SPECIAL ARTICLE

Myths of orthodontic gnathology

r Beverly McCollum established the Gnathologic Society in 1926. Gnathology is dened as the science that treats the biology of the masticatory mechanism as a whole: that is, the morphology, anatomy, histology, physiology, and the therapeutics of the jaws or masticatory system and the teeth as they relate to the health of the whole body, including applicable diagnostic, therapeutic, and rehabilitation procedures.1 Many gnathologic research endeavors have added much to our knowledge and understanding of the stomatognathic system, particularly those involving chewing (masticatory) kinematics2-13 and the early intraoral telemetry studies (to cite only a few).14-17 Although originally founded on scientic principles, the application of the valid gnathologic research to clinical practice has moved away from these founding tenets. Modern clinical gnathology (vs university-based gnathologic research) has become, for the most part, a pseudo-science based on mechanistic, perfunctory procedures, and instrumentation. There are many contemporary occlusal institutes that clearly have perverse views on gnathology that are not evidence-based. Dr Lysle Johnston18 sarcastically stated that gnathology is the science of how articulators chew. In the 1970s, Roth formally introduced the classic principles of clinical gnathology to orthodontics (orthodontic gnathology).19-21 The notions and considerations of modern orthodontic gnathology are not based on principles of science and do not correspond to contemporary evidence-based thinking. There might not be a unied orthodontic gnathologic view, but it seems that the one established by Roth is by far the most notable.
a Clinical professor, School of Dental Medicine, University of Pittsburgh; private practice, Greensburg, Pa. b Clinical senior lecturer in Orthodontics, Dental School, The University of Western Australia; private practice, Perth, WA, Australia; and adjunct assistant professor in Orthodontics, Centre for Advanced Dental Education, St. Louis, Mo. The authors report no commercial, proprietary, or nancial interest in the products or companies described in this article. Reprint requests to: Donald J. Rinchuse, 510 Pellis Rd, Greensburg, PA 15601; e-mail, [email protected]. Submitted, March 2008; revised and accepted, April 2008. Am J Orthod Dentofacial Orthop 2009;136:322-30 0889-5406/$36.00 Copyright 2009 by the American Association of Orthodontists. doi:10.1016/j.ajodo.2008.04.021

In general, the objectives of modern clinical and orthodontic gnathology are (1) to establish coincidence of maximum intercuspation (or centric occlusion) with centric relation (CR) in an anterosuperior seated condylar position, (2) to attain canine (mutually) protected occlusion (CPO) and anterior guidance, and (3) to mount pretreatment diagnostic casts on a fully adjustable articulator (with some also recommending pantographic tracings and many recommending deprogramming before taking centric-bite registrations).19-24 Gnathologists believe that failure to achieve at least 1 of these objectives will predispose patients to signs and symptoms of temporomandibular disorders (TMDs).19-21 The purpose of this article is to dispel and debunk 10 myths of orthodontic gnathology. We have recently written on many topics dealing with orthodontic gnathology, and this article will help to more clearly elucidate and integrate the topics to explain the big picture.22-29 The 10 myths of orthodontic gnathology are (1) occlusion and condyle position are the primary causes of TMD, (2) orthodontics causes TMD, (3) the modern view of TMD treatment is based on gnathologic principles, (4) orthodontic gnathology recognizes and evaluates patients parafunction and chewing cycle kinematics, (5) a high restoration provokes TMD, (6) TMD asymptomatic subjects with internal derangement (ID) need treatment, (7) CR is the key to the diagnosis and treatment of TMD, (8) CPO is the preferred functional occlusion type toward which to direct orthodontic patient treatment, (9) articulators play a critical role in orthodontic diagnoses, and (10) many valid scientic studies support orthodontic gnathology.
MYTH 1: OCCLUSION AND CONDYLE POSITION (CR POSITION) ARE THE PRIMARY CAUSES OF TMD

Occlusion and condyle position were once thought to be the primary causes of TMD.19-22,30,31 The temporomandibular joint (TMJ) pain dysfunction syndrome was thought to be a distinct disease caused by 1 etiologic agent (eg, occlusion or stress; later, it was thought to be caused by an eccentric condyle position).32-34 However, past etiologic agents such as occlusion and condyle position have not been proven to be the primary

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cause of TMD.35-49 Furthermore, TMD etiology and diagnosis are complicated because many diseases and dysfunctions can affect the TMJ complex and the neighboring structures of the head and neck.23-26,50 TMD is now considered a collection of 6 subclasses of diseases and dysfunctions, with many causes for each subclass.39,40 TMD treatments have changed from a dental-based model (ie, classic dental and jaw causative theories) to a biopsychosocial-medical model that emphasizes orthopedics, neuroscience, chronic pain theory, sleep neurophysiology, genetics, and psychosocial factors.51-70 Because occlusion and condyle position are currently believed to have secondary roles in the etiology of TMD, these should reduce the signicance of the orthodontic gnathologic view; gnathology is very much occlusion and condyle position oriented.23-26,28,29
MYTH 2: ORTHODONTICS CAUSES TMD

The orthodontic gnathologic view has argued that orthodontic treatment causes TMD from 2 possible perspectives. First, it causes TMD indirectly because nongnathologic orthodontists do not achieve a gnathologic occlusal nish and thereby produce an iatrogenic functional occlusion (ie, functional balancing interferences) and eccentric condyle (or CR) position that predisposes to TMD. The other possibility is that certain orthodontic appliances or techniques (eg, Class III mechanics, extractions, chincups, and so on) directly cause TMD.19-22,28,29 However, the evidence-based view clearly is that orthodontic treatment does not cause TMD.71-75 This should have been a tremendous wakeup call to the premises of clinical gnathology that are clearly dental-based. Parenthetically, because the data demonstrating that orthodontic treatment does not cause TMD are population-based, it is still possible for an occasional orthodontic patients TMJ complaint to be caused by treatment.
MYTH 3: THE MODERN VIEW OF TMD TREATMENT IS BASED ON GNATHOLOGIC PRINCIPLES (DENTAL BASED)

ment. Genetics related to pain and imaging of the pain-involved brain, central brain processing of thinking and emotions, endocrinology, and so on, are the exciting future. Treatments that are effective for all forms of chronic pain are equally effective in mitigating TMD pain.54,63,65,66 Cognitive behavioral therapies and biofeedback are becoming the recognized initial and early treatment modalities for TMD.51-53,55,56,63,64 However, there is support for the belief that occlusal splints (stabilizing-type splints are recommended) work best initially, and cognitive behavioral therapies and biofeedback work better later.56,59-61 Cognitive behavioral therapies involve many treatments emphasizing stress reduction and cognitive awareness: education regarding mind-body relationships with stress management, relaxation training, distraction and pleasant activity scheduling to reduce the impact of pain on activities, cognitive restructuring, self-instructional training, and maintenance skills.64

MYTH 4: ORTHODONTIC GNATHOLOGY RECOGNIZES AND EVALUATES PATIENTS PARAFUNCTION AND CHEWING CYCLE KINEMATICS

Contemporary TMD treatment has moved away from a historic, mechanical, dental-based model, no longer involving occlusal modication or jaw-repositioning protocols.50,65,66 The current evidence-based view of TMD treatment is now a biopsychosocial model.51-64 Dworkin76 stated that the biopsychosocial model remains the best approach to gaining an understanding for how to integrate the host of biologic, clinical and behavior factors that may account for the onset, maintenance and remission of TMD, as well as for understanding how to make rational choices for treat-

Two important aspects of human jaw function are not evaluated by the orthodontic gnathologic approach, particularly in relation to articulator mountings: parafunction and chewing cycle kinematics. The harshest and perhaps the most destructive occlusal forces are produced from parafunctionbruxing and clenching.77 In this regard, it seems that it is not so much the type of occlusion or CR position that a TMD patient has as it is how the patient uses his or her teeth and jaws.22-24 Patients with optimal and ideal static and functional occlusions (or condyle positions) have TMD, and vice versa. This stresses the importance of properly evaluating a patients parafunction irrespective of the type of occlusion or condyle position. Incidentally, it was once incorrectly thought some 50 years ago during the occlusionist era (and still espoused today) that parafunction was caused by occlusal prematurities or interferences and that bruxing was natures attempt to resolve the occlusal problems by grinding them away. Current evidence clearly supports the notion that parafunctional habits are basically a central nervous system phenomenon (mediated by the limbic system) and not of occlusal origin.78-85 The other aspect of human jaw function that is not evaluated by orthodontic gnathology (particularly by articulator mountings) is chewing cycle kinematics. It is understood that the chewing pattern shape as viewed from the frontal aspect is described as a tear drop.2,4,43 There are about a half dozen different chewing

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patterns.2-4,23,24 This elliptical chewing motion can vary signicantly from person to person.2,4 Simply stated, some patients have a more vertical chewing pattern; in others, it can be more horizontal.2,4,24 Chewing kinematics can vary based on several factors such as age, dental static occlusion, facial morphology, and so on.2-4,43,85 For instance, in the developmental stage of the deciduous dentition, chewing pattern shape (judged from the frontal aspect) is very much lateral, with the mandible circling out on opening and circling inward (medially) on closing in a narrow and tight loop.4 In the developmental stage of the permanent dentition, chewing pattern shape (judged from the frontal aspect) is not nearly as lateral; on opening, the mandible circles inward (medially) and, on closing, circles outward (laterally) in a larger loop than that in the deciduous dentition.4 The length of the chewing stroke is approximately 16 to 19 mm with about 20 masticatory strokes before swallowing, taking about 12 seconds.4 The consistency and shape of chewing kinematics vary for patients with deepbite malocclusions.86 A logical hypothesis might be that those with more vertical chewing pattern shapes adapt best to CPO, whereas those with more horizontal chewing patterns function best with group function or balanced occlusions.24 With the above in mind, how does the orthodontic gnathologic approach (and articulator recordings and mountings) account for, and take into consideration, each patients parafunction and chewing kinematics?
MYTH 5: A HIGH RESTORATION PROVOKES TMD

as to the role of high restorations causing TMD.89-92 TMD is certainly a potential consequence of a provoked high restoration, but so are headaches, tooth mobility, fremitus, and so on. Furthermore, most occlusal provocation studies are biased because they typically used dental students (or nurses) as subjects who had some notion of the possible outcome of the intervention. Curiously, some subjects in their control groups (with no high restorations) also had some of the same outcomes (eg, headaches and TMD) as those in the experimental group. Increasing the vertical dimension of occlusion does not generally negatively impact the TMJs unless there is a preexisting ID.93-96
MYTH 6: TMD ASYMPTOMATIC SUBJECTS WITH ID NEED TREATMENT

In 1995, Roth87 wrote: I would like to have the opportunity of placing a high molar restoration with balancing interferences in the mouths of all who believe that occlusion has nothing to do with TMD. He used this intuitively appealing argument to support the notion that occlusal interferences are the primary cause of TMD. Certainly, it would be illogical to argue that gross occlusal disharmonies would not adversely affect the stomatognathic system and potentially have some negative impact on the TMJs. The modern evidencebased paradigm does not argue that occlusal interferences (this is in sharp contract to balancing contacts that are generally considered benign and typically do not need occlusal adjustments) are no longer a possible etiologic agent for TMD. The argument is that they now are not primary and have a lesser (secondary) role than once thought. Occlusal equilibration of gross occlusal prematurities is still within the realm of evidence-based care.22-27,88 The occlusal provocation studies (provoked or produced occlusal interferences in subjects) are equivocal

It has been estimated that as many as 30% of TMD asymptomatic subjects have ID.97-99 The issue becomes whether TMJ ID predispose TMD asymptomatic subjects to TMD later on. And if this is true, the next question is whether these subjects need some form of dental or orthodontic treatment to mitigate future TMD. A relationship (studies were associational and not cause-and-effect) has been established between TMJ ID and craniofacial morphology (although the differences were small).100-102 TMJ disc abnormality was associated with reduced forward growth of the maxillary and mandibular bodies; for adolescents, there was reduced growth of the mandibular ramus.100,103 It is not a leap of faith to believe that TMJ disc pathology can affect condylar growth.100 It has been hypothesized that untreated (or inadequately treated) TMJ ID will most likely lead to pain, degenerative joint disease, compromised mandibular growth, and other negative conditions.103,104 There is general agreement that some consideration of this information should be factored into an orthodontists thought process during treatment planning.100-102 Nonetheless, the orthodontic gnathology camp (Dr Kazumi Ikeda105) argued that these subjects need treatment involving a nighttime occlusal stabilizing splint initially (in the past, the argument was for repositioning splints) followed perhaps by comprehensive orthodontic treatment. Roth87 always contended that it is not just good enough to maintain a patients status quo as related to TMJ health, but orthodontists have a higher obligationto improve their patients TMJ health status. It is believed that the best time to treat ID is early, before signicant disc, skeletal, and occlusal changes occur while patients have optimal capacity for tissue repair and growth: ie, when they are young.103 In addition, it is believed that most initially asymptomatic patients will become symptomatic usually after growth is

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complete and when the TMJs have progressed to a nonreducing disc displacement and degenerative joint disease; at this stage, treatment would be signicantly less effective.103,104 The contending view, and perhaps the logical and evidence-based view, is to let sleeping dogs lie and not to treat these patients because they are TMJ asymptomatic.106,107 To treat these patients might do more harm than good, since there seems to be no practical and evidence-based treatment options for correcting these TMJ anatomic disc derangements. In addition, no scientic evidence shows that treatment will mitigate future TMD. Furthermore, the relationship of disc displacement to pain, mandibular dysfunction, osteoarthrosis, and growth disturbances is unclear.106 Not all growing patients with disc displacements grow abnormally, nor do all patients with growth deciencies have disc displacements.54,107,108 Interestingly, it was also demonstrated that patients with moderate to severe TMD with associated disc displacement without reduction will improve without treatment over a 2.5-year period.108 It would seem that, if disc displacement were a signicant cause of mandibular growth deciency, its signs and symptoms would be more common in this population than in the normal population. Finally, the relationship between disc displacement and TMD is complex; the causes are multifactorial (eg, trauma, genetics, stress, and pathology) and therefore cannot be simply explained by disc displacement.107
MYTH 7: CR IS THE KEY TO THE DIAGNOSIS AND TREATMENT OF TMD

Roth87 stated: If condylar position is not important in orthodontics, how did the term Sunday Bite ever arise? CR has been dened in so many different ways that it has lost credibility.109 The concept of CR has historically and arbitrarily migrated from a posterior to a posterosuperior position to recently the most anterosuperior position of the condyles in the glenoid fossa.23 It would be difcult to prove that any CR position is correct for all patients. There appears to be a range of CR positions. In this respect, one study found that 89% of condyles were not concentric.110 It seems that mid to anterior sagittal CR positions might be better than a retruded position; however, in some patients, a retruded CR is the healthy norm.99,111 The American Dental Association in TMD conference reports in 1983 and 1990 stated that there is insufcient evidence that eccentricity of the condyles in the glenoid fossa will predispose to TMD or any other health consequence.39,40 Johnston18 sarcastically wrote about the absurdity of the many false notions of CR: it could

be argued that the progressive modication of Centric Relation (denition) has done more to eliminate centric slides than 20 years of grudging acquiescence to the precepts of gnathology. The gnathologic view dictates that maximum cuspation, or centric occlusion, should be coincident with CR (anterosuperior).2-4 In the early 1970s, Roth19-21 argued that the correct CR position was a retruded, posterosuperior position. Early intraoral telemetry studies did not support the concept of a retruded CR.14-17 Roths view (and that of gnathology per se) was proven fallacious, and he recanted his previous view of retruded CR and adopted the contemporary view of anterosuperior CR.19-23 The past notion of retruded (posterosuperior) CR by the orthodontic gnathologists was wrong despite the sad fact that many orthodontists blindly followed this thinking for decades. How much condence and credibility should we have for orthodontic gnathology with its mired history and false thinking? Furthermore, what happened to orthodontic gnathology patients treated to the old retruded centric position? Did they develop TMD? There are also many problems and issues related to CR records. As Nuelle and Alpern112 wrote: Doctor selected TMJ positioning at the dental chair is a blind procedure. Centric records have been shown to be somewhat reliable, but their validity has not been substantiated.22,23 The orthodontic gnathologic view that claims that the Roth power centric bite registration seats patients condyles in an anteroposterior CR needs to be veried by magnetic resonance imaging data. This becomes especially important because Alexander et al113 clearly demonstrated in a magnetic resonance imaging study that condyles are not exactly located in the CR positions that clinicians believe them to be. In addition, how do we know which of the many promulgated CR recordings (and positions) is correct? In this respect, there are at least 6 occlusal philosophies in dentistry (not limited to orthodontics).28 Five of the 6 views can be considered gnathologically based views: classic gnathology (dating back to Stallard, Stuart, Thomas, and Lucia); bioesthetic dentistry (based on the work of Robert L. Lee); Dawson, Pankey Institute; neuromuscular school (Las Vegas Institute, Jankelson Myotronics view); and the Roth orthodontic gnathologic view. The sixth view is the nongnathologic view, which essentially supports taking a reliable centric occlusion (maximum intercuspation) bite registration as has been traditionally done for the last century. Of course, there can be many variations of this nongnathologic view. The various occlusal schools differ mainly on their view of CRits position, but more so on how it is recorded. There are various philosophies

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concerning manipulation techniques to record CR, deprogramming, and whether to use a facebow or an earbow transfer. So, each occlusal philosophy is competing with the others on the proper denition and correct recording technique of CR; this further complicates and muddles the issue of CR, making any 1 view less valid and important.
MYTH 8: CPO IS THE PREFERRED FUNCTIONAL OCCLUSION TYPE TOWARD WHICH TO DIRECT ORTHODONTIC PATIENT TREATMENT

We have discussed the problems with the notion of ascribing to the philosophy and concept of CPO for all orthodontic patients and treatments.24 A summary of what we wrote in this comprehensive article follows. CPO, as the optimal type of functional occlusion to establish in orthodontic patients, is equivocal. Woda et al114 wrote, after a comprehensive review of the literature, Pure canine protection or pure group function rarely exists and balancing contacts seem to be the general rule in the population of contemporary civilizations. Modern evidence does not support a view that blindly adheres to the concept of CPO for all patients. One type of functional occlusion should not be considered optimal and preferred for all patients. CPO is merely 1 of a few possible functional occlusion schemes that might be attained with orthodontic treatment. Subjects with normal static occlusion (or Class I occlusions) tend to have balanced occlusion or else group function, and not CPO.115,116 Group function and balanced occlusion (with no interferences, only balancing contacts) appear to be acceptable functional occlusion schemes, depending on the patients unique characteristics. The stability and longevity of CPO is questionable. Reestablishing functional occlusion through orthodontic treatment back to the original type before treatment is problematic, since orthodontic treatment is often started before the permanent canines have fully erupted. It would also appear that consideration of chewing cycle kinematics, craniofacial morphology, static occlusion type, current oral health status, and parafunctional habits might provide important and relevant information about the most suitable functional occlusion type for each patient.24
MYTH 9: ARTICULATORS PLAY A CRITICAL ROLE IN ORTHODONTIC DIAGNOSES

on. Alpern and Alpern117 presented a strong argument that the polycentric hinge articulator might have some advantages over the others. Articulators can be useful for gross xed and removable prosthodontic and orthognathic surgical procedures to at least maintain a certain vertical dimension while preclinical laboratory procedures are performed on dental casts. A main criticism of articulators in orthodontics is based on the study by Lindauer et al.118 They found that, during opening and closing, the condyles not only rotate but simultaneously translate (move downward and forward); there is an instantaneous center of rotation. Articulators are based on the faulty notion of a terminal hinge axis, which goes back to a half-century-old claim of Posselt, that, in the initial 20 mm or so of opening and closing, the mandible rotates similarly to a door hinge (and does not simultaneously translate).118 However, Posselt formulated his view when CR was viewed as a posterosuperior, retruded (and not anterosuperior) CR position, and, during the recording of CR, distally guided pressure was applied to the chin, the most obvious reason for Posselts nding of a terminal hinge axis.22 Furthermore, Mohl35 believed that the sensitivity and specicity of articulator-mounted casts in the diagnosis of TMD are poor. In addition, there is no valid evidence that performing articulator mountings improves patients stomatognathic health. Interestingly, one of the most reliable and valid reports by the orthodontic gnathologic camp states that the difference between gnathologic and nongnathologic diagnostics is perhaps 1 to 2 mm, and this is only in the vertical plane.119 Also, articulators cannot accurately simulate jaw movements. Bite registrations are static, and patients are not asked to chew or function. There is no proven validity of bite registrations and where the condyles are located as a consequence of such recordings. Articulator mountings, for the most part, have not been shown to affect orthodontic diagnoses or treatment plans.120 After all the effort involved in mounting and the attention paid to the minute details of occlusion and condylar position, little consideration is given to the physiologic adaptation of the dentition after posttreatment occlusal settling. In children, the glenoid fossa complex changes with growth; this implies that new mountings would need to be routinely performed throughout treatment. Although argued by orthodontic gnathologists as not true, it takes more time and cost to perform the mountings.22
MYTH 10: MANY VALID SCIENTIFIC STUDIES SUPPORT ORTHODONTIC GNATHOLOGY

We have written several evidence-based reviews that argued against the validity of articulators in orthodontics.22,28,29 Therefore, this section will merely summarize some pertinent points in these articles. There are many types of articulators: arcon, nonarcon, fully adjustable, semi-adjustable, polycentric hinge, and so

We have published our criticisms of many orthodontic gnathology studies.22,25,28,29 We would, therefore,

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like to briey address only the recent study of Cordray.121 First, few studies are perfect and meet all requirements of great research. However, the study by Cordray (and others by orthodontic gnathologists) is more problematic than the typical published study.29 Cordray seemed to believe that it was possible to evaluate and test the effect of neuromuscular deprogramming (with a tongue blade) on centric bite registrations. However, the study design precluded such an evaluation. Two independent variables (deprogramming and gnathologic bite registration) were confounded and commingled into 1 recording, so that the single, isolated effect of deprogramming alone (vs no deprogramming) could not be accurately determined. To effectively ascertain the true inuence of deprogramming (if there was one), a third group would have had to be addeda gnathologic group without deprogramming. In addition, Cordray claimed to support the view that orthodontic gnathology (with articulators) is valid because it can help to better discern and elucidate the correct orthodontic diagnosis (by correctly determining the so-called correct centric bite registration). This conclusion was impossible for a number of reasons: not all the errors were accounted for, the large standard deviation was not explained, there were no blinding and no information on how the nongnathologic centric records were performed, and so on. Furthermore, Cordray did not mention the contradictory ndings of Kulbersh et al122 and Ellis and Benson.120 More importantly, even if there is a difference in centric recordings when deprogrammed or gnathologically determined, there is the problem in assuming that the newer, deprogrammed record is better (more physiologic) than the original one.22,23,123
CONCLUSIONS

embrace the concept of evidence-based treatment, the specialty will eventually have to carefully evaluate the quality of the evidence and its message within the context of a contemporary orthodontic practice. The dated ideas and art of orthodontic gnathology may actually be a waste of time for the average orthodontic patient. It is up to us to decide. In the end, the dayto-day application of any philosophy must ultimately measure up with literature that is pertinent to orthodontics. In orthodontics, everything works well enough to support a practice. Thus, the fact that something is used successfully does not mean that it is correct. Gnathology may make the orthodontist feel better; however, there is little evidence that the same benets accrue to the patient.
REFERENCES 1. The glossary of prosthodontic terms. 7th ed. J Prosthet Dent 1999;81:71. 2. Ahlgren J. Mechanism of mastication. Acta Odontol Scand 1966;24(supp 44):1-109. 3. Ahlgren J. Pattern of chewing and malocclusion of teeth: a clinical study. Acta Odontol Scand 1967;25:3-13. 4. Wickwire NA, Gibbs CH, Jacobson AP, Lundeen HC. Chewing patterns in normal children. Angle Orthod 1981;51:48-60. 5. Gibbs CH, Masserman T, Reswwick JB, Derda JH. Functional movements of the mandible. J Prosthet Dent 1977; 26:604-20. 6. Guttetman AS. Chop-stroke chewers. Dent Prog 1961;1:254-7. 7. Sheppard IM. The effect of extreme vertical overlap on masticatory stroke. J Prosthet Dent 1965;15:1035-42. 8. Alexander TA, Gibbs CH, Thompson WJ. Investigation of chewing patterns in deep-bite malocclusions before and after orthodontic treatment. Am J Orthod 1984;85:21-7. 9. Gillings BRD, Graham CH, Duckmanton NA. Jaw movements in young adult men during chewing. J Prosthet Dent 1973;29: 616-27. 10. Buschang PH, Hayasaki H, Throckmorton GS. Analysis of masticatory cycle kinematics: a new methodology. Arch Oral Biol 2000;45:461-74. 11. Throckmorton GS, Buschang PH, Hayaski H, Santos Pinto A. Changes in the masticatory cycle following treatment of posterior unilateral crossbite in children. Am J Orthod Dentofacial Orthop 2001;120:521-9. 12. Anderson K, Throckmorton GS, Buschang PH, Hayaski H. The effect of bolus hardness on masticatory kinematics. J Oral Rehab 2002;29:289-96. 13. Kiliaridis S, Karlsson S, Kjellberg H. Characteristics of masticatory movements and velocity in growing individuals and young adults. J Dent Res 1991;70:1367-70. 14. Pameijer JH, Brion M, Glickman I, Roeber FW. Intraoral occlusal telemetry. V. Effect of occlusal adjustment upon tooth contacts during chewing and swallowing. J Prosthet Dent 1970;24: 492-7. 15. Graf H, Zander HA. Functional tooth contacts in lateral and centric occlusion. J Prosthet Dent 1963;13:1055-66. 16. Glickman JI, Martigoni M, Haddad A, Roeber FW. Further observation on human occlusion monitored by intraoral telemetry [abstract 612]. IADR 1970;201.

It is time to reconsider the validity of the age-old ideas of orthodontic gnathology that are based on rhetoric, blind faith, art, emotionalism, and practice management rather than on science and evidence. Orthodontic gnathologists have proved no health benet to justify the many perfunctory exercises of the philosophy. The focus of orthodontic gnathology (and the clinical gnathologic view) was on the relationship of occlusion, then condyle position, and now TMJ disc position, dysfunction, and disease on the stomatognathic system (particularly regarding TMD). The view that occlusion and condyle position are the primary causes of TMD, and that diagnoses and treatments should be based on these notions, has been discredited. There is little to no evidence that treating subjects with TMJ ID will prevent or mitigate future TMD. If we are to

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17. Pameijer JH, Glickman I, Roeber FW. Intraoral occlusal telemetry. 3. Tooth contacts in chewing, swallowing, and bruxism. J Perodontol 1969;40:253-8. 18. Johnston LE Jr. Fear and loathing in orthodontics. Notes on the death of theory. In: Carlson DS, editor. Craniofacial Growth Series. Ann Arbor: Center for Human Growth and Development; University of Michigan; 1990. p. 75-90. 19. Roth RH. Temporomandibular pain-dysfunction and occlusal relationship. Angle Orthod 1973;43:136-53. 20. Roth RH. The maintenance system and occlusal dynamics. Dent Clin North Am 1976;20:761-88. 21. Roth RH. Functional occlusion for the orthodontist II. J Clin Orthod 1981;25:100-23. 22. Rinchuse DJ, Kandasamy S. Articulators in orthodontics: an evidence-based perspective. Am J Orthod Dentofacial Orthop 2006;129:299-308. 23. Rinchuse DJ, Kandasamy S. Centric relation: a historical and contemporary orthodontic perspective. J Am Dent Assoc 2006; 137:494-501. 24. Rinchuse DJ, Kandasamy S, Sciote J. A contemporary and evidence-based view of canine protected occlusion. Am J Orthod Dentofacial Orthop 2007;132:90-102. 25. Rinchuse DJ, Rinchuse DJ, Kandasamy S. Evidence-based vs experience-based views on occlusion and TMD. Am J Orthod Dentofacial Orthop 2005;127:249-54. 26. Rinchuse DJ, McMinn J. Summary of evidence-based systematic reviews of temporomandibular disorders. Am J Orthod Dentofacial Orthop 2006;130:715-20. 27. Rinchuse DJ, Sweitzer EM, Rinchuse DJ, Rinchuse DL. Understanding science and evidence-based decision making in orthodontics. Am J Orthod Dentofacial Orthop 2005;127:618-24. 28. Rinchuse DJ, Kandasamy S, Rinchuse DJ. Word of moutharticulators in orthodontics: chewing the facts. Part 1. Orthodontic Products 2007;14:152-5. 29. Rinchuse DJ, Kandasamy S, Rinchuse DJ. Word of mouth-articulators in orthodontics: chewing the facts. Part 2. Orthodontic Products 2007;14:40-2. 30. Rinchuse DJ, Rinchuse DJ. The impact of the American Dental Associations guidelines for the examination, diagnosis, and management of temporomandibular disorders on orthodontic practice. Am J Orthod 1983;83:518-22. 31. Rinchuse DJ. Counterpoint: preventing adverse effects on the temporomandibular joint through orthodontic treatment. Am J Orthod Dentofacial Orthop 1987;91:500-4. 32. Schwartz L. Conclusions of the TMJ clinic at Columbia. J Periodontol 1958;29:210-2. 33. Laskin DM. Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 1969;79:147-53. 34. Greene CS, Laskin DM. Long-term evaluation of treatment for myofascial pain-dysfunction analysis. J Am Dent Assoc 1983; 107:235-8. 35. Mohl ND. Temporomandibular disorders: role of occlusion, TMJ imaging and electronic devicesa diagnostic update. J Am Coll Dent 1991;58:4-10. 36. Gesch D, Bernhardt O, Kirbshus A. Association of malocclusion and functional occlusion with temporomandibular disorders (TMD) in adults: a systematic review of population-based studies. Quintessence Int 2004;35:211-21. 37. Gunn SM, Woolfolk MW, Faja BW. Malocclusion and TMJ symptoms in migrant children. J Craniomandib Disord 1988;2:196-200. 38. Seligman DA, Pullinger AG. The role of intercuspal occlusal relationships in temporomandibular disorders: a review. J Craniomandib Disord 1991;5:96-106.

39. Grifths RH. Report of the presidents conference on the examination, diagnosis and management of temporomandibular disorders. J Am Dent Assoc 1983;106:75-7. 40. McNeil C, Mohl ND, Rugh JD, Tanaka TT. Temporomandibular disorders: diagnosis, management, education, and research. J Am Dent Assoc 1990;120:253-60. 41. Dixon DC. Temporomandibular disorders and orofacial pain-diagnostic imaging of the temporomandibular joint. Dent Clin North Am 1991;35:53-74. 42. Katzberg RW, Westesson P, Tallents RH, Drake CM. Orthodontics and temporomandibular joint internal derangement. Am J Orthod Dentofacial Orthop 1996;109:515-20. 43. Gerstner GE, Marchi F, Haerian D. Relationship between anteroposterior maxillomandibular morphology and masticatory jaw movement patterns. Am J Orthod Dentofacial Orthop 1999; 115:256-66. 44. Gianelly AA. Orthodontics, condylar position and TMJ status. Am J Orthod Dentofacial Orthop 1989;95:521-3. 45. Gianelly AA, Hughes HM, Wohlgemuth P, Gildea C. Condylar position and extraction treatment. Am J Orthod Dentofacial Orthop 1988;93:201-5. 46. Gianelly AA. Condylar position and Class II deep bite, no overjet malocclusion. Am J Orthod Dentofacial Orthop 1989;96: 428-32. 47. Gianelly AA, Cozzanic M, Boffa J. Condylar position and maxillary rst premolar extraction. Am J Orthod Dentofacial Orthop 1991;99:473-6. 48. Gianelly AA, Anderson CK, Boffa J. Longitudinal evaluation of condylar postion in extraction and nonextraction treatment. Am J Orthod Dentofacial Orthop 1991;100:416-20. 49. LeResche L, Truelove EL, Dworkin SF. Temporomandibular disorders: a survey of dentists knowledge and beliefs. J Am Dent Assoc 1993;124:90-4. 97-106. 50. Klasser GD, Greene CS. Predoctoral teaching of temporomandibular disorders. J Am Dent Assoc 2007;138:231-7. 51. Mishra KD, Gatchel RJ, Gardea MA. The relative efcacy of three cognitive-behavioral treatment approaches to temporomandibular disorders. J Behav Med 2000;23:293-309. 52. Fernandez E, Turk DC. The utility of cognitive coping strategies for altering pain perception: a meta-analysis. Pain 1989;38: 123-35. 53. Flor H, Birbaumer N. Comparison of the efcacy of electromyographic biofeedback, cognitive-behavioral therapy, and conservative medical interventions in the treatment of chronic musculoskeletal pain. J Consult Clin Psychol 1993;61:653-8. 54. Dworkin SF, Massoth DL. Temporomandibular disorders and chronic pain: disease or illness? J Prosthet Dent 1994;72:29-38. 55. Dworkin SF, Turner JA, Wilson L, Massoth D, Whitney C, Huggins KH, et al. Brief group cognitive-behavioral intervention for temporomandibular disorders. Pain 1994;59:175-87. 56. Turk D, Zaki H, Rudy T. Effects of intraoral appliance and biofeedback/stress management alone and in combination in treating pain and depression in TMD. patients. J Prosthet Dent 1993;70:158-64. 57. Dworkin SF, Huggins KH, Wilson L, Mancl L, Turner J, Massoth D, et al. A randomized clinical trial using research diagnostic criteria for temporomandibular disorders-axis II to target clinic cases for a tailored self-care TMD treatment program. J Orofac Pain 2002;16:48-63. 58. Dworkin SF, Turner JA, Mancl L, Wilson L, Massoth D, Juggins KH, et al. A randomized clinical trial of a tailored comprehensive care treatment program for temporomandibular disorders. J Orofac Pain 2002;16:259-76.

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59. Turk DC, Rudy TE, Kubinski JA, Zaki HS, Greco CM. Dysfunctional patients with temporomandibular disorders: evaluating the efcacy of a tailored treatment protocol. J Consult Clin Psychol 1996;64:139-46. 60. Greco CM, Rudy TE, Turk DC, Herlich A, Zaki HH. Traumatic onset of temporomandibular disorders: positive effects of a standardized conservative treatment program. Clin J Pain 1997;13: 337-47. 61. Rudy TE, Turk DC, Kubinski JA, Zaki HS. Differential treatment response of TMD patients as a function of psychological characteristics. Pain 1995;61:103-12. 62. Dworkin SF, LeResche L. Research diagnostic criteria for temporomandibular disorders: review, criteria, examinations and specications, critique. J Craniomandib Disord 1992;6:301-55. 63. Gardea MA, Gatchel RJ, Mishra KD. Long-term efcacy of biobehavioral treatment of temporomandibular disorders. J Behav Med 2001;24:341-59. 64. Gatchel RJ, Stowell AW, Wildenstein L, Riggs R, Ellis E 3rd. Efcacy of an early intervention for patients with acute temporomandibular disorder-related pain: a one year outcome study. J Am Dent Assoc 2006;137:339-47. 65. Greene CS, Laskin DM. Temporomandibular disorders: moving from a dentally based to a medically based model. J Dent Res 2000;79:1736-9. 66. Greene CS. The etiology of temporomandibular disorders: implications for treatment. J Orofac Pain 2001;15:93-105. 67. Sessle BJ. The neural basis of temporomandibular joint and masticatory muscle pain. J Orofac Pain 1999;13:238-45. 68. Diatchenko L, Nackley AG, Slade GD, Fillingim RB, Maixner W. Idiopathic pain disorderspathways of vulnerability. Pain 2006;123:226-30. 69. Diatchenko L, Nackley AG, Slade GD, Bhalang K, Belfer I, Max MB, et al. Catechol-O-methyltransferase gene polymorphisms are associated with multiple pain-evoking stimuli. Pain 2006;125:216-24. 70. Diatchenko L, Slade GD, Nackley AG, Bhalang K, Sigurdsson A, Belfer I, et al. Genetic basis for individual variations in pain perception and the development of a chronic pain condition. Hum Mol Genet 2005;14:135-43. 71. Sadowsky C, BeGole EA. Long-term status of temporomandibular joint function and functional occlusion after orthodontic treatment. Am J Orthod 1980;18:201-12. 72. Sadowsky C, Polson AM. Temporomandibular disorders and functional occlusion after orthodontic treatment: results of two long-term studies. Am J Orthod 1984;86:386-90. 73. McNamara JA Jr, Seligman DA, Okeson JP. Occlusion, orthodontic treatment, and temporomandibular disorders: a review. J Orofac Pain 1995;9:73-89. 74. Kim MR, Graber TM, Vianna MA. Orthodontics and temporomandibular disorders: a meta-analysis. Am J Orthod Dentofacial Orthop 2002;121:438-46. 75. Reynders RM. Orthodontics and temporomandibular disorders: a review of the literature (1966-1988). Am J Orthod Dentofacial Orthop 1990;97:463-71. 76. Dworkin SF. TMD: is it out of occlusion? Proceedings of the 107th Annual Session of the American Association of Orthodontists. Seattle, Wash; 2007 May 20. 77. Shulman J, Deas DE, Mealey BL, Harrel SK, Hallmon WW, Nunn MM. Occlusal discrepancies. J Am Dent Assoc 2007; 138:30-2. 78. Seligman DA, Pullinger AG, Solberg WK. The prevalence of dental attrition and its association with factors of age, gender, occlusion and TMJ symptomology. J Dent Res 1988;67:1323-33.

79. Holmgren K, Sheikholeslam C, Riise C, Kopp S. The effects of an occlusal splint on the electromyographic activity of the temporal and masseter muscles during maximal clenching in patients with a habit of nocturnal bruxing and signs and symptoms of craniomandibular disorders. J Oral Rehabil 1990;17:447-59. 80. Kopp S. Pain and functional disturbance of the masticatory systema review of aetiology and principles of treatment. Swed Dent J 1982;6:49-60. 81. Young D, Rinchuse DJ, Pierce CT, Zullo T. Craniofacial morphology of bruxers versus non-bruxers. Angle Orthod 1999;69: 14-8. 82. Kato T, Montplaisir JY, Guitard F, Sessle BJ, Lund JP, Lavigne GJ. Evidence that experimentally induced sleep bruxism is a consequence of transient arousal. J Dent Res 2003;82: 284-8. 83. Kato T, Rompre P, Montplaisir JY, Sessle BJ, Lavigne GJ. Sleep bruxism: an oromotor activity secondary to micro-arousal. J Dent Res 2001;80:1940-4. 84. Macaluso GM, Guerra P, DiGiovanni G, Boselli M, Parrino L, Terzano MG. Sleep bruxism is a disorder related to periodic arousals during sleep. J Dent Res 1998;77:565-73. 85. Dube C, Rompre PH, Manzini C, Guitard F, de Grandmont P, Lavigne GJ. Quantitative polygraphic controlled study on efcacy and safety of oral splint devices in tooth-grinding subjects. J Dent Res 2004;83:398-403. 86. Buschang PH, Throckmorton GS, Austin D, Wintergerst AM. Chewing cycle kinematics of subjects with deepbite malocclusions. Am J Orthod Dentofacial Orthop 2007;131:627-34. 87. Roth R. Point: a three-dimensional comparison of condylar position changes between centric relation and centric occlusion using the mandibular position indicator. Am J Orthod Dentofacial Orthop 1995;107:315-8. 88. National Institutes of Health Technology Assessment Conference Statement. Management of temporomandibular disorders. J Am Dent Assoc 1996;127:1595-606. 89. Riise C, Sheikholeslam A. The inuence of experimental interfering occlusal contacts on the postural activity of the anterior temporal and masseter muscle in young adults. J Oral Rehabil 1982;9:419-25. 90. Randow K, Carlsson K, Edlund J, Obery T. The effect of an occlusal interference on the masticatory system. An experimental investigation. Odontol Revy 1976;27:245-56. 91. Magnusson T, Enbom L. Signs and symptoms of mandibular dysfunction after introduction of experimental balancing-side interferences. Acta Odont Scand 1984;42:129-35. 92. Rugh JD, Barghi N, Drago CJ. Experimental occlusal discrepancies and nocturnal bruxism. J Prosthet Dent 1984;51:548-53. 93. Kahn J, Tallents RH, Katzberg RW, Moss ME, Murphy WC. Association between dental occlusal variables and intraarticular temporomandibular joint disorders; horizontal and vertical overlap. J Prosthet Dent 1998;79:658-62. 94. Rivera-Morales WC, Mohl ND. Relationship of occlusal vertical dimension to the health of the masticatory system. J Prosthet Dent 1991;65:547-53. 95. Kovaleski WC, DeBoever J. Inuence of occlusal splints on jaw positions and musculature in patients with temporomandibular joint dysfunction. J Prosthet Dent 1975;33:321-7. 96. Manns A, Miralles R, Santander H, Valdivia J. Inuence of the vertical dimension in the treatment of myofacial pain-dysfunction syndrome. J Prosthet Dent 1983;50:700-9. 97. Kicos L, Ortendahl D, Arakawa M. Magnetic resonance imaging of the TMJ disc in asymptomatic volunteers. J Oral Maxillofac Surg 1987;114:76-7.

330

Rinchuse and Kandasamy

American Journal of Orthodontics and Dentofacial Orthopedics September 2009

98. Emshoff R, Brandlmaier I, Bertram S, Rudisch A. Comparing methods for diagnosing temporomandibular joint disk displacement without reduction. J Am Dent Assoc 2002;133:442-51. 99. Emshoff R, Brandlmaier I, Gerhard S, Stobl H, Bertram S, Rudisch A. Magnetic resonance imaging predictors of temporomandibular joint pain. J Am Dent Assoc 2003;134:705-14. 100. Flores-Mir C, Nebbe B, Heo G, Major PW. Longitudinal study of temporomandibular joint disc status and craniofacial growth. Am J Orthod Dentofacial Orthop 2006;130:324-30. 101. Nebbe B, Major PW, Prasad NG. Female adolescent facial pattern associated with TMJ disk displacement and reduction in disk length. Part I. Am J Orthod Dentofacial Orthop 1999;116: 167-76. 102. Nebbe B, Major PW, Prasad NG. Male adolescent facial pattern associated with TMJ disk displacement and reduction in disk length. Part II. Am J Orthod Dentofacial Orthop 1999;116: 301-7. 103. Hall HD. Intra-articular disc displacement. Part I: its signicant role in temporomadibular joint pathology. J Oral Maxillofac Surg 1995;53:1073-9. 104. Hall HD, Nickerson JW. Is it time to pay more attention to disc position? J Orofac Pain 1994;8:90-6. 105. Ikeda K. Disc displacement and orthodontics. Proceedings of the 107th Annual Session of the American Association of Orthodontists. Seattle: Wash; 2007 May 20. 106. Larheim TA, Westesson PL, Sano T. Temporomandibular joint disk displacement: comparison in asymptomatic volunteers and patients. Radiology 2001;218:428-32. 107. Dolwick LF. Intra-articular disc displacement. Part I: its questionable role in temporomandibular joint pathology. J Oral Maxillofac Surg 1995;53:1069-72. 108. Kurita K, Westesson PL, Yuasa H, Toyama M, Machida J, Ogi N. Natural course of untreated symptomatic temporomandibular joint disc displacement without reduction. J Dent Res 1998;77: 361-5. 109. Gilboe DB. Centric relation as the treatment position. J Prosthet Dent 1983;50:685-9. 110. Braun S. Achieving improved visualization of the temporomandibular joint condyle and fossa in the sagittal cephalogram and a pilot study of their relationship in habitual occlusion. Am J Orthod Dentofacial Orthop 1996;109:635-8.

111. Bean LR, Thomas CA. Signicance of condylar position in patients with temporomandibular disorders. J Am Dent Assoc 1987;114:76-7. 112. Nuelle DG, Alpern MC. Centric relation or natural balance. In: Alpern MC, editor. The ortho evolutionthe science and principles behind xed/functional/splint orthodontics. Bohemia, NY: GAC International; 2003. p. 37-47. 113. Alexander SR, Moore RN, DuBois LM. Mandibular condyle position: comparison of articulator mountings and magnetic resonance imaging. Am J Orthod Dentofacial Orthop 1993;104: 230-9. 114. Woda A, Vignernon P, Kay D. Non-functional and functional occlusal contacts: a review of literature. J Prosthet Dent 1979;42: 335-41. 115. Rinchuse DJ, Sassouni V. An evaluation of eccentric occlusal contacts in orthodontically treated subjects. Am J Orthod 1982;82:251-6. 116. Tipton RT, Rinchuse DJ. The relationship between static occlusion and functional occlusion in a dental school population. Angle Orthod 1991;61:57-66. 117. Alpern MC, Alpern AH. Innovation in dentistry: the polycentric occlusal system. In: Alpern MC, editor. The ortho evoluation the science and principles behind xed/functional/splint orthodontics. Bohemia, NY: GAC International; 2003. p. 55-68. 118. Lindauer SJ, Isaacson RJ, Davidovich M. Condylar movement and mandibular rotation during jaw opening. Am J Orthod Dentofacial Orthop 1995;107:573-7. 119. Kulbersh R, Kaczynski R, Freeland T. Orthodontics and gnathology. Semin Orthod 2003;9:93-5. 120. Ellis PE, Benson PE. Does articulating study casts make a difference to treatment planning? J Orthod 2003;30:45-9. 121. Cordray FE. Three-dimensional analysis of models articulated in the seated condylar position from a deprogrammed asymptomatic population: a prospective study. Part 1. Am J Orthod Dentofacial Orthop 2006;129:619-30. 122. Kulbersh R, Dhutia M, Mavarro M, Kaczynski R. Condylar distraction effects of standard edgewise therapy versus gnathologically based edgewise therapy. Semin Orthod 2003;9:117-27. 123. Klasser GD, Greene CS. Role of oral appliances in the management of sleep bruxism and temporomandibular disorders. Alpha Omegan 2007;100:111-9.