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Histopathology of the temporomandibular joint following bilateral extractions of molars in the rat
RESEARCH .
.
.
.
.
.
.
HISTOPATHOLOGY FOLLOWING
.
.
.
OF THE
BILATERAL
.
.
.
.
.
.
.
.
TEMPOROMANDIBULAR
EXTRACTIONS
.
.
.
.
.
.
JOINT
OF MOLARS
IN THE RAT A Preliminary
Report
Giorgio Cim.asoni, Dr. med. dent., M.X.D.,” Dental School, University
Geneva, Switzerland
of Geneva
the term temporomandibular joint pain-dysfunction syndrome has been proposed for a set of poorly defined disturbances specific for this joint, including clicking, subluxation phenomena, and pain.12 The cause of these disturbances has been- widely discussed, and a review of the pertinent literature reveals two hypotheses :
R
ECENTLY,
1. The structures proper of the temporomandibular joint would be involved and directly responsible for the disturbances. 2. The primary cause would be represented by altered function of the masticatory musculature. In fact, since Costens tried to explain the appearance of pain in the joint on the basis of anatomic considerations, other studies have pointed out the role played by the masticatory musculature.l~ 111I2 The relationship between the occlusal conditions and the status of structures of the temporomandibular joint has rarely been the object of experimental investigations. In 1952 Avant, Averill, and Hahn3 described, in four groups of rats, a number of pathologic findings in the temporomandibular joint 110 days after various groups of teeth had been extracted. The degree of joint disturbances was in direct relation to the severity of intermaxillary disturbances. The rats were all of the same age group, however, and the length of impaired occlusion was relatively short.3 This investigation. done at the Division oi’ Dental Medicine, School of Dentistry, and the George William Hooper Foundation, The University of California, San Francisco (Dr. Hermann Becks), was supported by grants of the University of California. *Present address: Institut de mddecine dentaire, 30, rue Lombard, Geneva, Switzerland.
In 1.954 Applchaum ant1 Levy” rc~portcd no significant clmngcs in the terr~poromandibnlar joints of ;I. group 01:young mice ~vho had worn orthotloutic bitt plates for 2 weeks. The present st,udy attempted to rc~producc the condition of t.hc long-term edentulous pat.ient (loss of vertical dimension) in ra1.s over 240 days of age. Bilateral extractions of the two uppw quadrants of rriohrs wrre IJtrforlnPd, and the length of impaired occlnsicm was over 200 days. METHODS
AND
;ZI~ATERL~L
Three groups of female Tdong-Evans rats wcrc nsctl in the present study. In some of the animals in each group the molars of the two upper quadrants were extracted by means of small forceps and elevators. TabIe I shows the over-all distribut,ion of the material. A total of twentytwo rats were used. In six animals c,f the first group the upper molars were extracted 200 days before the animals were killed (at. 240 days of age) ; four rats served as controls.
GROUP
AOE ( IME’S)
1
240
2 3
330 480
NO. OF ESPERIMENTAT, RATS
6 6 2
LENGTH OF EXPERIMENTAL TIME
---
200 270 300
NO.
OF COSTROT, RATS
.-.-__----4 2 I, __-__-
In Group 2 the molars of six older rats (330 days of age) were rxtractcd 270 days before the animals wcrc killed; two rats of this group served as controls. Group 3 consisted of four rats--two experimental and two control. This group was killed at 480 days, having lived 300 days with impaired occlusion. At autopsy, the masscter muscle was dissected and immediately utilized for an enzymologic study.G The temporomandibular structures were cut out, according to the method described by Decks and Evans.* They were fixed, decalcified, dehydrated, and embedded in nitrocellulose. They were sectioned in the frontal plane for histologic examinat.ion. Hematoxylin and eosin stain was used. Only the right temporomandibular joint of each rat was used. RESULTS
Group I.-Fig. 1 shows the normal appearance of a frontal histologic section of temporomandibular joint from a 240-day-old control rat. Notice the dense structure of bone in the condylar head (still irregularly covered by a layer of cartilage), the fibrous protection of the condyle, the compact structure of the meniscus, the layer of fibrous tissue, and cartilage lining the glenoid fossa. The meniscus seems to be closely adherent to the condyle (virtual space) ; this arrangement will be found in other specimens, in both the “upper” and “lower”
Volume 16 Number 5
HISTOPATHOLOGY
OF TEMPOROMANDIBULAR
JOlNT
615
articular spaces. It has already been reported as normally occurring4 and could be the result of pressure during the preparation of the sections. Very little or no deviation from the normal is noticed in the temporomandibular joint specimens of the six experimental rats of Group 1.
Fig.
L-Frontal
section
of a temporomandibular (Original magnification.
joint (control rat of Group X65 ; reduced l/5. )
1, aged
240 days).
Group Z-Fig. 2 shows a temporomandibular joint from a 330-day-old rat which had no teeth extracted. The meniscus adheres to both the fossa and the condylar head ; only the different orientation of fibers makes it possible to recognize the meniscus from the upper and lower structures. The thickness of cartilaginous covering, which would be too large for a rat of this age, is certainly the result of the section’s orientation .* The temporomandibular joint illustrated in Fig. 3 is from an experimental rat of Group 2. Notice that in the area indicated by a a structural alteration can be seen in the meniscus. Furthermore, the glenoid fossa shows some isolated sites of calcification surrounding a few chondrocytes (b) and an important zone of necrosis (c). Fig. 4 points out, under greater magnification, the peculiar feature found in the meniscus. Observation by polarized light suggests an actual different orientation of fibers, which could be interpreted as a repair phenomenon. Above this peculiar meniscal zone, and in direct relation wit,h it, a certain amount of liquid material is noticed (necrosis ? plasma ?) . *On histologic the plane of section.
preparations This must
the width of the cartilaginous layer may vary according to be kept in mind, particularly when studying mandibular growth.
616
Fig. 3.-Temporomand
Volume Number
16 5
HISTOPATHOLOGY
OF TEMPOROMANDIHULAR
JOINT
617
Atldhc~r inlportallt pa1hologic finding in some of the rats of Group 2 is the csistenec of a “pa,nnus. ” ~Presumably as a result of proliferation of the synovial membrane, an irregular rrmss of granulation tissue can be observed in some spccimcns, somet,imes showing large lacunae filled with blood. Fig. 5 shows one of thcsc features appearing in the upper articular space. On the left side of the pannus (a), the space is partially filled with blood (b), and the glenoid fossa shows some images of perichondrocytal calcifications (c). Fig. 6 shows, on a larger scale, a pannus found in another experimental anirnal of Group 2. Cr~zcp 3.---A limited numbrr of animals (two experimcnt.al and two control) were used in this oldest group. Fig. 7 shows the tenlporomandibular joint of one of the control rats. In the condylc, the separation line bctwccn the bone and the cartilage (itself generally more fibrous in older animals) is quite irregular. However, none of the alterations pointed out in Figs. 3, 4, 5, and 6 can be found here. On the contrary, the two rats whose upper molars were extracted 300 days before death showed signs of beginning osteoarthritic lesions. Fig. 8 shows one of the two specimens. It might be useful to point out that, by chance, the plant of sectioning passed through t,he zone of insertion and origin of the fibrous and heavily infiltrated proliferation, forming the pannus. The pathologic signs observed in the experimental specimens of Groups 2 and 0 can be summarized as follows: (L) isolated foci of calcification sur-
Volume
HISTOPATHOLOGY
16
Number 5
Fig.
S.-Section
of
a temporomandibular origin of a
OF TEMPOROMANDTRULAR
joint of an (Magnification,
pannus.
JOTNT
experimental rat ~65 ; reduceil
of Group I,$.)
619
3,
showing
the
rounding chondrocytes of the fossa, (2) necrosis of the cartilage lining the glenoid cavity, (3) isolated alteration of structure of the meniscus, and (4) pannus occupying the upper articular space. n’one of these signs is found in the control rats. The distribution of the observed lesions (+) is summarized in Table IT. TABLE II EXPERIMENTAL RAT NO.
Group
(-)
1
Group
2
Group
3
*One denote
or more complete
CONTROL
SI0N.S”
I
RAT
NO.
SIGNS
-
1 (Fig.
-
2
3 4 5 6
-
3 4
i: 3 4 :
+ t++ (Figs.- 3 and 4) +++ (Fig. 5) ++++ (Fig. 6) ++
21 (Fig.2)
-
1 2
+++ ++++ fFie.
1 (Fig.7) 2
-
i
plus signs absence
of
(+) indicate lesions.
lesions
81 in
varying
degrees
1)
of
severity;
-
minus
signs
Observation of Table Il. reveals the following : 1. In spite of t,he limited number of control rats iti C:roups Z and il. there is good evidence that long-standing loss of “vctrtical tlimcnsion” can cause histologically visible signs of osteoarthritis iit the temporomandibular joint structures. 2. The pathologic findings in the temporomandibular ,joint resulting from loss of molars arc more likely to be found in oltlcr animals. DIXCUSSlON
It is known that osteoarthritic lesions increase with advancing agel* HOWever, publications dealing with the normal development of the temporomandibular joint in the rat, even beyond the age studied in the present report,,4. 7 hart not pointed out the occurrence of lesions similar to the ones illustrated in this article. The present results confirm the observations reported by Avant, Averill, and Hahn.3 Bernick5 recently reported an investigation of the vascular and nerve supplies of the temporomandibular joint in the rat. His work showed that “nerve fibers could be traced entering t,he disc at its attachment margin, continuing Bernick’s demonstration is in centrally to the thin avascular central portion.” and modifies the classic view that nerve agreement with the findings of Masson10 fibers and vascular supply would be especially rich in the loose connective tissue behind the discI Probably, degenerative and inflammatory lesions, such as the ones described in the present study, in close relation with nervous receptors, may be responsible for pain in the temporomandibular joint. In the complex problem of the temporomandibular joint pain-dysfunction syndrome the role played by muscular tension and spasm must also be taken into account. In fact, the two views expressed in the introduction of this paper (involvement of the structures proper of the temporomandibular joint and participation of the masticatory musculature) do not exclude each other. SUMMARY
Twenty-two female ra.ts were divided into three groups. In each group some of the animals were kept as controls, while the upper molars of the other animals were extracted. Rats of the three groups were killed at the ages of 240 days, 330 days, and 480 days, respectively. The length of time that the animals lived with impaired occlusion increased from 200 days in Group 1 to 300 days in Group 2. One temporomandibular joint from each rat was prepared for histologic study. In the rats of Group 1, temporomandibular joint sections did not show any abnormal signs, whereas in most of the experimental rats of Groups 2 and 3 the following lesions were observed : 1. Perichondrocytal calcifications (glenoid 2. Necrosis of the cartilage of the fossa
fossa)
Volume 16 Number 5
HISTOPATHOLOGY
3. Structural 4. Pawns
alterations
OF TEMPOROMANDIBULAR
JOINT
621
of the meniscus (repair ?)
The lesions were more frequent in older rats. 311 of the control hat1 histologically normal telnporomandil)ular joints.
animals
of Oral Medicine at the: The author is deeply grateful to Dr. A. J. Held, Professor Medical and Dental School of the University of Gcncva, and to Dr. R. Lagier, Department for their help in the interpretation of the histologic of Pathology of the same University, spec~lmcns.
Elec1. Angelone, L., Clayton, J. A., and Brandhorst, W. C.: An Approach to Quantitative tromyography of the Masseter Muscle, J. I). Res. 39: 17, 1960. Condyle of Mice Following 2. Applebaum, E., and Levy, H. P.: Changes in the Mandibular the Use of Orthodontic Bite Plates, Am. J. Orthodontics 40: 775, 1954. 3. Avant, F. B., Averill, Ch. J., and Hahn, W. E.: Changes in the Temporomandibular Joint of Rats Caused by Alterations in the Intermaxillary Relationships of the Teeth (Abst.), J. D. Res. 31: 499, 1952. 4. Becks, H., and Evans,, H.: Atlas of the Skeletal Development of the Rat, Berkeley, Calif., 1953, American Institute of Dental Medicine. and Nerve Supply of the Temporomandibular Joint of the 5. Bernick, S.: The Vascular Rat, ORAL SURG., ORAL MED. & ORAL PATH.~~: 485,1962. ti. Cimasoq G., Myers, H., and Smudski, J.: Acetylcholinesterase Activity in the Masseter of the Rat. International iissociation for Dental Research Meeting, St. Louis, MO., 1962 (Abstract). 7. Collins, D. A., Becks, H., Simpson, M. E., and Evans, H.: Growth and Transformation of the Mandibular Joint in the Rat. I. Normal Female Rats, Am. J. Orthodontics 32: 431, 1946. of Ear and Sinus Symptoms Dependent Upon Disturbed 8. Costen, J. B.: A Syndrome Function of the Temporomandibular Joint, Ann. Otol. Rhin. & Laryng. 43: 1, 1934. Q. Jarabak, J. R.: An Electromyographic Anal,ysis of Muscular and Temporomandibular Joint Disturbances Due to Imbalance in Occlusion, Angle Orthodontist 26: 170, 1956. IO. Masson, G.: Structure et innervation du mbnisque temporo-mandibulaire, Rev. mensuelle suisse d’odonto-stomatol. 63: 739, 1953. 11. Moyers, R. E.: Electromyographical Analysis of Certain Muscles Involved in the Temporomandibular .Movements, Am. J. Orthodontics 35: 837, 1949. 12. Schwartz, L.: Disorders of the Temporomandibular Joint, Philadelphia, 1959, W. B. Saunders Company. 13. Sicher, H.: Structural and Functional Basis for Disorders of the Temporomandibular Articulation, J. Oral Surg. 13: 275, 1955. 14. Smyth, C. J., and others: Rheumatism and Arthritis; Review of the American and English Literature of Recent Years, Ann. Tnt. Med. 53: 1, lQ6O.
.
.
.
.
.
.
HISTOPATHOLOGY FOLLOWING
.
.
.
OF THE
BILATERAL
.
.
.
.
.
.
.
.
TEMPOROMANDIBULAR
EXTRACTIONS
.
.
.
.
.
.
JOINT
OF MOLARS
IN THE RAT A Preliminary
Report
Giorgio Cim.asoni, Dr. med. dent., M.X.D.,” Dental School, University
Geneva, Switzerland
of Geneva
the term temporomandibular joint pain-dysfunction syndrome has been proposed for a set of poorly defined disturbances specific for this joint, including clicking, subluxation phenomena, and pain.12 The cause of these disturbances has been- widely discussed, and a review of the pertinent literature reveals two hypotheses :
R
ECENTLY,
1. The structures proper of the temporomandibular joint would be involved and directly responsible for the disturbances. 2. The primary cause would be represented by altered function of the masticatory musculature. In fact, since Costens tried to explain the appearance of pain in the joint on the basis of anatomic considerations, other studies have pointed out the role played by the masticatory musculature.l~ 111I2 The relationship between the occlusal conditions and the status of structures of the temporomandibular joint has rarely been the object of experimental investigations. In 1952 Avant, Averill, and Hahn3 described, in four groups of rats, a number of pathologic findings in the temporomandibular joint 110 days after various groups of teeth had been extracted. The degree of joint disturbances was in direct relation to the severity of intermaxillary disturbances. The rats were all of the same age group, however, and the length of impaired occlusion was relatively short.3 This investigation. done at the Division oi’ Dental Medicine, School of Dentistry, and the George William Hooper Foundation, The University of California, San Francisco (Dr. Hermann Becks), was supported by grants of the University of California. *Present address: Institut de mddecine dentaire, 30, rue Lombard, Geneva, Switzerland.
In 1.954 Applchaum ant1 Levy” rc~portcd no significant clmngcs in the terr~poromandibnlar joints of ;I. group 01:young mice ~vho had worn orthotloutic bitt plates for 2 weeks. The present st,udy attempted to rc~producc the condition of t.hc long-term edentulous pat.ient (loss of vertical dimension) in ra1.s over 240 days of age. Bilateral extractions of the two uppw quadrants of rriohrs wrre IJtrforlnPd, and the length of impaired occlnsicm was over 200 days. METHODS
AND
;ZI~ATERL~L
Three groups of female Tdong-Evans rats wcrc nsctl in the present study. In some of the animals in each group the molars of the two upper quadrants were extracted by means of small forceps and elevators. TabIe I shows the over-all distribut,ion of the material. A total of twentytwo rats were used. In six animals c,f the first group the upper molars were extracted 200 days before the animals were killed (at. 240 days of age) ; four rats served as controls.
GROUP
AOE ( IME’S)
1
240
2 3
330 480
NO. OF ESPERIMENTAT, RATS
6 6 2
LENGTH OF EXPERIMENTAL TIME
---
200 270 300
NO.
OF COSTROT, RATS
.-.-__----4 2 I, __-__-
In Group 2 the molars of six older rats (330 days of age) were rxtractcd 270 days before the animals wcrc killed; two rats of this group served as controls. Group 3 consisted of four rats--two experimental and two control. This group was killed at 480 days, having lived 300 days with impaired occlusion. At autopsy, the masscter muscle was dissected and immediately utilized for an enzymologic study.G The temporomandibular structures were cut out, according to the method described by Decks and Evans.* They were fixed, decalcified, dehydrated, and embedded in nitrocellulose. They were sectioned in the frontal plane for histologic examinat.ion. Hematoxylin and eosin stain was used. Only the right temporomandibular joint of each rat was used. RESULTS
Group I.-Fig. 1 shows the normal appearance of a frontal histologic section of temporomandibular joint from a 240-day-old control rat. Notice the dense structure of bone in the condylar head (still irregularly covered by a layer of cartilage), the fibrous protection of the condyle, the compact structure of the meniscus, the layer of fibrous tissue, and cartilage lining the glenoid fossa. The meniscus seems to be closely adherent to the condyle (virtual space) ; this arrangement will be found in other specimens, in both the “upper” and “lower”
Volume 16 Number 5
HISTOPATHOLOGY
OF TEMPOROMANDIBULAR
JOlNT
615
articular spaces. It has already been reported as normally occurring4 and could be the result of pressure during the preparation of the sections. Very little or no deviation from the normal is noticed in the temporomandibular joint specimens of the six experimental rats of Group 1.
Fig.
L-Frontal
section
of a temporomandibular (Original magnification.
joint (control rat of Group X65 ; reduced l/5. )
1, aged
240 days).
Group Z-Fig. 2 shows a temporomandibular joint from a 330-day-old rat which had no teeth extracted. The meniscus adheres to both the fossa and the condylar head ; only the different orientation of fibers makes it possible to recognize the meniscus from the upper and lower structures. The thickness of cartilaginous covering, which would be too large for a rat of this age, is certainly the result of the section’s orientation .* The temporomandibular joint illustrated in Fig. 3 is from an experimental rat of Group 2. Notice that in the area indicated by a a structural alteration can be seen in the meniscus. Furthermore, the glenoid fossa shows some isolated sites of calcification surrounding a few chondrocytes (b) and an important zone of necrosis (c). Fig. 4 points out, under greater magnification, the peculiar feature found in the meniscus. Observation by polarized light suggests an actual different orientation of fibers, which could be interpreted as a repair phenomenon. Above this peculiar meniscal zone, and in direct relation wit,h it, a certain amount of liquid material is noticed (necrosis ? plasma ?) . *On histologic the plane of section.
preparations This must
the width of the cartilaginous layer may vary according to be kept in mind, particularly when studying mandibular growth.
616
Fig. 3.-Temporomand
Volume Number
16 5
HISTOPATHOLOGY
OF TEMPOROMANDIHULAR
JOINT
617
Atldhc~r inlportallt pa1hologic finding in some of the rats of Group 2 is the csistenec of a “pa,nnus. ” ~Presumably as a result of proliferation of the synovial membrane, an irregular rrmss of granulation tissue can be observed in some spccimcns, somet,imes showing large lacunae filled with blood. Fig. 5 shows one of thcsc features appearing in the upper articular space. On the left side of the pannus (a), the space is partially filled with blood (b), and the glenoid fossa shows some images of perichondrocytal calcifications (c). Fig. 6 shows, on a larger scale, a pannus found in another experimental anirnal of Group 2. Cr~zcp 3.---A limited numbrr of animals (two experimcnt.al and two control) were used in this oldest group. Fig. 7 shows the tenlporomandibular joint of one of the control rats. In the condylc, the separation line bctwccn the bone and the cartilage (itself generally more fibrous in older animals) is quite irregular. However, none of the alterations pointed out in Figs. 3, 4, 5, and 6 can be found here. On the contrary, the two rats whose upper molars were extracted 300 days before death showed signs of beginning osteoarthritic lesions. Fig. 8 shows one of the two specimens. It might be useful to point out that, by chance, the plant of sectioning passed through t,he zone of insertion and origin of the fibrous and heavily infiltrated proliferation, forming the pannus. The pathologic signs observed in the experimental specimens of Groups 2 and 0 can be summarized as follows: (L) isolated foci of calcification sur-
Volume
HISTOPATHOLOGY
16
Number 5
Fig.
S.-Section
of
a temporomandibular origin of a
OF TEMPOROMANDTRULAR
joint of an (Magnification,
pannus.
JOTNT
experimental rat ~65 ; reduceil
of Group I,$.)
619
3,
showing
the
rounding chondrocytes of the fossa, (2) necrosis of the cartilage lining the glenoid cavity, (3) isolated alteration of structure of the meniscus, and (4) pannus occupying the upper articular space. n’one of these signs is found in the control rats. The distribution of the observed lesions (+) is summarized in Table IT. TABLE II EXPERIMENTAL RAT NO.
Group
(-)
1
Group
2
Group
3
*One denote
or more complete
CONTROL
SI0N.S”
I
RAT
NO.
SIGNS
-
1 (Fig.
-
2
3 4 5 6
-
3 4
i: 3 4 :
+ t++ (Figs.- 3 and 4) +++ (Fig. 5) ++++ (Fig. 6) ++
21 (Fig.2)
-
1 2
+++ ++++ fFie.
1 (Fig.7) 2
-
i
plus signs absence
of
(+) indicate lesions.
lesions
81 in
varying
degrees
1)
of
severity;
-
minus
signs
Observation of Table Il. reveals the following : 1. In spite of t,he limited number of control rats iti C:roups Z and il. there is good evidence that long-standing loss of “vctrtical tlimcnsion” can cause histologically visible signs of osteoarthritis iit the temporomandibular joint structures. 2. The pathologic findings in the temporomandibular ,joint resulting from loss of molars arc more likely to be found in oltlcr animals. DIXCUSSlON
It is known that osteoarthritic lesions increase with advancing agel* HOWever, publications dealing with the normal development of the temporomandibular joint in the rat, even beyond the age studied in the present report,,4. 7 hart not pointed out the occurrence of lesions similar to the ones illustrated in this article. The present results confirm the observations reported by Avant, Averill, and Hahn.3 Bernick5 recently reported an investigation of the vascular and nerve supplies of the temporomandibular joint in the rat. His work showed that “nerve fibers could be traced entering t,he disc at its attachment margin, continuing Bernick’s demonstration is in centrally to the thin avascular central portion.” and modifies the classic view that nerve agreement with the findings of Masson10 fibers and vascular supply would be especially rich in the loose connective tissue behind the discI Probably, degenerative and inflammatory lesions, such as the ones described in the present study, in close relation with nervous receptors, may be responsible for pain in the temporomandibular joint. In the complex problem of the temporomandibular joint pain-dysfunction syndrome the role played by muscular tension and spasm must also be taken into account. In fact, the two views expressed in the introduction of this paper (involvement of the structures proper of the temporomandibular joint and participation of the masticatory musculature) do not exclude each other. SUMMARY
Twenty-two female ra.ts were divided into three groups. In each group some of the animals were kept as controls, while the upper molars of the other animals were extracted. Rats of the three groups were killed at the ages of 240 days, 330 days, and 480 days, respectively. The length of time that the animals lived with impaired occlusion increased from 200 days in Group 1 to 300 days in Group 2. One temporomandibular joint from each rat was prepared for histologic study. In the rats of Group 1, temporomandibular joint sections did not show any abnormal signs, whereas in most of the experimental rats of Groups 2 and 3 the following lesions were observed : 1. Perichondrocytal calcifications (glenoid 2. Necrosis of the cartilage of the fossa
fossa)
Volume 16 Number 5
HISTOPATHOLOGY
3. Structural 4. Pawns
alterations
OF TEMPOROMANDIBULAR
JOINT
621
of the meniscus (repair ?)
The lesions were more frequent in older rats. 311 of the control hat1 histologically normal telnporomandil)ular joints.
animals
of Oral Medicine at the: The author is deeply grateful to Dr. A. J. Held, Professor Medical and Dental School of the University of Gcncva, and to Dr. R. Lagier, Department for their help in the interpretation of the histologic of Pathology of the same University, spec~lmcns.
Elec1. Angelone, L., Clayton, J. A., and Brandhorst, W. C.: An Approach to Quantitative tromyography of the Masseter Muscle, J. I). Res. 39: 17, 1960. Condyle of Mice Following 2. Applebaum, E., and Levy, H. P.: Changes in the Mandibular the Use of Orthodontic Bite Plates, Am. J. Orthodontics 40: 775, 1954. 3. Avant, F. B., Averill, Ch. J., and Hahn, W. E.: Changes in the Temporomandibular Joint of Rats Caused by Alterations in the Intermaxillary Relationships of the Teeth (Abst.), J. D. Res. 31: 499, 1952. 4. Becks, H., and Evans,, H.: Atlas of the Skeletal Development of the Rat, Berkeley, Calif., 1953, American Institute of Dental Medicine. and Nerve Supply of the Temporomandibular Joint of the 5. Bernick, S.: The Vascular Rat, ORAL SURG., ORAL MED. & ORAL PATH.~~: 485,1962. ti. Cimasoq G., Myers, H., and Smudski, J.: Acetylcholinesterase Activity in the Masseter of the Rat. International iissociation for Dental Research Meeting, St. Louis, MO., 1962 (Abstract). 7. Collins, D. A., Becks, H., Simpson, M. E., and Evans, H.: Growth and Transformation of the Mandibular Joint in the Rat. I. Normal Female Rats, Am. J. Orthodontics 32: 431, 1946. of Ear and Sinus Symptoms Dependent Upon Disturbed 8. Costen, J. B.: A Syndrome Function of the Temporomandibular Joint, Ann. Otol. Rhin. & Laryng. 43: 1, 1934. Q. Jarabak, J. R.: An Electromyographic Anal,ysis of Muscular and Temporomandibular Joint Disturbances Due to Imbalance in Occlusion, Angle Orthodontist 26: 170, 1956. IO. Masson, G.: Structure et innervation du mbnisque temporo-mandibulaire, Rev. mensuelle suisse d’odonto-stomatol. 63: 739, 1953. 11. Moyers, R. E.: Electromyographical Analysis of Certain Muscles Involved in the Temporomandibular .Movements, Am. J. Orthodontics 35: 837, 1949. 12. Schwartz, L.: Disorders of the Temporomandibular Joint, Philadelphia, 1959, W. B. Saunders Company. 13. Sicher, H.: Structural and Functional Basis for Disorders of the Temporomandibular Articulation, J. Oral Surg. 13: 275, 1955. 14. Smyth, C. J., and others: Rheumatism and Arthritis; Review of the American and English Literature of Recent Years, Ann. Tnt. Med. 53: 1, lQ6O.