rv with no gum (15 minutes). An arch wire adjustment or placebo adjustment was then made. Subjects returned after 48 h0urs, and the EMG measurements were made under the same conditions. After 3 weeks, subjects received arch wire or placebo treatment in a crossover design with identical recording procedures. The EMG levels while chewing peanuts decreased in 18 of 22 subjects after treatment, compared with 9 of 22 subjects after the placebo. While watching TV with gum, the EMG levels of 20 of 22 subjects decreased after treatment, compared with 9 of 22 subjects after the placebo. The number of chewing strokes before swallowing increased significantly after treatment compared with after placebo. The results suggest that orthodontic pain on teeth tend to reduce muscle activity during function. (AM J ORTHODDENTOFACORTHOP1994;106:365-70.)
A
common clinical observation is that after the application or adjustment of orthodontic arch wires, a patient will avoid chewing hard foods for a few days? This avoidance could be the result of conditioned, and/or nociceptive reflexes in re: sponse to the pain associated with the initial tooth movement after orthodontic arch wire activation. Ngan et aI? found a significant increase in the levels of discomfort after insertion of either separators or arch wires at 4- and24-hour intervals but n6t at 7 days. Pain receptors exist in the periodontal ligament: Pain is believed to be a result Of the effects of compression or tension of these endings? It has been shown that pain has an effect on muscle activity even When it does not originate in the muscle itself Or in the related joint. High et al. 3 measured maximum biting force and subjective pain levels before and after the extraction of third
Supported by grants from Alpha Omega and by NIH/NIDR training grant DEO7160. "Orthodontic Resident, Baylor College of Dentistry, Dallas, Texas. bProressor and Chair, Department of Occlusion, Tel Aviv University. CProfessor and Chair, Department of Orthodontics, Tel Aviv University. aProfessor, Department of Orthodontics; Director of Research, UTHSCSan Antonio Dental School. Copyright 9 1994 by the American Association of Orthodontists. 0889-5406/94/$3.00 + 0 811/45393
molars. They found that the maximum biting force of almost all subjects was much less after surgery. In a study by Stohler 4 and quoted by Lund et al., s pain was associated with a decrease in electromyographic (EMG) activity of a muscle acting as an agonist and an increase when the muscle acts as an antagonist. Lund and others 5 have described a theoretical model to explain the changes in muscle activity caused by chronic pain. They suggest "that motor programs control the premotor nociceptive interneuron to agonist and antagonist motoneurons in a reciprocal way. To account for the lowering of agonist output in the presence of pain, the motor command includes excitation (or facilitation) Of the inhibitory group and the inhibition (or disfacilitation) of the excitatory group supplying agonist motoneurons. The increase of antagonist muscle EMG activity is explained by facilitation of the excitatory pathway and reduction of transmission through the inhibitory interneurons." In other words, agonist and antagonist muscles are controlled by two pathways. One that excites the muscle when stimulated and another that inhibits the muscle when stimulated. The effects of these pathways on agonist and antagonis~ muscles is reciprocal (if the agonist is excited, the antagonist 365
Goldreich el al.
366
AmericanJournalof Orthodonticsand DentofacialOrthopedics October 1994
Table I. Raw data for all conditions
EMG muscle activity hi uV*seconds Chewingpeanuts Patient No. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22
lVatching re,vision relaxed -
-
IVatching television with gum
Treatment
Placebo
Treaonent
Placebo
Treatment
Placebo
Before [After
Before [After
Before latter
Before latter
Before [After
Before I After
1608 7319 9121 4296 660 1265 8107 547 1178 5621 152 22 2881 i377 2871 975 66 20,200 1971 3108 20 52
4268 1033 1658 3219 1537 946 1900 550 3473 4999 120 116 127 901 846 294 15 10,640 12,119 1468 343 344
186 413 259 889 189 42 177 171 419 331 188 55 380 325 246 424 95 709 541 188 144 303
104 195 99 380 138 7 230 0 239 265 11 99 289 373 1 111 16 568 741 20 33 168
256 430 230 865 131 129 134 132 283 303 146 92 207 281 257 426 92 865 1456 262 195 259
204 306 249 660 287 150 209 141 400 258 i88 11 352 300 148 437 155 836 1158 322 187 318
1104 81 24 0 41 25 0 35 11 0 10 0 60 26 0 89 27 862 1485 529 94 0
67 12 22 0 0 4 0 0 18 0 38 0 0 30 0 0 42 85 1820 0 1 0
583 206 69 16 8 15 0 20 6 6 0 0 2 2 1 10 0 0 6180 110 '19 0
562 138 51 3 6 C/O* 2 30 17 2 10 0 C/O* 0 4 104 0 9 3128 102 0 0
284 2425 2972 336 94 374 2022 2 25 5241 15 5 3187 2602 70 97 4 5631 1378 5 6 1
499 1453 2265 5617 2409 777 4273 1114 2765 2514 152 0 57 1210 1312 1089 473* 8706 14,978 1685 178 74
*Faulty or loose electrodes.
will be inhibited). In the presence of pain, the agonist muscles' activity is lowered because of the inhibitory pathway being stimulated and the excitatory pathway being inhibited. The opposite is true for the antagonist muscle. This model is proposed "to explain why pain arising from joints, teeth, and other nonmuscular tissues can sometimes cause the same signs of dysfunction as muscle pain; because the interneurons receive convergent excitatory inputs from different tissues." 9 of the pain iassociated with the constant forces on the fibers'of the periodontal ligament during orthodontictreatment, one would expect agonist muscle activity to decrease after the activation of orthodontic arch wires. If pain and muscle activity (chewing) are affected by the activation of arch wires, it is possible that the swallow could be affected as well. There is still debate over the determination of the swallowing threshold, i.e., the numbei" o f chews before swallowing. The purpose of this investigation was to test the model proposed by Lund et al.5 in the context of orthodontic treatment. The study evaluates the
effects of orthodontic forces and its associated pain on the muscles of the maxillofacial region. The specific aims were to determine the effects of orthodontic force application on masseter muscle EMG activity, to test the effect of arch wire activation on the number of chewing strokes before swallowing and :to determine whether perceived pain is 9 with changes in EMG activity. METHODS AND MATERIALS The overall study design was a within-subject comparison of masseteric EMG levels before and after an
arch wire Change; Each subject received an active adjustment and a placebo adjustment. Twenty-two subjects were selected from an orthodontic practice in Tel-Aviv, Israel. Informed subject consent was obtained from each subject and the parent or guardian before entry into the study. Subjects ranged in age from 11 to 15 years. Each subject Wag screened by one of the investigators (E.G.) for evidence of TMD and/or dental pain and eliminated if either of these conditions were present. All subjects were receiving comprehensive orthodontic treatment in: volving the beginningstages of tooth alignment, withoiat altering jaw position. Integrated EMG data were collected under the following conditions before and after
Goldreich et al. 367
American Journal of Orthodontics and Dentofacial Orthopedics Volume 106, No. 4
Number of chew strokes before swallow
Treatment Before 31 29 52 38 25 25 22 26 25 17 26 19 30 14 22 33 33 45 19 23 28 22
I
Subjective pabz 1 to I00 mm scale
Placebo After
Before
27 33 62 35 21 35 17 31 28 16 57 17 27 22 140" 33 45 43 16 40 37 18
23 29 30 38 40 25 16 30 28 26 30 20 25 ll 41 40 30 42 16 32 28 21
[
Treatment After
Before
31 25 33 34 28 30 14 22 24 20 26 20 34 15 32 34 38 47 18 28 25 21
5 1 I 2 .3 1 10 3 2 3 1 3 15 2 27 3 3 0 2 0 0 2
active and placebo treatments: (1) EMG muscle activity while chewing five peanuts for 10 seconds, (2) watching a videotape for 15 minutes while relaxed, and (3) watching a videotape for 15 minutes while chewing gum. Integrated EMG levels were recorded with a portable EMG unit (AL-200, Aaron Laboratories, San Antonio, Texas). 6 The area over the right masseter muscle was cleansed with alcohol, and an acetate template was used to ensure repeatable placement of a tripod electrode (J & J model SE-45, J & J Engineering, Poulsbo, Wash.). The threshold of the EMG unit was set at 25 uV. The subjects were asked to count from 1 to 10 to ensure that muscle activity related to talking and swallowing would not be recorded. The same brand of gum was used during each visit, and the same videotape was shown with the patient starting the video tape at the position where the last appointment ended. Assessments were also made of the number of chewing strokes before swallowing the peanuts, and the subjective pain rating during chewing on a 0 to 100 mm scale. The subjects were asked to raise their hands when the bolus was swallowed so that the number of chewing strokes could be counted. See Table I. During the first visit, subjects were randomly assigned either to receive an active arch wire treatment or to receive a placebo treatment, in which case the orth-
Placebo
[After 33 49 68 48 3 67 58 56 46 75 70 17 58 87 89 27 68 28 12 51 100 13
Before 1 3 3 1 l 3 4 1 0 1 1 0 1 1 3 2 11 0 0 25 0 1
[After 2 2 3 l l 20 5 1 I l 1 0 20 2 4 2 7 3 l 0 0 1
odontist would remove the arch wire and replace the identical wire. The subjects returned after a 48-hour period and the measurements were repeated. Each subject returned after 3 weeks and the same procedure was followed except in the reverse order; i.e., subjects who received a placebo adjustment at the first visit received the true adjustment and those who received the true adjustment at the first visit received a placebo adjustment. This counterbalance procedure was to control for order effects. A 3-week time lapse between arch wire changes was required to assure complete patient comfort with the appliance at the time the baseline was established.
RESULTS T h e d a t a for i n d i v i d u a l subjects are p r o v i d e d in T a b l e I. A s s h o w n in T a b l e I, m u s c l e activity while c h e w i n g p e a n u t s d e c r e a s e d i n 18 of the 22 subjects after t r e a t m e n t a n d in 9 of t h e 22 subjects with n o t r e a t m e n t . T h e E M G while chewing g u m a n d w a t c h i n g T V d e c r e a s e d in 20 subjects after treatm e n t a n d in 9 subjects with n o t r e a t m e n t . O n the subjective p a i n scale, 21 subjects r e p o r t e d a n increase o f p a i n after arch wire a d j u s t m e n t , w h e r e a s
368 Goldreich et aL
American Journal of Orthodontics and Dentofacial Orthopedics October 1994
EMG PERCENT DIFFERENCE EMQ % Difference
T R E A T M E N T VS. P L A C E B O CHEWING PEANUTS
9
I
i,oot
'i
150
_._
. . . . . .
i J i i i i 1 2 3 4 5 6
i i i i i i i i i i i i i t i i i I 7 8 9 10 It 12 13 14 15 16 17 18 19 20 21 22 AVERAGE t-3.41, pc.05 PATIENT # TREATMENT
~
PLACEBO
Fig. 1. Eating peanuts.
EMG PERCENT DIFFERENCE
EMG % Difference 300-
_~
T R E A T M E N T VS. P L A C E B O CHEWING
GUM/WATCHING
T.V.
i l 200 100 -
0-
-100 -o -
2 t
0 2 3 4 5 6
m 9k
0 ~ 7 8 9 10 11 12.13 14 15 16 17 18 19 20 21 22 AVERAGE PATIENT # t-3.89, p,.05 TREATMENT
[~
PLACEBO
patient deleted due to f a u l t y electrode
F i g . 2. C h e w i n g
gum/watching
9 of the 22 subjects reported very small increases in pain after the placebo. The avei'age pain increase after treatment was 46 mm compared with 7 mm after placebo on a 100 mm scale. No correlation was found between EMG change scores and subjective pain scales. The percent differences in EMG and chewing strokes were calculated between the treatment and placebo condition for all but one parameter. Watching television while relaxed was excluded because of the frequent number of zero EMG readings. This was due to the muscle activity being below the instrumental threshold. The percent dif-
television.
ferences and the average of the percent differences are shown in Figs. 1, 2, and 3. A single tailed paired t test was used to compare the treatment and nontreatment outcomes for the three of the four conditions. A single tailed test was used because the direction of the expected differences were predicted by the hypotheses being tested~ Statistically significant differences were found in all three parameters. While chewing peanuts after treatment, the EMG decreased significantly compared with the EMG after the placebo. (t21 = 3.41, p < 0.05). The same was true after chewing gum (t19 = 3.89, p < 0.05). The number-of chewing strokes before
Goldreich et aL
American Journal of Orthodontics and Dentofacial Orthopedics Volume 106, No. 4
369
# OF CHEWING STROKES PERCENT DIFFERENCE % dlfferencq In r
TREATMENT VS. PLACEBO
strokes
140 120
,o
~
~o $0
~ -o
0
~ tg
zo -40 2
3
4
5
6
7
8
9
10 11 12 13 14 15 16 17 18 19 2 0 21 2 2
PATIENT # m *
TREATMENT
~
Average
t.-l.77,pr PLACEBO
patient deleted due to faulty electrode
Fig. 3. Chewing strokes percent difference.
swallowing increased significantly after treatment compared with after placebo (t20 = -1.77, p < 0.046). The t test could not be applied for subjects not chewing gum while watching television because of the frequent number of zero EMG readings. The number of subjects used in calculating these statistics varied because of exclusion of subjects in whom electrodes were faulty (two subjects) or electrodes came loose (two subjects) identified by asterisks in Table I. Unpaired t tests,were also used to test for differences in sex and age. No differences were detected. Order effects of treatment were tested with a nonpaired two-tailed test. No significant order effects were found. The mean and standard deviation of the EMG percent differences for subjects receiving treatment first (x = -56.5, SD = 54.2) were not significantly different than those who received treatment after the placebo treatment (x = -73.1, SD = 37.9). DISCUSSION
Masseter EMG activity decreased while subjects watched TV (chewing gum) and while eating peanuts after arch wire treatment. In this study a true arch wire treatment was compared with a placebo arch wire treatment. These results are consistent with the results of the study by Smith et a17 who reported a significant decrease in masseter EMG levels integrated over 11 hour periods in three of five subjects after arch wire changes. In the
study by Smith, masseter EMG was recorded in the patients' natural environment during wakefulness and during sleep. The decrease in EMG after arch wire adjustment suggests a reluctance of the subjects to use as much force while chewing. It should be noted that the total EMG activity was recorded, therefore one cannot separate agonist (jaw closing) from antagonist (jaw opening) activity. However, even if antagonist activity increases in pain, it is unlikely to pass the threshold used in this study, and therefore all the changes seen are probably occurring in the closing phase. These results are consistent with the model proposed by Lund et al. 5 in the introduction. This model proposed that, "pain arising from nonmuscular tissues can sometimes cause the same signs of dysfunction as muscle pain, because the interneurons receive convergent excitatory inputs from different tissues." In our study, the perceived pain did not arise from the masseter muscle but rather from the paradental tissues in subjects receiving the treatment. Other explanations for the reduction in EMG could be that the noxious input arising from teeth, periodontal membrane, and perioral structures produce a protective reflex with inhibition of the jaw closing muscles, s Also, in addition to the role of the cortex in the voluntary act of mastication, evidence indicates that the cortex may be receiving peripheral feedback from intraoral receptors during the masticatory act and be implicated in our ability to make' contact with the food bolus and crush it. An obvious source of
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Goldreich et al.
the information would be the periodontal receptors, providing a form of positive feedback on jaw closing muscle activity. And at the level of the brain stem, periodontal receptors are capable of inducing both facilitatory and inhibitory effects on jaw closing motoneurone activity.9"~~ A significant difference was also found between treatment and placebo for the number of chewing strokes before swallowing. A net increase was found after treatment, whereas no change was found after the placebo. The fact that the subject takes more strokes to prepare the food in the presence of pain and the EMG activity decreases suggests that particles of constant size are being swallowed. The results of this study are limited by a few general concerns. Although an attempt was made to blind the subjects to their treatment condition, it is possible that they were aware of the true treatment. However, there is no reason to believe that this knowledge would bias the study, as the subjects were not aware of the anticipated direction of change. Another potential limitation is that this study assessed pain at 48 hours after treatment. Although it has been found that there is a significant increase in pain at 24 hours, 2 completing the study in a private practice setting required that we assess pain at 48 hours. Our subjective level of pain after 48 hours was found to be elevated. However, our results may have been more dramatic at 24 hours. A last limitation is that this study did not provide a naeasure of arch wire forces. In summary, our findings confirm the clinical observation that adjustment of orthodontic arch wires reduces muscle activity in chewing 48 hours after activation of arch wires. This reduction of muscle activity during function is possibly due to the noxious stimulation of the periodontal membrane and paradental receptors triggering a reflex mechanism and thus causing inhibition of the jaw closing muscles, or to the Painarising in nonmuscular tissues causing the same signs of dysfunction as muscle pa!n because the interneurons receive
American Journal of Orthodontics and Dentofacial Orthopedics October 1994
convergent excitatory signals from different tissues. These findings also suggest that the periodontal receptors could play an important role in the triggering of a swallow. We thank Drs. Arthur Storey and James Lund for their critical comments and advice. REFERENCES
1. Gianelly AA, Goldman ttM. Tooth movement. In: Gainclly AA, Goldman HM, eds. Biologic basis of orthodontics. Philadelphia: Lea & Febiger, 1971:116-204. 2. Ngan P, Kess B, Wilson S. Perception of discomfort by patients undergoing orthodontic treatment. AM J ORTtIOD DENTOFAC ORTttOP 1989;96:47-53. 3. High AS, Macgregor AJ, Tomlinson GE. A gnathodynamometer as an objective means of pain assessment following wisdom tooth removal. Br J Oral Maxillofac Surg 1988;26: 284-91. 4. Stohler CS, Ashton-Miller, Carlson DS. The effects of pain from the mandibular joint and muscles on masticatory motor behavior in man. Arch Oral Biol 1988;33:175-82. 5. Lund JP, Donga R, Widmer CG, Stohler CS. The painadaptation model: a discussion of the relationship between chronic musculoskeletal pain and motor activity. Can J Phys Pharm 1991;69:683-94. 6. Burgar CG, Rugh JD. An EMG integrator for muscle activity studies in ambulatory subjects. IEEE Trans Biomed Eng 1983;30:66-9. 7. Smith BR, Flanary CM, Hui'st CL, Rugh JD. Effects of orthodontic archwire changes on masseter muscle activity. J Dent Res 1984;63:258. 8. Dubner R. Chairman's introduction. In: Sessle BJ, Hannam A, eds. Mastication and swallowing: biologic and chemical correlates. Toronto: University of Toronto Press, 1976:81-2. 9. Lund JP, Lamarre Y. The importance of positive feedback from periodontal pressoreceptors during voluntary isometric contraction of jaw closing muscle in man. J Biol Bucc 1973;1:345-51. 10. Lund JP, Sessle BJ. Oral-facial and jaw muscle afferent projections to neurones in cat frontal cortex. Exp Neurol 1974;45:314-31. Reprint requests to:
Dr. John D. Rugh Department of Orthodontics UTHSC-San Antonio 7703 Floyd Curl Dr. San Antonio, TX 78284-7910