Internal derangement of the TMJ: Changes associated with mandibular repositioning and orthodontic therapy

American Journal of and DENTOFACIAL Founded

in 1915

ORT Volume 96 Number 5

Copyright

0 1989 by The C.V. Masby Company

al derangement of the l’MJ: Changes ssociated with mandibular repositioning an hodontic therapy Stephen D. Keeling, DDS, MS,” Charles Gibbs, PhD,b Matthew B. Hall, DDS, MD,” and S&fan Lupkiewicz, BS, MSd Gainesville,

Fla.

Because of its apparent success in relieving symptoms, especially pain, anterior mandibular repositioning therapy is a popular mode of nonsurgical treatment for patients with painful, clicking internal derangement of the temporomandibular joint. Posterior open bites are a frequent consequence of such therapy and may necessitate either continued appliance wear or closure by equilibration, prosthetics, or orthodontics. The anatomic and functional changes that occur subsequent to mandibular repositioning during orthodontic closure of the posterior open bite are not well understood. A case of a patient with a Class II, deep bite malocclusion and painful internal derangement of the TMJ is presented. Transcranial and cephalometric radiographs, arthrograms, and mandibular movement recordings were obtained before treatment and after both repositioning therapy and orthodontic treatment. Regarding occlusal improvement and pain relief, the treatment was successful. However, not all of the changes that occurred during repositioning therapy were maintained after orthodontic treatment. The strategy used in this case (mandibular repositioning/orthodontic finishing) was evaluated by an examination of these anatomic an functional changes with a discussion centered on the possible mechanisms involved. (AM J QRTHOD DENTOFACORTHOP1989;96:363-74.)

nternal derangement of the temporomandibmar joint has been defined as an abnormal relationship of the articular disk to the condyle,’ characterized by mechanical disturbances and impediments to joint function .2 This condition may involve displacement / deformation of the articular disk, alteration of condylar position, osseous remodeling, and joint hypermobility; clinical signs include clicking, limitation of mandibular movement, and/ or locking. * Patients may complain of capsular pain, muscular pain, and/or temporal headaches.3 From the University of Florida. aDepartment of Orthodontics. %kpxtment of Oral Biology. ‘Department of Oral and Maxillofacial dDivision of Computer Science. 8l411146.3

Surgery

Clicking is often the result of anterior displacement of the disk,4-6 although joint sounds may occur because of adhesions between a normally positioned condyle and disk.7 Displacement often is associated with reciprocal clicking’; the opening click generally is louder than the closing click and occurs at a point of more condylar translation.6 The disk does not undergo active remodeling, but passively deforms and/or displaces to accommodate changes in the temporal. and condylar units.’ However, osseous structures of the joint can remodel in response to biomechanical stress to maintain equilibrium between joint form and function.g-12 When the disk is displaced, the posterior attachment (bilaminar zone) is placed in a position of repetitive loading.6 Clinically many people with such displacements function without problems when, it has been suggested, the forces directed to these nonsecular tis363

Fig. 1. Pretreatment Left.

facial

and

intraoral

photographs.

sues do not exceed the joint’s capacity to undergo metaplasia without inflammation. l3 However, when stresses exceed adaptive capacity, it is hypothesized that the balance between form and function shifts to a pathologic state with breakdown or loss of articular tissues, which may result in friction and eventual disk perforation’; associated cellular changes in the osseous tissues are referred to as osteoarthrosis.’ Repositioning of the mandible has become a popular mode of nonsurgical treatment for internal derangement because of its success in normalizing symptoms, especially pain. 14-16It has been hypothesized that concentric repositioning of the condyle in the fossa restores the integrity of the disk, promotes stability, and thereby improves muscle coordination.* However, Ash3 recently reported a “. . . dramatic increase in the referral to the

A, Frontal.

, Profile.

C, Anterior.

[TMJ pain] clinic of patients for whom [swh] irreversible treatment has failed.” This dichotomy suggests that the results of mandibular repositioning are not well understood. In addition the consequences of rnand~bnl~ repositioning to subsequent occlusal relationships are not predictable: some patients return to their previous occlusal position without complication; in others a posterior open bite persists.3 In these latter cases: continued appliance wear to support the mandible, occlusal adjustment, prosthetic rehabilitation, and o~hodonti~s to erupt posterior teeth have been reported.2,3,i4,‘5,!7,~~ The anatomic and functional changes that occur subsequent to mandibular repositioning after orthodontic closure of a posterior open bite are not clear. Changes in condylar position have been shown with banscranial

V&me 96 Yumber 5

PRE-TREATMENT

Fig.

a 2. Pretreatment

orthodontic

models.

radiography and in mandibular position with cephalometric radiography; functional changes have been assessed by evaluating (1) clinical signs of dysfunction, (2) self-reports of symptoms, and (3) mandibular movement patterns. Frequently one method has been used in initial diagnosis (condylar position, for example) and another method to evaluate treatment success (selfreport of pain severity, for example). Surprisingly, few well-documented cases have been reported in the literature. The following is a report of a patient with a Class II, deep bite malocclusion and signs and symptoms of chronic, painful internal derangement. Transcranial radiographs, arthrograms, lateral cephalometric radiographs, and recordings of mandibular movement were obtained before treatment and after both mandibular repositioning and orthodontic therapy.

of pretreatment

lateral

cephalogram.

developed during the day. He denied muscle tenderness, paresthesia, joint-associated headaches, hearing or visual problems, and facial trauma. He did not express concern about his facial appearance. There was a history of previous orthodontic therapy: (1) nonextraction headgear treatment between 8 and 10 years of age and (2) four-premolar extraction therapy from 12 to 14 years of age. He reported an allergy to penicillin, no current medication, and no previous hospitalization. Clinical examination. The patient (Figs. 1 and 2) had a Class II, Division 2, subdivision right malocclusion with 2 mm of overjet, an impinging overbite, and 1 mm of crowding in each arch. The maxillary arch had a reverse curve of Spee, the mandibular arch a mild curve of Spee. The maxillary dental midline was centered with the patient’s face; the mandibular dental midline was 2% mm to his right. His face was symmetric; the soft-tissue profile was convex with a strong nose, obtuse nasolabial angle, fiat lip support, moderate mental sulcus, good soft-tissue chin button, and competent lip function. Maximum mouth opening was 40 mm with 10 mm of right and left lateral movement and 7 mm of protrusive move-

ment. An opening click in the right TMJ occurred at 30 mm

CASEREPORT ETREATMENT

3. Tracing

FlNDlNGS

History. The patient was an 1%year-old male college student whose chief complaints were “collapse of alignment” of the teeth and painful clicking in the right TMJ. Clicking had started 2 years previously with pain that progressively

and was audible. The patient could execute opening and closing movements without clicking when the incisors were in an end-to-end relation; the dental midlines remained unchanged. His muscles were not tender to palpation. There were neither signs nor symptoms of left TMJ dysfunction. Cephalometric analysis. The lateral cephalogram (see

Table

I. Cephaiornetric

Ba-S-Na SN-FH SNA A to Na perpendicular (mm) SNB Pogonion to Na perpendicular (mm) Co-Gn (mm) ANB 1toNA 1. to NA (mm)

1 to SN I~ONB i to NB (mm) IMPA

SN-GoGn FMA Soft-tissue pogonion to subnasale perpendicular (mm)

measurements*

117.7 4.2 84.5 - 1.3

118.8 4.4 83.2 - 2.2

118.5 3.6 85.3 - 1.5

79.9 -4.1

79.2 -6.6

81.4 -3.3

127.1 4.6 9.7 - 1.9 93.6 17.8 3.1 97.0 20.9 16.8 - 17.6

128.5 4.0 9.7 -2.1 92.9 22.6 4.4 99.4 24.1 19.7 19.1

127.2 3.9 26.7 1.6 112.0 26.3 4.8 IO5.5 19.4 15.8 - 16.7

*All measures are in degrees, unless noted otherwise, and represent the average of three tracing determinations.

Fig. 4. Transcranial

radiographs. A and B, Pretreatment, teeth in occiusion. E and D, Pretreatment, maximum opening. E and F, After 12 weeks of mandibular repositioning therapy, taken with splint in place. G and H, After 12 weeks of mandibular repositioning therapy, taken with teeth in occlusion (anterior teeth had contact, posteriors did not). I and J, After orthodontic therapy with teeth in occlusion. K and L, After orthodontic therapy, maximum opening.

Fig. 3, Table I) showed a mild Class II relation of the maxilla to the mandible. The cranial base flexure was acute with a fiat, short anterior crania1 base. This relation affected SNA and SNB. making them more protrusive than the facial profile suggested. The upper incisors were retroclined and bodily retrusive: the lower incisors tended toward bodily retrusion. Measurements of facial divergence showed a closed vertical

pattern. Soft-tissue pogonion was markedly retrusive In relation to the soft-tissue subnasale perpendicular. TMJ radiogruph~. Transcranial radiographs (Fig. 4, A and B) showed what might be interpreted as flattening of the posterosuperior surface of both condyles. Both condyles did not appear to be centered in the fossa with the teeth in occlusion, but they translated past the eminence in function (Fig. 4, C and D). Because there were no signs of erosion or cratering, the osseous elements of the joint were considered normal. Arthrography of the painful, clicking right joint (Fig. 5) was performed with dye injected into the inferior joint space. There was no sign of perforation; late reduction (recapture) of the displaced disk was inferred. Artb~ograp~y was not performed on the asymptomatic left joint. Mandibular movement. Tracings of mandibular movement were obtained with the Replicator system (Fig. 6).‘y-21 Right condylar movement in the sagittal plane (Fig. 7, upper) showed the typical “figure 8” pattern5 of a clicking joint with late reduction during opening and late loss of the disk during closure. Movement of the left condyle appeared normal. Tracings of border movement at the incisor point in the sagittal plane (Posselt’s diagram**) (Fig. 8, upl7e.r left) appeared normal, with a small anterosuperior slide from retruded contact (RC) to intercuspal position (IF’). Tracings of the border movement at the incisor point in the frontal plane (Fig. 8. lower lefi) demonstrated a “flatness” in the lower right (patient’s left) of the pattern, indicating restricted movement of the right condyle during mediotrusive translation, which suggests anteromedial displacement of the disk of the right TMJ.

Fig. 5. Pretreatment anterior to condyle disk.

arthograms of painful, clidking rrght temporomandibular at the maximum opening position (in D), suggesting

joint. Note absence of die late reduction of the displaced

These findings suggested chronic, painful internal derangement of the right TMJ with late reduction and without pathologic degenerative changes of the articular surfaces. There was a Class II, Division 2 deep bite malocclusion with retroclined upper incisors. The facial profile was convex with a mild Class II denture base relation, retrognathic maxilla and mandible, and a closed vertical pattern. The four permanent first premoiars were absent. EATMENT

OPTIONS

The following treatment options were presented to the patient: (1) phcation surgery of the right TMJ, (2) anterior repositioning therapy and reevaluation for orthodontic correction of his malocclusion, and (3) observation without active therapy. He was considered an excellent surgical candidate because of the self-reducing nature of the click. This feature plus the absence of meniscus perforation also made for mandibular repositioning therapy. We whim a candidate stressed the evanescent nature of pain to support the option of observation. His choice of option 2 appeared to address both of his chief complaints (occlusal collapse and pain), whereas options 1 and 3 did not. TERlOR

POSITIONING

THERAPY

An anterior repositioning splint was fabricated for the mandibular arch (Fig. 9). Deep fossae with guiding planes directed the mandible forward so the patient could open and close on the splint without clicking. On the ninth day of wear, the patient reported, “less tension, a lot more comfort, no more pain; the teeth do not fit in the back position [with the splint out]; there is pain when I try to squeeze my teeth all together.” Clinically there

Fig. 6. Patrent during Replicator recording session with intraoral clutches and external face-bow consisting of upper and lower arms connected by six photooptical transducers.

was no clickmg on opening or closing with or without the splint. A posterior open bite existed; the Iower midline remained off to the right. The patient remained comfortable and was an exceiient full-time splint wearer during the following 10 weeks. At that time a lateral cephalometric film, transcranial radiographs, and mandibular movement recordings with the Replicator were obramed. POSTSPLINT

FINDINGS

A brlateral posterior open bite with in&al contact persisted (Fig. 10). The cephalometric tracmg (Fig. I 1, A) with the splint in place superimposed on the pretreatment tracing suggested that

3

Keeling

et al.

LEFT

Fig. 7. Tracings produced movement in the sagittal center, after repositioning orthodontics

by the Replicator system of condylar plane. Upper, Pretreatment tracings; therapy; lower, after completion of

Fig.

9. Mandibular

anterior

repositioning

splint.

Fig. 10. Occlusal relationship after 12 weeks of anterior repositioning therapy. Note posterior open bite, improved anterior overbite, and midline deviation.

but less so with the teeth in occlusion (anterior teeth had contact, posterior teeth did not) (Fig. 4, G and N). Recordings of mandibular movement were made without the splint. Tracings of condylar movement in the sag&al plane The classical “‘figure 8” appeared normal (Fig. 7, center). pattern of a clicking joint was not evident. The posterior portion of the tracing was nearly horizontal and not inclined with the articular eminence. Posselt’s diagram (Pig. 8, upper center) had changed. An RC to IP anterosuperior slide was not evident. The posterior limit of the diagram was more anterior than it was before splint therapy. This change was evident when the diagrams (Fig. 12) were superimposed on the upper incisor concavity tracing (i.e., the positions of the incisors had not been intentionally altered at this point). A flatness remained in the lower right corner of the frontal pattern of incisal point movement (Fig. 8, lower center). Fig. 9. Upper, Tracings produced by the Replicator system of border movement at the mandibular incisor point in the sagittal plane (Posseit’s diagramz*); lower, tracings of border movement at the mandibular incisor point in the frontal plane.

in this deep bite case the splint served more as a vertical repositioning appliance than an anterior repositioning one. Condylion was positioned anteroinferiorly, but pogonion and I3 point moved inferiorly and posteriorly. Transcranial radiographs suggested an anteroinferior positioning of both condyles with the splint (Fig. 4, E and F)

ORTHODONTIC

TREATMENT

The maxillary arch was banded/bonded 5 weeks later with a straight-wire 0.01%inch slot appliance. During the following 6% months, the maxillary reverse curve of Spee was leveled and anterior torque corrected. The mandibular splint was continuously worn during tbis time; the patient remained comfortable. The maxillary arch was stabilized with a 0.016 x 0.022-inch arch wire. At this time the mandibular splint was replaced with an occlusal coverage flat plane maxillary acryhc appliance and the mandibular arch was banded/bonded. A periodontal graft

Yolume

96

Number

5

PRE-TREATMENT

-

POST-TREATMENT

.. . .. .. . ..

PRE-TREATMENT

-

SPLINT

------

POSITION

SPLINT \

Pos1Tm4

POST-TREATMENT

---_-.. .. . . .. . ..

\

’ / )

c ~ ‘Il. Superimpositions of tracings of lateral splint in place and pretreatment occlusal position. in place and posttreatment occlusal position.

was placed in the lower incisor region before arch wire engagement and allowed to heal for 1 month. The maxillary acrylic appliance was not well tolerated; during the month of graft healing, the patient stopped wearing it. A 40% anterior overbite with incisor contact and a posterior open bite persisted. The mandibular arch was aligned, leveled, and worked up to a 0.016~inch arch wire. Right-side Class elastics, an anterior diagonal elastic, and a left box elastic were placed to correct the right side Class II relation, midline deviation, and posterior open bite. Three months later vertical elastics were added to the right second molars. Within a week, the patient returned complaining of occasional popping in the right joint. The right vertical elastic to the second molars, left box elastic,

cephalometric B, Pretreatment

radiographs. A, Anterior repositioning and posttreatment tracings. C, Splint

and anterior diagnonal elastic were stopped. In their place right and left check elastic? were placed, extending from the upper second molars through a hook on the lower first molar bands to a hook on the maxillary arch wire mesial to the canines. These elastics had short vertical and long Class II vectors. The right side Class II elastic was continued. Tne case continued without further patient complaints for 5 months at which time appliances were removed and upper/lower Hawley retainers were placed. POW-TREATMENT

FINDINGS

The patient appeared to have subtle facial changes with a decrease in mental sulcus depth (Figs. 13 and 14). There was a Class I occlusion with ideal overjet and overbite. The

Am. J. Orthod.

Keeling et al.

PRE-TREATMENT

Dent&c. Orthop. November 1989

condyles were intermediate between their pretreatment position and splint held position. Tracings of condylar movement in the sagittal plane did not show the “figure 8” pattern of a clicking joint (Pig. 7, lower). The posterior portion of the condylar curve no longer showed the horizontal flattening. Opening and closing movements of the right condyle were more “separated” than those of the left. The right path was shortened. A small RC to IP anterosuperior slide was evident in Posselt’s diagram (Pig. 8, upper right). Superimposition of these diagrams (Fig. 12) demonstrated that the sagittal envelope of motion was more confined than in previous recordings. The tiontal movement pattern at the lower incisor point (Fig. 8, lower righr) appeared more symmetric after orthodontic treatment with a well-defined IP spike and lateral disclusion paths. The previously recorded flatness in the lower right corner remained. Because the patient was free of signs and symptoms of dysfunction, TMJ arthrography was not performed. The patient has remained asymptomatic for 2 years at the time of this report. DISCUSSION

AND CONCLhl

Regarding occlusal improvem sence of pain, the patient’s chief to have been addressed. The s Fig. 12. Composrte tracing of Posselt’s diagramsz superimposed on the lingual concavity of the maxillary incisors. midlines remained slightly off. Maximum mouth opening measured 42 mm: with 9 mm of right and left lateral movement and 7 mm of protrusive movement. There was no clicking during mandibular movement and no report of discomfort. Superimposition of the pretreatment and posttreatment cephalometric radiographs (Fig. 11, B, and Table I) showed the maxillary position as unchanged, the mandible more anteriorly positioned, and the ANB difference reduced. The maxillary and mandibular incisors had been proclined and advanced. The mandibular plane angle was reduced slightly. Soft tissue pogonion was advanced slightly in relation to the subnasale perpendicular. The cephalometric superimpositions (Fig. 11) indicated that menton point was held inferiorly and slightly posteriorly in the splint; after treatment menton approached its pretreatment position. The gonial point was positioned inferiorly and posteriorly with the splint; after treatment its vertical position established with the splint remained unchanged but had moved anteriorly. It appeared as though the vertical position of the mmus was lowered by the splint and maintained by orthodontic treatment, while the mandible rotated in an upward and forward direction. Transcranial radiographs (Fig. 4, I and J) did not show further obvious remodeling. Both condyles translated past the articular eminence as before (Fig. 4, K and L). Superimposition tracings (Fig. 15) registered on the outline of the temporal fossa suggested that the posttreatment positions of both

be related to the treatment rendered, a placebo effect, or the natural history of the condition (or all three).24,25 The strategy used in this case was evaluated by examining the anatomic and functional changes that occurred during treatment in light of the current literature. This case study provided an opportunity to focus on unanswered questions; it did not provide hard answers. Underlying assumptions made by the proponents of repositioning therapy are that internal d~rangemeut is a progressive disorder and the threshold between adaptive remodeling and tissue degeneration is reversible in the early stages; such therapy attempts to reverse this progressive process.‘3 Whether the favorabble changes achieved during repositioning therapy are maintained during orthodontic therapy to reestablish the occlusion remains problematic. However, the natural history of TMJ disorders is not well understood.3 The suggestion that clicking is a progressive disturbance leading to disk p ration’ and/or degenerative joint disease* has not n substantiated.3,26 A recent 5year ~o~gi~d~~a~ study suggesting a cyclic nature to these disorders concluded, “TMJ clicking may come and go spontaneously and seldom is associated with more severe dys~nction.“27 Thus cessation of clicking in this case can not be attributed solely to the therapy received. In patients with painful clicking who receive anterior repositioning therapy and become pain-free and nonclicking, can it be assumed the disk has been “‘re-

Fig. 13. Posttreatment facial and intraoral photographs. E, Left.

captured”? Right condylar movement (Fig. 7) apparently was normalized during repositioning therapy; the ‘“figure 8” pattern of a clicking joint had disappeared. At the completion of orthodontic treatment, the “figure 8” pattern also was absent, but the translatory path appeared abruptly shortened. This feature, plus the persistent flatness in the lower right comer of the frontal movement pattern (Fig. S), suggested anterior and medial displacement of the disk. These Replicator data suggested that the condylar movement pattern that occurred during repositioning therapy was a function of splint wear and was not maintained during orthodontic correction. Absence of postorthodontic clicking could have resulted from an anteriorly displaced disk.‘* Superimpositions of cephalometric (Fig. 11) and transcranial (Fig. 15) tracings suggested that ramus/condylar position had been lowered. In the ab-

A, Frontal.

, Profile. C, Anterior.

sence of “‘true capture,” perhaps this change served to decrease the repetitive loading of the posterior attachment tissues to allow healing and metaplasia (scarring with extension of the disk). This mechanism has been suggested previously’3 and might have accounted for pain reduction in this case. Cephalometric superimpositions (Fig. 11) indicated that the mandible was more anteriorly displaced after treatment. In addition Replicator data demonstrated that the patient was functioning more anteriorly (see Fig. 12, superimposition of Posselt’s diagrams). Anterior mandibular posturing, mandibular/condylar growth, and/or glenoid fossa relocation might have accounted for these changes. Superimposition of the transcranial tracings (Fig. 15) suggested that the condylar positions were intermediate between their pretreatment and splint-held po-

72

Keeling

Fig.

et al.

14. Posttreatment

orthodontic

models.

sitions. The condyles did not appear to be positioned anteriorly against the articular eminence nor distracted from the fossa. However, transcranial radiographs have limitations in assessing condylar morphology and concentricity in the fossa.’ Repeated attempts to produce a larger slide in centric during the posttreatment Replicator recording were unsuccessful. In addition the patient was free from signs and symptoms of muscle/joint pain that often accompany mandibular posturing.30 Repeated measures of mandibular length (Table I) did not show differences that could be interpreted as significant mandibularicondylar growth, although such growth might be expected in postadolescent or even adult males.31 These differences are not easily demonstrated on lateral cephalometric radiographs. Perhaps these skeletal and functional changes suggest (albeit indirectly) glenoid fossa remodeling. This interpretation would be consistent with the recent conclusions of Woodside, Metaxas, and Altuna” that “Skeletal jaw relationships may be altered by both glenoid fossa remodeling and condylar extension in young primates, thereafter by glenoid fossa re-

location.” This raises a further question: Is integrity of the soft-tissue components of the joint necessary for osseous remodeling and/or growth? These data suggest otherwise. Pain relief in this case could have been unrelated to any of the anatomic and functional changes observed and could be explained by the placebo effect associated with any treatment.24.25 In this regard our patient had become more adjusted to college life during the treatment time and had established a close relationship with his girlfriend. The relationship between orthodontistpatient was also judged good. TMJ disorders have a multifactorial cause that is not completely understood.3 Our patient did not report a history of external trauma. His joint problem could have existed before, developed during (and independent of), or occurred spontaneously after his adolescent orthodontic treatment. Systematic orthodontic therapy has not been implicated as a primary causative factor in mandibular dysfunction (for review, see Moyers3’). Deep bite and Class II malocclusions have been associated with signs and symptoms of dysfu~ctio~,3~ but a cause-effect relationship has not been established. In short, the cause of this patient’s joint problem was unknown. Definitive treatment should be based on a specific diagnosis.’ The inability to define the causative factor(s) in these cases suggest that this popular strategy (repositioning/orthodontic finishing) is being nonspecifically applied. Predicting success is difficult and understanding the basis for success/failure even more so. It is ironic perhaps that although orthodontists assess occlusal deficits, skeletal morphology, signs of dysfunction, and patient desires, treatment successdepends on adaptability, favorable growth, cooperation (for which there are neither reliable nor valid measures), and perhaps on choosing from among several therapeutic approaches (for which there are no comparable data). Was repositioning therapy necessary to achieve the treatment goals (occlusal correction and pain relief)? If the favorable changes produced during mandibular repositioning (improved condylar movement of the affected condyle) are not routinely maintained after ortbodontic therapy, could these goals have been obtained by orthodontic therapy alone? Orthodontists have been correcting deep bite malocclusions for decades by erupting posterior teeth and (perhaps unknowingly) repositioning condyles. The challenges in orthodontics are many; we live in an exciting professional era.

Volume 96 Number 5

PRE-TREATMENT SPLINT POSITION

---. .. .. . . .

POST-TREATMENT

Fig. 15. Tracings of transcranial radiographs

REFERENCES 1. Dolwick MF, Katzberg RW, Helms CA. Internal derangements of the temporomandibular joint: fact or fiction? J Prosthet Dent 1983;49:415-8. 2. Solberg WK. Temporomandibular disorders: management of internal derangement. Br Dent J 1986;160:379-85. 3. Ash MM. Current concepts in the aetiology, diagnosis and treatment of TMJ and muscle dysfunction. J Oral Rehabil 1986;13:120. 4. Ireland VW. Tbe problem of the clicking jaw. Proc R Sot Med 1951;44:191. 5. Farrar WB. Characteristics of the condylar path in internal derangements of the TMJ. J Prosthet Dent 1978;39:319-23. 6. Isberg-Ho!m AM, Westesson PL. Movement of the disc and condyle in temporomandibular joints with clicking. An arthrographic and cineradiographic study on autopsy specimens. Acta Odontol Stand 1982;40:15 l-64. 7. Sanders B. Buoncristiani R. Diagnostic and surgical arthroscopy of the temporomandibular joint: clinical experience with 137 procedures over a 2-year period. J Craniomandib Disord 1987;1:202-13. 8. Moffett BC, Westesson PL. Diagnosis of internal derangements of the temporomandibular joint. Vol 1. Double-contrast arthrography and clinical correlation. Seattle: University of Washington Continuing Dental Education, 1984. 9. Moffett SC, Johnson LC, McCabe JB, Askew HC. Articular remodeling in the adult human temporomandibular joint. Am J Anat 1964;115:I19-30. 10. Stockh PW, Willert HG. Tissue reactions in the temporomandibular joint resulting from anterior displacement of the mandible in the monkey. AM J ORTHOD 1971;60:142-55. 1 I. McNamara JA Jr. Neuromuscular and skeletal adaptation to altered hunzion in the orofacial region. AM J ORTHOD 1973;64:578606. 12. Woodside DG, Metaxas A, Altuna G. The influence of functional appliance therapy on glenoid fossa remodeling. AM J ORTHOD DENTOFAC

superimposed

17.

18.

19. 20.

21. 22. 23.

24. 25.

26.

27.

28.

OKTTNOP 1987;92:181-98.

13. Solberg WK. Temporomandibulardisorders: clinical significance of TMJ changes. Br Dent J 1986;160:231-6. 14. Williamson EN, Sheffield JW Jr. The treatment of internal derangement of the temporomandibularjoint: a survey of 300 cases. Cranio 1987;5: 119-24. 15. Owen AH III. Grthodonticiorthopedic treatment of craniomandibular pain dysfunction. Part 2. Posterior condylar displacement. J Craniomandibular Pratt 1984;4:333-49. 16. Clark GT. Treatment of jaw clicking with temporomandibular

29.

30.

3 1.

on outline of the glenoid fossa.

repositioning: anaiysis of 25 cases. J Craniomandibular Pratt 1984;2:263-70. Weinberg LA. Definitive prosthodontic therapy for TMJ patients. Part I. Anterior and posterior condylar displacement. J Prosthet Dent 1983;50:544-57. Abadi BJ, Okeson JP. Alteration of vertical dimension in the treatment of craniomandibular disorders. J Craniomandibuiar Pratt 1983;1:55-9. Gibbs CH, Messerman T, Reswick JB. Functional movements of the mandible. J Prosthet Dent 1971;26:601-10. Gibbs CH, Wickwire NA, Jacobson AP, Lundeen HG, Mahan PE. A comparison of typical chewing patterns in children and adults. J Am Dent Assoc 1982;105:33-42. Lundeen HC, Gibbs CH. Advances in occlusion. Littleton, Massachusetts: John Wright-PSG, 1982. Posselt U. Movement areas of the mandible. J Prosthet Dent 1957;7:375-85. Hocevar RA. Understanding, planning, and managing tooth movement: orthodontic force system theory. Am J Orthod 1981;80:457-77. Epstein JB. Understanding placebos in dentistry. J Am Dent Assoc 1984;109:71-4. Greene CS, La&in DM. Long-term evaluation of treatment of myofascial pain-dysfunction syndrome: a comparative analysis. J Am Dent Assoc 1983;107:235-8. Eriksson L, Westersson PL. Clinical and radiographic study of patients with anterior disk displacement of the temporomandibular joint. Swed Dent J 1983;7:55. Magnusson T, Egermark-Eriksson I, Carlsson GE. Five year longitudinal study of signs and symptoms of mandibular dysfunction in adolescents. J Craniomandibular Prac 1986;4:33844. McCarty W Jr. Diagnosis and treatment of internal derangements of the articular disc and mandibular condyle. In: Solberg WK, Clark GT, eds. Temporomandibular joint problems: biologic diagnosis and treatment. Chicago: Quintessence, 1980. Pullinger AG, Hollender L, Solberg WK, Petersson A. A tomographic study of mandibular condyle position in an asymptomatic population. J Prosthet Dent 1985;53:706-13. Rocabado M. Diagnosis and treatment of abnormal craniocervital and craniomandibular mechanics. In: Solberg WK, Clark GT, eds. Abnormal jaw mechanics. Chicago: Quintessence, 1984. Behrents RG. An atlas of growth in the aging craniofacial skeleton. Monograph 18, Craniofacial Growth Series. Ann Arbor:

Keeling

et al.

1985. Center for Human Growth and Development, University of Michigan. 32. Moyers RR. The development of occlusion and temporomandibulat joint disorders. In: Carlson DS, McNamara JA, Ribbens KA, eds. Developmental aspects of temporomandibular joint disorders. Monograph 16, Craniofacial Growth Series. Ann Arbor: 1985. Center for Hnman Growth and Development, University of Michigan. 33. Brandt D. Temporomandibular disorders and their association with morphologic malocclusion in children. In: Carlson DS, McNamara IA, Ribbens KA, eds. Developmental aspects of temporomandibular joint disorders. Monograph 16, Craniofacial

Growth Series. Ann Arbor: and Development, University Reprint requests to: Dr. Stephen D. Keeling University of Florida .I. Millis Miller Health Center College of Dentistry Department of Orthodontics Box J-444 Gainesville, FL 32610

1985. Center of Michigan.

for Human

Growth