NIH Technology Conference April 29-May 1,1996!

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Joseph J Marbach, D.D.S. Christian S Stohler, D.D.S., Ph.D.

Robert and Susan Carmel Professor D.M.D. Professor and Chair in Algesiology Department of Biologic and Department of Oral Pathology, Biology, Materials Diagnostic Sciences and Department of Sciences and Center for Human Psychiatry Growth and Development University of Medicine and Dentistry of School of Dentistry New Jersey University of Michigan Newark, New Jersey Ann Arbor, Michigan.

James A McNamara, Jr., D.D.S., Ph.D. Dennis C Turk, Ph.D. Professor Director, Pain Evaluation and Department of Orthodontics and Pediatric Treatment Institute Dentistry and Center for Human Growth University of Pittsburgh Medical and Development University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania

School of Dentistry Professor of Psychiatry, University of Michigan Anesthesiology and Behavioral Ann Arbor, Michigan Science

Charles McNeill, D.D.S. Joseph P Vacanti, M.D. Director, Center for TMD and Orofacial Associate Professor of Surgery Pain Department of Surgery Department of Restorative Dentistry Harvard Medical School School of Dentistry Children's Hospital University of California, San Francisco Boston, Massachusetts San Francisco, California

Michael R Von Korff, Sc.D. Stephen B Milam, D.D.S., Ph.D. Associate Director Associate Professor Center of Human Studies Department of Oral and Maxillofacial Group Health Cooperative of Surgery Puget Sound Department of Surgery Seattle, Washington

Medical School University of Texas Health Science Larry M Wolford, D.D.S. at San Antonio Clinical Professor San Antonio, Texas Department of Oral and Maxillo-facial Surgery

Baylor College of Dentistry Gerald J Murphy, D.D.S. Baylor University Medical President American Academy of Head, Neck and Dallas, Texas Facial Pain Grand Island, Nebraska

Jeffrey P Okeson, D.M.D. Director, Orofacial Pain Center College of Dentistry University of Kentucky Lexington, Kentucky (10)

PLANNING COMMITTEE

Chairperson: James A. Lipton, D.D.S.,Ph.D. Special Assistant for Training and Career Development National Institute of Dental Research National Institutes of Health Bethesda, Maryland

Judith E N Albino, Ph.D. Jerry M Elliott

Panel Chairperson Program Analyst

President Emerita and Professor of Office of Medical Applications

Psychiatry of Research

University of Colorado Health Sciences National Institutes of Health Center Bethesda, Maryland

Denver, Colorado

Patricia S Bryant, Ph.D. John H Ferguson, M.D.

Program Director Director

Behavior, Pain, Oral Function, and Office of Medical Applications of

Epidemiology Program Research

Division of Extramural Research National Institutes of Health

National Institute of Dental Research Bethesda, Maryland

National Institutes of Health

Bethesda, Maryland William H Hall

Director of Communications

Elaine Collier, M.D. Office of Medical Applications of

Chief Autoimmunity Section Research

Division of Allergy, Immunology National Institutes of Health

and Transplantation Bethesda, Maryland

National Institute of Allergy and Infectious Diseases

Stephen P Heyse, M.D., M.P.H. National Institutes of Health Director Bethesda, Maryland Office of Prevention, Epidemiology and Clinical

Raymond A Dionne, D.D.S., Ph.D. Applications

Chief, Clinical Pharmacology Unit National Institute of Arthritis and

Neurobiology and Anesthesiology Branch and Musculoskeletal and Skin Division of Intramural Research Diseases

National Institute of Dental Health National Institutes of Health

National Institute of Health Bethesda, Maryland Bethesda, Maryland Cheryl Kitt, Ph.D. Health Science Administrator Division of Demyelinating, Atrophic, and Dementing Disorders National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda, Maryland

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Mary Lucas-Leveck, Ph.D., R.N. Christian S Stohler, D.D.S., Ph.D.

Chief, Acute and Chronic Illnesses Branch D.M.D. Professor and Chair

National Institute of Nursing Research Department of Biological and National Institute of Health Materials

Bethesda, Maryland Sciences and Center for Human Growth and Development William Maas, D.D.S. School of Dentistry Chief Dental Officer University of Michigan Agency for Health Care Policy and Ann Arbor, Michigan

Research

Rockville, Maryland Carolyn Tylenda, D.D.S.,Ph.D. Dental Reviewer

Stephen B Milam,D.D.S., Ph.D. Dental Devices Branch Associate Professor Food and Drug Administration Department for Oral and Maxillofacial Rockville, Maryland

Surgery

Department of Surgery John T Watson, Ph.D.

Medical School Scientific Group Leader

University of Texas Health Science Center Division of Heart and Vascular at San Antonio

Diseases San Antonio, Texas National Heart, Lung, and Blood Institute

Jeffrey P Okeson, D.M.D. National Institutes of Health Director, Orofacial Pain Center Bethesda, Maryland

College of Dentistry University of Kentucky Susan Wise Lexington, Kentucky Program Analyst

National Institute of Dental Joyce Rudick Research Senior Program Analyst National Institutes of Health Office of Research on Women's Health Bethesda, Maryland

Office of the Director National Institutes of Health Bethesda, Maryland

Patricia G Sheridan

Project Officer

National Oral Health Information Clearinghouse

National Institute of Dental Research National Institutes of Health Bethesda, Maryland

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ABSTRACTS

The following abstracts of presentations to the NIH Technology Assessment Conference on Management of Temporomandibular Disorders were furnished by presenters in advance of the conference. This book is designed for the use of panelists and participants in the conference and as a pertinent reference document for anyone interested in the conference deliberations. We are grateful to the authors who have summarized their materials and made them available in a timely fashion.

James A Lipton, D.D.S., Ph.D. Special Assistant for Training and Career Development National Institute of Dental Research National Institutes of Health Bethesda, Maryland

Jerry M Elliott Program Analyst Office of Medical Applications of Research National Institutes of Health Bethesda, Maryland

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History and Evolution of Temporomandibular Disorder Concepts Charles McNeill, D.D.S.

Historians explain that the management of temporomandibular disorders (TMD) began with ancient Egyptians manually treating jaw dislocations.1 Modern history reveals a more aggressive TMD approach, with Annandale receiving credit for the first surgical repositioning of an articular disc in the late 1800's2 and Pringle being recognized as one of the first surgeons to perform a menisectomy in the early 1900's.3 Then a dramatic change in the evolution of TMD management occurred basically on two fronts. First, Costen, an otolaryngologist, published his legendary treatise in 1934 claiming that pain in and around the jaw and "related ear symptoms" improved with alteration of the bite.4 Secondly, with the formation of the Gnathological Society by McCollum in 1926. the role of occlusion rapidly gained in popularity.5 Dentists became extremely interested in complex occlusal techniques, including prophylactic and therapeutic occlusal equilibration, in order to provide optimum dental treatment, including treatment for TMD. 6-10 Even though most, if not all, of Costen's hypotheses were refuted by Sicher11 and others, many dentists continued to embrace the concept that occlusal disharmonies were the primary cause of TMD. 12-14

However, in the 1950's the association between occlusal and TMD was beginning to be questioned by Schwartz and co-workers who emphasized the importance of the masticatory musculature and specifically emotional tension as a primary etiologic factor.11 In 1969, Laskin and coworkers published their psychophysiologic concept that also stressed the roles of muscle spasm and fatigue produced by chronic oral habits as the factors responsible for the symptoms of pain-dysfunction syndrome and further de-emphasized the mechanical role of occlusion in TMD.16 Supporting the importance of the neuromuscular system, Jankelson developed clinical instrumentation, reportedly to establish optimum neuromuscular jaw relationships as a basis for occlusal and TMD treatment. 17

Using arthrography in the late 1970's, Farrar and McCarty challenged the neuromuscular concepts and refocused on internal derangements as the primary cause of TMD signs and symptoms. 18 Numerous procedures were performed by enthusiastic dentists who believed that they could recapture malpositioned articular discs. This enthusiasm led to a disastrous time in TMD history due to the tragic sequelae that followed the use of alloplastic materials for disc replacement.19 As a result of questionable treatment outcome and with an increased awareness for its importance of a scientific foundation, dentists began to focus more on a medical approach to TMD treatment.20

Responding to the need for further study, the American Academy of Craniomandibular Disorders, founded in 1975, published a position paper on the state of art of TMD in 1980.21 Three years later the paper was updated to include more recent findings in the area of diagnosis.22 Understanding the critical need for definitive guidelines, the American Dental Association (ADA) held an important conference on the examination, diagnoses, and management of TMD in 1982.23 The conference stressed the importance of an improved classification system that would permit proper comparison of epidemiologic, diagnostic, and treatment data. As interest in TMD grew, the first issue of the Journal of Orofacial Pain (formerly the Journal of Craniomandibular Disorders: Facial and Oral Pain) was (15) published in 1986.34 The journal was the first peer-reviewed scientific journal exclusively devoted to TMD and orofacial pain, although a more clinically oriented journal, Cranio: The Journal of Craniomandibular Practice, had been published since 1982.25

As the demand for specific diagnostic criteria and treatment outcome data increased the American Academy of Craniomandibular Disorders and other organizations published more extensive classification guidelines with the intent to establish more specific diagnostic criteria. 26-28 Three years later, the Academy, now known as the American Academy of Orofacial Pain (AAOP), published an expanded and improved edition of the 1990 guidelines.29 At the same time, a multicenter research center group established specific research diagnostic criteria for patient questionnaires and clinical findings associated with TMD.30 It had become evident that operational definition guidelines were of paramount importance as the proliferation of TMD devices, both diagnostic and therapeutic helped foster clinical belief systems that had little or no scientific basis. 31 The following definition clinical presentation, and prevalence data are from the 1993 AAOP TMD Guidelines:

1. Temporomandibular disorders is a collective term that embraces a number of clinical problems that involve the masticatory musculature, the temporomandibular joint (TMJ) and associated structures, or both. TMDs are considered to be a subclassification of musculoskeletal disorders.

2. TMDS are characterized by the following clinical presentation: pain in the muscles of mastication, preauricular area and/or TMJ that is usually aggravated by manipulation or function; limited range of motion, asymmetric mandibular movement, and/or locking, and joint sounds described as clicking, popping, or crepitus.

3. Common complaints include headache, earache, and orofacial pain as well as masticatory muscle hypertrophy and abnormal occlusal wear. Unexplained complaints include tinnitus, ear fullness, and perceived hearing loss.

4. Cross-sectional epidemiologic studies of specific nonpatient populations show that approximately 75 percent of those studied have at least one sign and approximately 33 percent have at least one symptom; however, only 5-7 percent are estimated to be in need of treatment. Prevalence data from clinical reports reveal a female to male ratio of 4:1 to 6:1 in persons seeking care primarily in the second through fourth decade of life.

In a coordinated effort to establish research priorities, a National Institutes of Health International workshop on TMD and related pain conditions was held in 1994 and the proceedings were published by the International Association for the Study of Pain.32 A significant 30-year study on the progression of TMD was published soon after the conference by Boering and co-workers.33

Their conclusions provided some of the first longitudinal results regarding the natural progression of TMD. An unrelated but extreme revealing scientific monograph on treatment outcome was published by an international panel in Spine on whiplash-associated disorders.34

Their conclusions questioned the need for expensive diagnostic procedures and invasive, irreversible treatment and stressed the need for a biopsychosocial approach, including self-care for chronic musculoskeletal pain. Based on similar concepts, the AAOP is presently publishing guidelines for orofacial pain emphasizing that the (16) differential diagnosis of all head and neck conditions is essential to the management of TMD.35 In order to establish credentials in these complex areas, the American Board of Orofacial Pain was established by an independent medical testing agency in 1994.36 The evolutionary process appears to be moving in the direction of more comprehensive orofacial pain diagnosis and biopsychosocial management of chronic pain and away from the mechanical approaches of the past.

References

1. Ruffer MA. Studies in the palaeopathology of Egypt. Chicago: University of Chicago Press, 1921.

2. Annandale T. On displacement of the interarticular cartilage of the lower jaw and its treatment by operation. Lancet 1987;1: 41.

3. Pringle J. Displacement of the mandibular meniscus and its treatment. Br J Surg 1918;6:385.

4. Costen JB. A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otol 1934;43:1-15.

5. McCollum BB. Factors that make the mouth and teeth a vital organ. (Articulation Orthodontia) ADAJ 1927;14:1261-71.

6. Schuyler CH. Fundamental principles in the correction of occlusal disharmony, natural and artificial. J Am Dent Assoc 1935;22:1193.

7. Granger ER Biomechanics of periodontal disease. J Periodont 1950;21:98.

8. Shore NA. Equilibration of the occlusion of natural dentition. J Am Dent Assoc 1952;44:414.

9. Stuart CE. Articulation of human teeth. In: McCollum BB, Stuart CE, eds. A research report. South Pasadena: Scientific Press, 1955.

10. Lauritzen AG. Atlas of Occlusal Analysis. Boulder, Colorado: Johnson Publishing Co., 1974.

11. Sicher H. Temporomandibular articulation in mandibular overclosure. J Am Dent Assoc 1948;30:131-9.

12. Ramfjord SP. Dysfunctional temporomandibular joint and muscle pain. J Prosthet Dent 1961;11:353-74.

13. Dawson PE. Evaluation, diagnosis, and treatment of occlusal problems. St Louis: C.V. Mosby Co., 1974.

14. Guichet NF. The Denar system and its application in everyday dentistry. In: Boucher LJ, ed. Occlusal Articulation. Dent Clin North Am 1979;23:243-57.

15. Schwartz L. Pain associated with the temporomandibular joint. J Am Dent Assoc 1955;51:39.

(17) 16. Laskin DM. Etiology of the pain dysfunction syndrome. J Am Dent Assoc 1969;79:147-53.

17. Jankelson B. Neuromuscular aspects of occlusion. Dent Clin North Am 1979;23:151-68.

18. Farrar NB, McCarty Jr WL. Inferior joint space arthrography and characteristics of condylar paths in internal derangements of the TMJ. J Prosthet Dent 1979;41:548-55.

19. U.S. Food and Drug Administration. Safety Alerts. Department of Health and Human Services. Rockville, Maryland, 1990-91.

20. Bell WE. Clinical management of temporomandibular disorders. Chicago: Year Book Medical Publishing Co., 1982.

21. McNeill C, Danzig WM, Farrar WB, Gelb H, Lerman M, Moffett BC, Pertes R, Solberg WK, Weinberg L,

Craniomandibular (TMJ) disorders--The state of the art. Postition paper of the American Academy of Craniomandibular Disorders. J Prosthet Dent 1980;44:434-7.

22. McNeill C, ed. Accept diagnosis and treatment modalities. In Craniomandibular (TMJ) Disorders--The state of the art.

Part II. Accept diagnosis and treatment modalities. J Prosthet Dent 1983;49:393-7

23. Griffiths RH. Report of the President's conference on examination; diagnosis and management of temporomandibular disorders. J Am Dent Assoc 1983;106:75-7

24. Journal of craniomandibular disorders: facial and oral pain. Chicago: Quintessence Publishing Co., 1987;1:3-78.

25. Cranio: The journal of craniomandibular practice. Chattanooga, TN 1982.

26. McNeill C, ed. Craniomandibular disorders: guidelines for evaluation, diagnosis, and management. Chicago: Quintessence Publishing Co., 1990.

27. Eversole LR, Machado L. Temporomandibular joint internal derangements and associated neuromuscular disorders. J Am Dent Assoc 1985;110:69-79

28. Stegenga B, DeBont LGM, Boering. A proposed classification of temporomandibular disorders based on synovial joint pathology. J Craniomand Pract 1989;7:107-18

29. McNeill C, ed. Temporomandibular disorders--guidelines for classification, assessment, and management Chicago: Quintessence Publishing Co., 1993.

30. Dworkin SF, LeResche L, eds. Research diagostic criteria for temporomandibular disorders. Review, criteria, examinations and specifications critique. Chicago Quintessence Publishing Co., 1993.

(18) 31. American Association Dental Research (Draft). Statement on Temporomandibular Diseases. IADR Reports (Newsletter) 1995;17:3.

32. Sessle BJ, Bryant PS, Dionne RN, eds. TMD and related pain conditions. In: Fields HL, ed. Progress in pain research. Vol. 4 Seattle: IASP Press, 1995.

33. Boering G, Stegenga B, deBont LGM. Clinical sign of TMJ osteoarthrosis and internal derangement 30-years after nonsurgical treatment. J Orofacial Pain 1994;8:18-24.

34. Cassidy JD, ed.Scientific monograph of the Quebec task force on whipash-associated disorders; relining whiplash and its management. Spine 1995;20:8S-68S.

35. Okeson JP, ed. Orofacial pain: guidelines for assessment, diagnosis and management. Chicago: Quintessence Publishing Co., 1996.

36. American Board of Orofacial Pain. Lafayette, CA, 10 Joplin Court, established 1994.

(19) (20)-blank page CURRENT TERMINOLOGY AND DIAGNOSTIC CLASSIFICATION SCHEMA

Jeffrey P. Okeson, D.M.D.

Introduction

The ability to understand any disorder begins with common terminology and a classification schema. Nothing is more basic to communication within the profession. Common terminology within the profession is essential to begin the investigation, discussion, and ultimately understanding of a disorder. Because all functional disturbances of the masticatory system are not the same, it is important that a systematic classification be established that enhances communications between clinicians, researchers, academicians, and patients.

A classification schema begins by grouping disorders according to common signs and symptoms. Each of these groups are then subdivided by the signs and symptoms that differentiate them. If this grouping is successful, each subcategory will consist of a collection of related disorders that are likely to respond to similar treatment approaches. In this manner, the diagnostic classification schema can assist the clinician in treatment selection. From a clinical prospective, it is not important to further divide subgroups when all the disorders within a given subgroup are managed by the same therapy. Therefore, from a therapeutic stand point subcategories are only useful when therapy demands it.

Another purpose for a common diagnostic classification schema is to assist the researcher in gaining insight into the prevalence, etiology, and natural course of a specific disorder. The profession can only advance knowledge in the field when agreement is met on specific disorders so that research efforts can be compared between patients and various research groups. At this time there is uncertainty as to whether diagnostic criteria for research purposes are compatible with diagnostic criteria for determining therapy. For example, it is quite reasonable to separate muscle disorders from intracapsular joint disorders for the purpose of studying the natural course of these disorders. However, merely identifying that a patient is suffering from one of these major disorders may not be adequate to effectively manage the condition. The most useful classification schema would provide both research and diagnostic advantages.

This paper discusses past and present terminology and diagnostic classification schemes that have been offered for functional disorders of the masticatory system and concludes with some recommendations for future direction in this area.

TERMINOLOGY

Over the years, functional disturbances of the masticatory system have been identified by a variety of terms, which has likely led to confusion in this area. In 1934, James Costen described a group of symptoms that centered around the ear and temporomandibular joint (TMJ).1 Because of his work, the term "Costen Syndrome" developed. Later the term "temporomandibular joint disturbances" became popular, and then in 1959, Shore2 introduced the term "temporomandibular joint dysfunction syndrome." Subsequently, the term "functional temporomandibular joint disturbances" was introduced (21) by Ramfjord and Ash.3 Some earlier terms described the suggested etiologic factors such as "occlusomandibular disturbance"4 and "myoarthropathy of the temporomandibular joint.5 Othersewmphasized the term "pain," such as "myofascial pain-dysfunction syndrome,"6 and "temproromandibular pain-dysfunction syndrome."7 Since the symptoms are not always isolated to theTMJ, some authors believe that the previously mentioned terms are too limited and that a broader,more collective term should be used, such as "craniomandibular disorders."8 Bell suggested the term"temporomandibular disorders (TMD),"9 which has gained wide acceptance and popularity. This termnot only includes problems related to the TMJs but also all functional disturbances of the masticatory system.

Diagnostic Classification Schemes

Over the years many classifications schemes have been offered with varying advantages and disadvantages. Some classifications utilize etiologic factors to group disorders while others use common signs and symptoms. Still other classifications use tissue origin or functional relation of the body. Some classifications combine several of these parameters, often requiring greater expertise from the clinician.

Perhaps the first classification schema for TMJ problems was offered by Weinmann and SIcher in 1951.10 They classified TMJ problems into (1) vitamin deficiencies, (2) enocrine disorders, and (3) arthritis. Two years later, Schwartz11 introduced the term11 tempromandibular joint pain dysfunction syndrome11 to distinguish the masticatory muscle disorders from organic disturbances in the joint proper. In 1960, Bell 12 offered a classification composed of six groups, recognizing both intracapsular and muscle (extracapsular) disorders. Acknowledging the need for a suitable classification for functional disorders of the masticatory system, a group of clinicians, researchers, and academicians published a position paper with suggested classification schema.8 Soon after this publication the president of the American Dental Association (ADA) recognized the need to organize the profession's focus on these disorders and called for a national confernence.13 During this conference, Bell offered the term temporomandibular disorders and a revised classification of TMDs consisting of five categories. Both the term and classification were accepted by the ADA.13

In 1989, Stengenga et al.14 proposed a classification with its main emphasis on articular disorders of the TMJ. They divided their classification into inflammaroty and nononflammatory articular disorders with a third category that included nonarticular disorders. The subcategories of osteoarthritis and internal derangements were further divided accordinng to staging over time. Athough this classification provided insight into intracapsular disorders, it placed little emphasis on masticatory muscle disorders.

As the dental profession began to appreciate the similarity between many TMDs and other medical conditions, a need grew to include TMD in a more inclusive medical classification for pain disorders. In 1986, the International Association for the Study of Pain (ISAP)15 published a classifi-cation of pain conditions. Of the 32 categories of pain disorders, category III was designated as "Craniofacial Pain of Musculoskeletal Origin." Within this category were subcategories:

(1) tempromandibular pain and dysfunction syndrome and (2) osteoarthritis of the TMJ. ALthough this classification provided for (22) Pain conditions originating from the TMJ's, it again failed to adequately recognize any pain disorders arising from the masicatory muscles.

Two years after IASP classifications was published, the Internatinal Headache Society (IHS)16 proposed a classification for headache made up of 13 broad categories. The eleventh category was designated as "Headaches or facial pain associated with disorders of cranium, neck, eyes, nose, sinuses, teeth, mouth or other facial or cranial structures." The IHS committee elected not to elaborate the specific subcategories related to TMJ and masicatory muscle pain disorders. The American Academy of Orofacial Pain (AAOP) offered input to the ISH committee regarding the specific TMD sub-categories to be included in the eleventh categoty of the IHS classification.17 Diagnostic criteria were included for each subcategory. These subcategories have recently undated.18

In 1990, the American Academy of Head, Neck, and Facial Pain and TMJ Orthopedics offered a classification with five TMD ccategories and two non-TMD categories.19 The subcategories represented a mixture of both traditional and nontraditional disorders. There were brief explanations for most subcategories but no diagnostic criteria were offered. There were 19 subcategories under the main category of myofascial disorders, some of which were separated by the specific muscle or tendon involved. Some diagnostic categories, such as bruxism, might better represent a precipitating or contributing factor of muscle pain and not necessarily a muscle pain disorder itself.

A few more recent classification schemes also offer certain advantages. Truelove et al.20 proposed a classification schema that allowed for multiple diagnoses within the same subject group. Required operational criteria were listed for each diagnostic group allowing the researcher to investigate a sample population and determine the types and severity of disorders present. This concept was further elaborated through the research diagnostic criteria offered by Dworkin and LeResche.21

This classification not only provided very specific diagnostic criteria for eight TMD subgroups, but also recognized another level or Axis that must be considered when evaluating and managing TMD pain. This second Axis represents the psychosocial influence on the patient's pain experience. For the first time in any classification schema a dual diagnosis was established tht recognizes not only the physical condition (Axis I) that contriburtes to the pain but also the pschosocial issues (AxisII) that contribute to the suffering, pain behavior, and disability associated with the patient's pain experience. This dual Axis classification approach has recently been incorporated in a diagnostic schema not only for TMD but for all orofacial pain disorders.22

Presently there is little consensus regarding the most favorable diagnostic classification schema. Recenty many medical and dental clinicians have favored the IHS classification because of its inclusive considerations of all head pains. This classification, however requires the clinician to have a very high level of appreciation for all head pain disorders before a diagnosis can be properly established. The research validity of the various diagnostic criteria have not yet been established and the classification does not provide for dual Axis diagnoses. It is therefore concluded that the ideal classification scema has not yet been developed.

(23) Recommendations

1. Recently, it has become increasingly clear that complaints about TMD are very similar to those from many other types of musculoskeletal disorders. Solutions to these problems must come from a thorough understanding of the pathophysiology of musculoskeletal pain. With thisunderstanding, one might question the need for a separate term for musculoskeletal pain disordersof the masticatory structures (i.e., TMD). Yet in another sense, the masticatory system is unique with teeth and its own dual joint system. THere are also certain treatment considerations that are unizue to the masticatory system. It would therfore appear that temporomandibular disorders is an appropriate collective term to describe musculoskeletal disorders arising from the masticatory structures. However, the clinician needs to be cognitive of the fact that these complaints have comon pathophysiology with other musculoskeletal disorders of the body and therefore should be diagnosed and treated by means of a medical model.

It is recommended that temporomandibular disorders be maintained as an appropriate collective term to describe musculoskeletal disorders of the masticatory system.

2. There is a need for a well-described, scientifically based, diagnosic classification for TMD. Each diagnostic category needs to have specific inclusionary and exclusionary criteria. Presently the research diagnostic criteria21 offers the best classification for grouping disorders for research purposes. Future effort needs to be directed to refining tese categories so that they may be more useful for both research purposes and therapy selection.

It is recommended that continued research be directed toward gaining greater insight into the pathophysiology of TMD. Beter understanding will improve the dignostic classficationof TMD. Efforts should be directed toward establishing a single diagnostic classification schema that is compatible for both research and therapeutic purposes.

3. The classification of TMD would be greatly enhanced by the use of reliable diagnostic instrumentation. Presently, however, there are few diagnostic instruments that have been proven reliable for use. Most of the instruments presently being used today have not met the reliability, validity, and efficacy standards that are necessary to consistently assist in determining diagnostic classification.23-29

It is recommended research be directed toward the development and evaluation of valid and reliable diagnostic instruments and/or tests that will assist in the accurate diagnosis of TMD subcategories.

References

1. Costen JB. Syndrome of ear and sinus symptoms dependent upon functions of the tempromandibular joint Ann Otol RHinol Laryngol 1934;3:1-4.

2. Shore NA. Occlusal equilibration and temporomandibular joint dysfunction. Philadelphia: JB Lippincott Co., 1959. (24)

3. Ramfjord SP, Ash MM. Occlusion. Philadelphia: WB Saunders Co, 1971.

4. Gerber A. Kiefergelenk und Zahnokklusion. Dtsch Zahnaerztl 1971;26:119.

5. Graber G. Neurologische und psychosomatische Aspekte der Myoarthropathien des Kauorgans. Zwr 1971;80:997.

6. Laskin DM. Etiology of the pain-dysfunction syndrome. J Am Dent Assoc 1969;79(1):147-`53.

7. Schwartz L. Disorders of the temporomandibular joint. Philadelphia: WB Saunders., 1959.

8. McNeill C, Danzig D, Farrar W, Gelb H, Lerman MD, Moffett BC, Pertes R, Solberg WK, Winberg LA.

Craniomandibular (TMJ) disorders--state of the art J Prosthet Dent 1980;44:434-7.

9. Bell WE. Clinical management of temporomandibular disorders. Chicago: Year Book Medical Publishers. 1982

10. Weinmann JP, Sicher H. Pathology of the temporomandibular joint. In: Sarnat BG, ed. The temporomandibular joint. Springfield: Charles C Thomas Publishers 1951:65-81

11. Schwartz LL. A temporomandibular joint pain-dysfunction syndrome. J Chron Dis 1956;3:284.

12. Bell WE. Temporomandibular joint disease. Dallas: Egan Company, 1960.

13. Griffiths RH. Report of the President's Conference on examination, diagnosis, and management or temporomandibular disorders. J Am Dent Assoc 1983;106:75-7.

14. Stegenga B, de Bont LG, Boering G. A proposed classification of temporomandibular disorders based on synovial joint pathology. J Craniomand Pract 1989;7(2):107-18.

15. Merskey H. Classification of chronic pain: Descriptions of Chronic pain syndromes and definitions of pain terms. Pain 1986;suppl 3:S1-S226.

16. Oleson J. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8(Suppl 7):1-97.

17. McNeill C, ed. Temporomandibular disorders: guidlines for classification, assessment, and management. 2nd ed. Chicago: Quintessence Publishing Co., 1993.

18. Okeson J, ed. Orofacial pain: guidlines for classification, assessment, and management. 3rd ed. Chicago: Quintessence Publishing Co., 1996.

Talley RL, Murphey GJ, Smith SD, Baylin MA, Haden JL. Standards for the history examination, diagnosis, and treatment of temporomandibular disorders (TMD); a position paper. J Craniomand Pract 1990;8:60-77

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20. Truelove El, Sommers EE, LeResche L, Dworkin SF, Von KM. Clinical diagnostic criteria for TMD. New classification permits multiple diagnoses (see comments). J AM Dent Assoc 1992; 123(4):47-54. (Comment in J Am Dent Assoc 1992 Oct;123:(10:12).

21. Dworkin Sf, LeRescheL. Research diagnositic for temporomandibular disorders: review, criteria, examinations and specifications, critique. J Craniomand Disord 1992;6(4):301-55.

22. Okeson Jp. Bell's Orofacial Pains. 5th ed. Chicago, IL:Quintessence Publishing Co, Inc. 1995:135-84.

23. Lund Jp, Widmer CG, Feine JS. Validity of diagnostic and monitoring tests used for temporomandibular disorders. J Dent Res 1995;74(4):1133-43.

24. Mohl ND. Reliability and validity of diagnositic modalities for temporo-mandibular disorders. Adv Dent Res 1993;7(2):113-9.

25. Lund Jp, Widmer CG. Evaluation of the use of surface electromyography in the diagnosis, documentation, and treatment of dental patients. J Craniomand Disord 1989;3(3):`25-37.

26. Mohl ND, McCall WS, Lund JP, Plesh O. Devices for the diagnosis and treatment of temporomandibular disorders: Part 1. Introduction, scientific evidence, and jaw tracking. J Prosthet Dent 1990;63:198-201.

27. Mohl ND, Lund Jp, Widmer CG, McCall WD Jr. Devices for the diagnosis and treatment of temporomandibular disorders. Part II: Electromyography and sonography [published erratum appears in J Prosthet Dent 1990 May;63(5):13A]. J Prosthet Dent 1990;63(3):332-6.

28. Mohl Nd, Ohrback RK, Crow HC, Gross AJ. Devices for the diagnosis and treatment of temporomandibular disorders. Part III. Thermography, ultrasound, electrical stimulation and EMG biofeedback. J Prosthet Dent 1990; 63:472-7.

29. Okeson J, ed. Orofacial pain: guidelines for classification, assessment, and management. 3rd ed. Chicago: Quintessence Publishing Co., 1996:28-36.

Psychosocial and Behavioral Assessment

of Temporomandibular Disorder Patients

Dennis C. Turk, Ph.D.

Despite major advances in our understanding of the nervous system, in the development of potent analgesic preparations, and in increasingly sophisticated surgical procedures, permanent amelioration of pain for patients with persistent pain has not been achieved. To understand and appropriately treat a patient whose primary symptom is pain begins with a comprehensive history and physical examination.

Patients are usually asked to describe the characteristics, location, and severity of pain. Physical examinations procedures have been detailed in texts, and sophisticated laboratory and imaging techniques are readily available for use in detecting organic pathology. Thus, assessment of the complaint of pain may at first seem to be quite an easy task; however, this assessment is complicated by the psychological, social, and behavioral characteristics of the individual patient.

Review of the chronic pain literature reveals that a number of factors, in addition to physical pathology, play a role in reports of pain and disability associated with chronic medical conditions. Specifically, research suggests that patients' perceptions of pain, the impact of pain on their lives, dysphoric mood, responses of significant others, and levels of activity all contribute to the patient's suffering and disability. Thus, it is important to consider classification of pain patients themselves in addition to the classification of their diseases according to location, severity, and etiology.

In addition to this standard medical approach, an adequate pain assessment also requires evaluation of the myriad psychosocial and behavioral factors that influence the subjective report. Turk and Meichenbaum (1994) have suggested that three central questions should guide assessment of people who report pain.

1. What is the extent of the patient's disease or injury (phyisical impairment)?

2. What is the magnitude of the illness? That is, to what extent is the patient suffering, disabled, and unable to enjoy usual activities?

3. Does the individual's behavior seem appropriate to the disease or injury or is there any evidence of amplification of symptoms for any of a variety of psychological or social reasons or purposes?

This presentation focuses on the second two questions and in particular how they apply to the assessment of temporomandibular disorder (TMD) patients. A multiaxial approach to assessment is described and an empirically based classification system based on the comprehensive assessment is presented.

(27) It is concluded that a dual-diagnostic approach would make use of the two axes--physical and psychological--simultaneously. For example, it is suggested that the physical treatment should be directed toward the disease classification and that other treatments would supplement this by focusing on a classification based on relevant psychological characteristics. Thus, a patient might have a physical diagnosis that fits with axis 1 of the Research Diagnostic Criteria (Dworkin & LeResche, 1992) and a diagnosis based on the empirically derived psychosocial classification proposed by Turk, Rudy, and colleagues. Adopting such an approach would serve the valuable function of encouraging diagnosticians to think concurrently in terms of the two relevant areas for TMD.

BIBLIOGRAPHY

1. Dworkin SF, LeResche L, eds. Research diagnostic criteria for temporomandibular disorders: Review, criteria, examinations and specifications, critique. J Craniomand Disord Facial Oral Pain 1992;6:301-355.

2. Rudy TE, Turk DC, Zaki HS, Curtain HD. An empirical taxometric alternative to traditional classification of temporomandibular disorders. Pain 1989;36:311-320.

3. Turk DC, Rudy TE, Toward a comprehensive assessment of chronic pain patients: A multiaxial approach. Behav Res. Ther 1987;24:237-49.

4. Turk DC, Rudy TE. Toward an empirically derived taxonomy of chronic pain patients: Integration of psychological assessment data. J Consult Clin Psychol 1988;56:233-8.

5. Kerns RJ, Turk DC, Rudy TE. The West Haven-Yale Multidimensional Pain Inventory (WHYMPI). Pain 1985;23:245-56.

6. Turk DC, Meichenbaum D. A cognitive-behavioral approach to pain management. In: Wall PD, Melzack R, eds. Textbook of pain, 3rd ed. London: Churchill Livingstone, 1994:1337-48.

7. Turk DC, Rudy TE. Robustness of an empirically derived taxonomy of pain patients. Pain 1990l43L27-36.

8. Turk Dc, Rudy TE, Zaki HS. Multiaxial assessment and classification of TMD pain patients. Implications for treatment. In: Friction JR, Dubner R, eds. Orofacial and temporomandibular disorders. New York: Raven Press, in press.

9. Turk DC. Customizing treatment for chronic pain patients: Who, what, and why? Clin J Pain 1990;6:255-70. (28)

Health Care Services Issues Concerning Temporomandibular Disorders Michael R. Von Korff, Sc.D.

Like back pain, temporomandibular pain might be thought of as "an illness in search of a disease."1 Although standardized and reliable diagnostic criteria for temporomandibular disorders (TMD) have been recently developed,2 the validity of these criteria and how specific diagnoses relate to either etiology or response to specific treatments is largely unknown. Temporomandibular pain is rarely associated with a well-understood disease. In most instances, evidence is lacking that dental, medical, or behavioral treatments produce appreciably better outcomes than those that can be achieved without treatment.

Given this uncertain state of affairs, developing rational strategies for the provision of health care for persons with temporomandibular pain is a difficult task. Efforts to define guidelines for and to ensure diagnosis and treatment of patients with TMD are likely to be controversial. Differing views about appropriate diagnosis and treatment are held by providers who treat patients in different ways, by patients with different treatment preferences, and by health care insurers. Efforts to promulgate treatment guidelines could be expected to generate conflict among providers with an interest in providing particular services. Such conflict is nurtured by the lack of rigorous scientific data on what kinds of treatment are effective and how therapeutic services can be provided in a cost-effective manner.

This paper draws on epidemiologic and health services data on the care of persons with temporomandibular pain to identify critical issues and to suggest how health services research might contribute to their resolution. At present, a scientific basis is lacking for consensus regarding the kinds of services likely to benefit the typical patient with temporomandibular pain. Three alternative strategies for the care of the typical patient with temporomandibular pain, i.e., specialty care, generalist care, self-care, may be characterized as follows:

Specialty care. The typical patient requires a comprehensive diagnostic evaluation followed by specific treatment to address the underlying disorder.

Generalist care. The typical patient requires a brief screening examination conducted by a generalist (primary care physician or general dentist) to assess whether significant diseases may be present. Most patients are managed with palliative care to control pain and inflammation. A small percentage of patients (less than 10 percent) are referred to a specialist for further evaluation and treatment.

Self-care. Temporomandibular pain is typically a condition, like the common headache, that usually does not require diagnostic evaluation or medical management.

Adequate data are lacking of the direct costs (treatment costs) and indirect costs (disability costs) associated with TMD in the United States. It is likely that hundreds of millions of dollars are spent annually on diagnostic and therapeutic services for persons seeking care for these conditions. Despite (29) the resources expended on care of patients with temporomandibular pain, little research has examined the magnitude of treatment services provided to patients with temporomandibular pain, where they are cared for, what kinds of services they receive, what those services cost, the short- and long-term outcomes of treated and untreated patients, and whether the services provided are effective and cost-effective. Applying health services research to the provision of services for persons with temporomandibular pain is needed to identify how to effectively care for persons with temporomandibular pain at a cost that individual patients and society can afford.

Like other common pain symptoms, approximately one in four of those experiencing temporomandibular pain seek health care for their pain.3,4, People whose pain is more severe, more persistent, and of more recent onset are more likely to seek treatment.5 Consistent with a large body of research on how people manage common symptoms, self-care appears to be the most common form of management of temporomandibular pain. Although self-care is the most common form of management of most common pain symptoms, including temporomandibular pain, there has been remarkably little research studying how people self-manage pain and how self-management of pain might be enhanced. Important exceptions are the growing body of research on minimal interventions for headache6 and on self-care of arthritis.7

Insurance arrangements and the organizations of health care affect the setting in which persons with a pain symptom are treated. First, contact for temporomandibular pain may often be with a primary care physician or a general dentist, but there is no research concerning how primary care providers can effectively assess and manage these patients. Although temporomandibular pain has many features that make it appropriate for management by a primary care physician or general dentist, generalists often feel inadequately prepared to evaluate and manage patients with temporomandibular pain. As a result, there may be greater utilization of specialty care for this common pain symptom than would otherwise be warranted.

The most essential criterion for evaluating the relative benefits of specialty care, generalist care, and self-care is their impact n patient out-comes, the two most critical of which are pain (Intensity and persistence) and interference with activities. Rigorous comparison of the effects of specialty care, generalist care, and self-care on patient outcomes is likely to require randomization of patients to these different modalities of care.

A second criterion for evaluating health care services is their contribution to patient satisfaction. Patient preferences are increasingly recognized as important in deciding how services should be organized. Patient satisfaction may be greater with specialty care in which providers are able to spend more time with each patient and have more experience with the presenting complaint. An unresolved issue in the provision of health services in whether publicly subsidized insurance benefits should provide for services that are more satisfactory to patients, regardless of whether they produce more favorable outcomes. With the social provision of health insurance, the interests of business and of government in limiting coverage to services that have health benefits commensurate with their cost may come in conflict with the desires of individual patients for care from a specialist who spends more time and who is highly experienced in treating the patient's particular problem. Differences in patient outcomes and satisfaction between specialist care, generalist care, and self-care need to be balanced against differences in the costs of care.

(30) A critical concern in the organization of health care services for patients with a poorly defined pain condition is that patients may be exposed to expensive treatments that are ineffective or the cause harm. These risks are likely to increase as patients move from care by a generalist to care by a specialist. At present, the safety and efficacy of some nonconservative interventions for TMD have not been established by scientifically valid methods.

Patients with temporomandibular pain, like patients afflicted with common pain problems, sometimes cycle through multiple providers and treatments over the course of their patient career. A patient career in which large numbers of providers are consulted may be harmful to some patients while wasting health care resources. Williams and Hadler characterized the distinction between management of acute and chronic illness as follows."The quest to define the disease response for a patient's distress is important when the disease is acute or potentially remediable or both...A disease-specific focus deemphasizes the dominant issue in the management of chronic illness, which is the maximization of the patient's productivity, creativity, well-being, and happiness. This goal of improving patient function and satisfaction to the utmost is usually achieved without curing the underlying diease."7

Surprisingly little research attention has been paid to determine how to organize services to prevent patients with chronic pain from developing an expensive and potentially harmful "chronic patient" career. While extended patient careers may bring patients into contact with many different providers, patients exposed to multiple providers are likely to observe heterogeneous diagnostic and therapeutic practices across providers.8 Variation in clinical methods across providers may not be a benign phenomenon. Since patients affected by chronic pain often seed care from multiple providers, they are likely to observe that providers diverge in their diagnostic assessments, tests ordered, and treatments prescribed. Such variation may contribute to patient uncertainty and may encourage patients to seek care from different practitioners until they find a diagnostic explanations and a therapeutic regiment to their liking. The search for the cure of a chronic pain condition may be both an expensive and a risky undertaking. An antidote to the costs and risks of doctor shopping may be greater uniformity in practice standards for diagnosis and treatment of chronic pain conditions like TMD, and greater scientific rigor in the evaluation of commonly prescribed treatments.

There has been relatively little health services assessing the effectiveness of these services, how satisfactory they are to patients, what forms of service are most cost-effective, or whether nonconservative interventions are safe. Health services research that rigorously evaluates the effectiveness, costs, patient satisfaction, and safety of services for patients with temporomandibular pain is urgently needed. In particular, it needs to be determined whether and under what circumstances patients with temporomandibular pain are best cared for by a specialist or a generalist and whether self-care is adequate for the typical patient.

(31) References

1. Van Korff M, Dworkin SF, LeResche L, Kruger A. An epidemiologic comparison of pain complaints. Pain 1988a;32:173-83.

2. Williams M, Hadler N. The illness as the focus of geriatric medicine. N Engl J Med 1983;308:1357-60.

3. Dworkin S, LeResche L. eds. Research diagnostic criteria for temporomandibular disorders. Washington Dc: National Institute of Dental Research, 1992.

4. Linet MS, Stewart WF, Celantano DD, Ziegler D, Sprecher M. An epidemiologic study of headache among adolescents and young adults. JAMA 1989;261:2211-16.

5. Von Korff M, Wagner EH, Dworkin SF, Saunders KW. Chronic pain and use of ambulatory health care. Psychosom Med 1991;53:61-79.

6. Nash J, Holroyd K. Home-based behavioral treatment for recurrent headache: a cost-effective alternative? Am Pain Soc Bull 1992;2:1-6

7. Lorig K. Holman H. Arthritis self-management studies: a twelve-year review. Health Educ Q 1993;20:17-28.

8. Von Korff M, Howard JA, Truelove EL, Wagner E, Dworkin S. Temporomandibular disorders: variation in clinical practice. Med Care 1988b;26:307-14.
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Epidemiology and Natural Progression of
Temporomandibular Joint
Intracapsular and Arthritic Conditions
Lambert G.M. de Bont, D.D.S., Ph.D.

 The prevalence rates of temporomandibular disorders (TMD) differ from study to study, probably because of methodologic errors and the lack of a standardized definition of TMD and their characteristics. 1,2,  These studies suggest that the prevalence of clinically significant TMD-related jaw pain is at least approximately 5 percent in the general population. Nearly 2 percent of the total population demanded treatment for a TMD symptom.2,3  Figures from epidemiologic studies frequently suggest a much higher prevalence of TMD-related signs and symptoms and a corresponding need for treatment. 4,5  Gender differences in TMD are hardly reported in epidemiologic studies; this is in contrast with the observation of a considerable female predominance in TMD clinics. Female susceptibility for TMD may be the result of a sex-linked molecular biologic nature of the onset of TMD. Because of the progress in the area of molecular biology, research in this field probably has the potential to answer questions related to the female predominance in several degenerative joint diseases, especially in adolescents. The degenerative nature of many TMJ intracapsular and arthritic conditions has been reported frequently by many arthroscopists.6  Osteoarthrosis (OA) is widely accepted as the basic process that occurs in degenerative joint diseases. 7,8  By modern definitions, OA is a disruption of a steady-state balance in a complex of interacting degradative and repair processes in cartilage, bone and synovium with secondary inflammatory components. Degenerative joint diseases result from an imbalance between predominantly chondrocyte-controlled anabolic and catabolic processes, characterized by progressive degradation of components of the extracellular matrix of articular cartilage with secondary inflammatory components. A unique initiating factor has not yet been identified. The primary insult may be local or systemic, and of a mechanical, chemical, or inflammatory nature. The result is chondocyte of synovial cell breakdown, release of proteolytic enzymes, and matrix degradation.
Throughout life, articular cartilage and underlying bone display shifting equilibria between changes in form and function by tissue remodeling. Increased loading may stimulate remodeling, involving increased synthesis of proteoglycans and collagen fibrils. Overloading may disturb the equilibrium between form and function and give rise to tissue breakdown. With the loss of matrix, the mechanical properties of the cartilage may become insufficient to withstand functional joint loads. Cartilage breakdown is caused by collagenolytic and proteolytic enzymes; cartilage repair is expressed by chondrocyte proliferation and increased synthesis of collagen and proteoglycans.
 Chondrocytes are surrounded by numerous peptide factors that modulate cell growth and differentiation. These factors interact such that one factor may influence the production and also the biological effects of others. The involved peptide factors are nowadays categorized as proteases, protease inhibitors, cytokines, growth factors, and arachidonic acid metabolites. They all seem to play an important role in the etiopathogenesis of OA. A general feature in these complex and interacting degradative and repair processes in cartilage, bone and synovium is an imbalance of protease versus
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protease inhibitor concentrations. Biochemically, OA can be classified in several phases, based on the grade of degradation of articular cartilage.9
Temporomandibular joint (TMJ) OA and disc displacement seem to be strongly related, but may also represent mutually independent TMD. In our classification of TMJ disorders, primary OA with disc displacement is distinguished from primary OA without disc displacement. Secondary OA of the TMJ would be the result of other joint disorders such as rheumatoid arthritis, but also disc displacement and hypermobility can be considered as causes of secondary OA. Considering pathology of TMJ OA, we are dealing with synovial joint pathology, basically connective tissue diseases.10
 Because biochemical and biomechanical adaptive mechanisms seem to play a major role in the natural course of TMJ degenerative disorders, treatment should be oriented toward promoting a joint condition that is most likely to repair. Because of the nonprogressive nature of TMJ OA and its self-limiting behavior, TMJ nonsurgical management of TMJ can be highly successful.11
 Surgical therapies should be considered only after reasonable nonsurgical efforts, directed to symptom relief and tissue adaptation, have failed and the patient's quality of life is being significantly affected. Arthroscopy is the least invasive surgical technique that has the potential of successful surgical outcome with minimal sequelae. Arthroscopic surgery originally included only lysis and lavage techniques. Increase in range of motion, improvement of joint function, and reduction of pain were observed. It became clear that successful surgical outcome may not be predicated on the restoration of disc position, but probably in the effects on concomitant findings associated with osteoarthritis and internal derangements, such as synovitis, adherence of discal tissue and its attachments to the temporal articulating surface, fibrous connective tissue adhesions, and capsular fibrosis.
 Successful surgical outcome of any TMJ procedure will be based on eliminating the etiological, contributing and perpetuating factors responsible for the disease and localized dysfunction of the joint. However, these factors are not yet determined.12
Summary
 The TMJ obeys the same biologic laws as do other synovial joints in the body. It is becoming more and more obvious that enzymatic pathways, in addition to mechanical factors, are involved in osteoarthrotic cartilage matrix degradation.9  To establish an effective regimen of therapy to minimize the extent of joint destruction, it is important to understand how matrix degradation develops and what enzymes mediate the process.
 TMJ osteoarthrosis and disc displacement seem to be strongly related, but may also represent mutually independent TMD.10 Therefore, TMJ treatment modalities that simply focus on TMJ disc position neglect that osteoarthrosis affects all joint components.
 TMJ disc perforation, disruption, and severely changed disc shape cannot be repaired. Only displaced discs with minimal changes in disc morphology and reduction in nature can be surgically
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repositioned. However, the nature of TMJ osteoarthrosis and internal derangement is nonprogressive in the majority of cases.7 Therefore, there is no rationale for disc-repositioning procedures.
 TMJ degenerative diseases are self-limiting in a very high percentage of cases,7,11 and nonsurgical management is appropriate in these cases. Therefore, surgical therapy should be considered only after reasonable nonsurgical efforts have failed and the patient's quality of life is being significantly affected.
 Because TMJ degenerative diseases are self-limiting, there is no rationale for differentiation in nonsurgical treatment modalities. 7,11 (The primary approach should be explanation of the natural course of the disorder, so that reasonable expectations can be met, and patient reassurance.)
 Surgery has the potential to remove the destroyed or affected joint structures. Surgery does not have the potential to heal the joint or joint structures, or to restore the integrity of the tissues; at most it creates a starting point for the natural healing process.
 Since the etiology and pathogenesis of TMJ degenerative diseases are not yet fully understood., causal therapy is not feasible.
REFERENCES
1.  De Kanter RJ, Truin GJ, Burgersdijk RCW, Van't Hof MA, Battistuzzi PG, Kalsbeek H, Kayser AF. Prevalence in the Dutch population and a meta-analysis of signs and symptoms of temporomandibular disorders. J Dent Res 1993;72:1509-18.
2.  Goulet JP, Lavigne GJ, Lund JP. Jaw pain prevalence among French-speaking Canadians in Quebec and related symptoms of temporomandibular disorders. J Dent Res 1995;74:1738-44.
3.  De Kanter RJ, Kayser A, Battistuzzi PG, Truin GJ, Van't Hoff MA.  Demand and need for treatment of craniomandibular dysfunction in the Dutch adult population. J Dent Res 1992;71:1607-12.
4.  Dworkin SF, Huggins KH, LeResche L, Von Korff M, Howard J, Truelove E, Sommers E. Epidemiology of signs and symptoms in temporomandibular disorders: clinical signs in cases and controls. J Am Dent Assoc 1990;120:273-81.
5.  Salonen L, Hellden L, Carlsson GE, Prevalence of signs and symptoms of dysfunction in the masticatory system: An epidemiologic study in an adult Swedish population. J Cranio Disord 1990;4:241-50.
6.  McCain JP. Principles and practice of temporomandibular joint arthroscopy. St. Louis: C. V. Mosby Co. 1996.
7.  Boering G. Temporomandibular joint osteoarthrosis: an analysis of 400 cases, a clinical and radiographic investigation. Thesis, University of Groningen, 1966, Dept. of Oral and Maxillofacial Surgery, reprinted in 1994.
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8.  Stegenga B, de Bont LGM, Boering G. Osteoarthrosis as the cause of craniomandibular pain and dysfunction: a unifying concept. J Oral Maxillofac Surg 1989;47:249-56.
9.  Dijkgraaf LC, deBont LGM, Boering G, Liem RSB. The structure, biochemistry, and metabolism of osteoarthritic cartilage: a review of the literature. J Oral Maxillofac Surg 1995;53:1182-92.
10. De Bont LGM, Stegenga B. Pathology of temporomandibular joint, internal derangement and osteoarthritis. Int J Oral Maxillofac Surg 1993;22:71-4.
11. De Leeuw R, Boering G, Stegenga B, de Bont LGM. Symptoms of temporomandibular joint osteoarthrosis and internal derangement 30 years after non-surgical treatment. J Craniomand Pract 1995;13:81-8.
12. Stegenga B. Temporomandibular joint osteoarthrosis and internal derangement. Diagnostic and therapeutic outcome assessment. Thesis, University of Groningen, 1991.
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Epidemiology and Natural Progression of
Muscular Temporomandibular Disorder Conditions
Christian S. Stohler, D.D.S., Ph.D., D.M.D.

INTRODUCTION
 Current knowledge does not support the notion that the masticatory muscle disorders are any different from the painful muscle afflictions in other regions of the human body. However, the tactile, sensibility of the tooth support makes the masticatory apparatus unique insofar as differences can be perceived in this region that are significantly smaller than those in any other musculoskeletal system of the body. Therefore, it is not surprising that complaints of teeth no longer fitting correctly have been expressed in the context of temporomandibular disorders (TMD) and their subsets. This fact does explain (1) the long-standing interest of the dental profession in these disorders and (2) the plethora of occlusal treatments that have been developed to address these pain conditions.
 Many providers believe that most patients with masticatory myalgia are treated effectively by management of the dental occlusion. Therefore, it is not surprising that failure to resolve a jaw pain problem is perceived as the clinician's inadequacy to provide the patient with an acceptable occlusal scheme. In recent years, however, a reassessment of this point of view was triggered by the impression gained in facial pain clinics that there exists a subpopulation of jaw muscle pain patients for whom this treatment paradigm does not provide any relief. The question arose whether one should work harder within the popular occlusal treatment paradigm or abandon this paradigm that appears to be incorrect.
CLINICAL SPECTRUM
 Since muscle pains are the most frequent of any pains in the body, the high prevalence of painful, involvement of the muscles of mastication is not surprising. Muscle pains occur in various forms,  ranging from a response to unaccustomed exercise or trauma, to persistent, localized, regional, or even generalized involvement without obvious or known cause. Many muscle pains resolve without intervention, whereas for others a therapeutic benefit may exist.
 Although episodic and relatively infrequent masticatory muscle pain may be a nuisance, frequent or lasting conditions can be disabling. Attempts to bring order to the perceived heterogeneity of the masticatory muscle pain conditions have not matured to the point that a reliable and valid classification scheme is currently available to the clinician. Although it is unclear whether subgroups of the painful masticatory muscle conditions are characterized by differences in etiology, variances between the milder or episodic forms, and presentations that involve a great deal of suffering, will likely call for a refined therapeutic approach.
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CASE DEFINITION
 As in any other field of clinical research, different designations have often been used by different investigators, and based on the review of the relevant literature, the need for reproducible, reliable clinical measurement in this field cannot be overemphasized. Disagreement in prevalence figures resulted from applying different criteria to the same clinical condition or from the use of arbitrary, often inconsistent cutoff points in a continuous distribution of a measurement variable. Data on the reliability of measurement are provided on rare occasions. The absence of a tight case definition not only limits comparisons of published work and adds to the confusion among clinicians but also has hindered scientific progress. Case definitions that were based on the presence of at least one symptom or sign have shown to be too sensitive on the one hand while lacking the specificity on the other.
 To address this problem, the National Institute of Dental Research has sponsored the development of operational diagnostic criteria for making a clinical decision about the existence of masticatory myalgia (and other TMD entities) based on a cluster of symptoms and clinical features.1  The impression is gained that this first endeavor to bring order to research has resulted in a higher quality of the TMD literature by raising the awareness of and concern for critical methodologic issues.
EPIDEMIOLOGY
 Given the perceived heterogeneity among the masticatory muscle pain conditions, the necessity for long-term epidemiologic followup studies on large numbers of community cases has been recognized. Although the persistent forms are encountered in high numbers among patients in tertiary care pain clinics, episodic forms are likely more frequent in the primary care environment. On the other hand, subjects with the trivial forms of jaw muscle pain are less likely to seek any form of care. Since prognostic distinctions appear to be in order between these masticatory myalgias, pooling extremes in  an overall prevalence figure is misleading. In addition, although masticatory muscle pain represents the main attribute, spread and secondary effects may coexist and can have a bearing on the level of needed care; a comorbid condition may have a major impact on the patient's prognosis. However, issues like these have not been sufficiently addressed by epidemiologic work. Overtreatment of mild and episodic forms and undertreatment of the disabling forms of masticatory myalgia represent an impression of the status of care today.
Cross-sectional studies suggest that the TMD, including the masticatory myalgias, are more prevalent in childbearing ages than in any other group. The prevalence also appears to decline with age for both sexes. Tertiary care clinics report a preponderance of females among patients with TMD that is even more pronounced than the proportion of women in community controls. However, factors like gender differences in health service utilization and symptom perception appear to be insufficient to explain this observation. Physiologic gender differences are increasingly becoming the focus of interest.
ETIOLOGY AND PATHOGENESIS
 Most probably because the episodic muscle pains are so frequent and often trivial, the chronic, disabling forms have not been subject to intense systematic study. However it is becoming apparent
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that the central nervous system (CNS) plays a major role in the pathogenesis of the masticatory myalgias. Long-term potentiation of the nociceptive system and attenuation of antinociceptive mechanism are being investigated as causes of the persistence of these muscle pain conditions. Experimental evidence suggests neuroplastic changes in the CNS and alteration in the responsivity of peripheral nociceptors in clinical cases of muscle pain. Although the cause of the masticatory myalgias has not been identified, it is fair to conclude that the older concepts of "overworked" jaw muscles resulting from an imbalance of the bite or craniofacial skeleton are too simplistic to be considered valid.
CONCLUSIONS
 Masticatory myalgias come in various forms. Although some are trivial, others are disabling. Since a comorbid ailment may have a major impact on the patient's course, appropriate consideration is in order. Pooling the heterogeneous group of masticatory muscle pain conditions under one label is misleading. Differences between the various forms need to be recognized by health care providers to prevent overtreatment of the trivial forms and undertreatment of the chronic, disabling masticatory muscle pain conditions. Many of the older etiologic concepts that have "justified" specific treatments no longer appear to have sufficient support to be taken seriously.
REFERENCES
 1.  Dworkin SF, LeResche L.  Research diagnostic criteria for temporomandibular disorders: review, criteria, examinations and specifications, critique. J Craniomand Disord 1992;6:301-55.
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(40) BLANK PAGE
Assessing Physical and Behavioral
Outcomes of Treatment
Linda LeResche, Sc.D.

 Temporomandibular disorders (TMD) are musculoskeletal pain conditions affecting the temporomandibular joint (TMJ) and/or muscles of mastication, that typically run a recurrent or chronic course. A number of approaches to assessing TMD treatment outcomes are generic to the assessment of treatment outcomes for any recurrent or chronic pain. However, because the specific structures involved in TMD differ from those in other pain conditions, assessment of TMD outcomes relating to physical signs and symptoms will also make use of approaches specific to TMD.
 There is now overwhelming consensus that persistent pain conditions involve not only biologic but also psychological and social components and that assessment approaches must consider all these dimensions. We have proposed a model for understanding chronic and recurrent pain conditions that is heuristic for organizing existing research in this area and for identifying gaps in our current knowledge base.1  The model suggest that chronic pain involves the dynamic interaction of nociception (i.e., the physiologic processes involved in responding to noxious stimuli, including neurotransmission and modulation of pain-related signals), pain perception, appraisal of the cognitive and affective meaning of pain, pain-related behavior, and social rules for persons with pain within the context of the family, the workplace, the health care delivery system, and the social welfare system.
 Management of TMD problems can be directed at any of these levels, and consequently, the outcomes of treatment must at a minimum be evaluated in terms of the specific pain outcomes that the treatments are designed to influence. In addition, because of the multidimensional nature of pain phenomena, assessment of outcome at other levels is also necessary. For example, a narcotic analgesic medication might be quite effective for decreasing perception of pain intensity but have addictive properties and keep the patient drowsy and unable to function in a work role. Thus, at the levels of pain behavior and social role, the outcomes of treatment with this medication would not be considered optimal. This presentation addresses the availability of reliable and valid assessment approaches at each of these levels, identifies gaps in our assessment procedures, and briefly discusses methodologic issues related to research design.
CLINICAL SIGNS AND SYMPTOMS (NOCICEPTION AND PAIN PERCEPTION)
 Signs that are thought to indicate the pathologic processes involved in various TMDs include limitations in the range of mandibular motion, joint sounds (clicking.popping and crepitus), and deviation in mandibular path. In addition, pain on mandibular movement and pain on palpation of the TMJ and masticatory muscles are often assessed through clinical examination. The results of several studies evaluating the reliability of assessment for these measures are remarkably consistent2-4 and indicate that:
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  1.  All measures are more reliable when examination specifications are provided and examiners are calibrated.
2.  Range of motion measurement shows high interexaminer reliability; however, reliability of assessment of deviations in mandibular path is generally unacceptable using clinical methods.
  3.  Assessment of joint sounds can be conducted with acceptable reliability; reliability can be increased by identifying only sounds that are present on repeated assessments and by identifying only those sounds that are also detected by the subject.
4.  Muscle palpation pain and pain on mandibular movement can be assessed with marginally acceptable reliability, although reliability of assessment of palpation pain in intraoral muscles is sometimes unacceptably low.
 A number of the clinical signs and symptoms (e.g., joint clicking, intraoral muscle palpation pain) that are prevalent in TMD patients are also present in significant numbers of persons without TMD pain. This raises questions about the validity of these individual signs as pathognomonic indicators of TMD. However, changes in these clinical measures may still provide useful information concerning treatment effects in properly designed trials.
PAIN PERCEPTION
 Perception of pain involves not only the intensity but also the quality, duration, and location of the pain. Because pain quality, duration, and location are rarely used as outcome measures, this review focuses on measures of pain intensity. Self-reporting instruments developed to assess pain intensity include verbal descriptor scales, visual analog scales and numerical rating scales.5 Such scales have been used for a variety of pain conditions, and their reliability appears to be similar across pain sites. Since the patient's self-report is taken as the "gold standard" in pain research, the validity of these approaches is assumed. In addition to traditional self-reporting approaches, psychophysical stimulus matching methods using experimental pain stimuli have been employed to develop internally consistent measures of clinical pain intensity.6  The psychometric properties of the resulting instruments are excellent, and these scale have been used extensively in research. However, the simultaneous direct scaling of experimental and clinical pain has rarely been used to assess outcome of treatment, probably because these approaches are time-consuming and logistically difficult.
PAIN APPRAISAL
 Cognitive aspects of pain appraisal include explanatory models for pain, pain coping, and self-efficacy for controlling pain. Although these cognitive aspects have rarely been targeted as outcomes in treatment trials, interventions directed at modifying pain-related cognitions have been conducted for TMD as well as other chronic pain problems. Psychometrically sound scales for the assessment of pain coping are available.7,8  Assessment approaches for other aspects of pain-related cognitions are less well developed.
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 Modifications of the appraisal of the affective aspects of pain is frequently a primary focus of pain treatment trials or is a secondary focus, after pain intensity. The affective dimension of pain can be measured using self-reporting approaches similar to those employed to assess pain intensity (e.g., visual analog scales, verbal descriptor scales, and instruments derived using psychophysical methods).5 In addition, numerous standardized instruments are available to assess various aspects of psychological distress (e.g., depression, anxiety) that frequently accompany pain.
PAIN BEHAVIOR
 Assessment in the pain behavior domain includes evaluation of activity level, expressive behaviors, pain-related modifications of motor behaviors (e.g., guarding bracing), use of medications, and use of health services. Pain behaviors encompass a broad range of activities that are usually measured either directly or through the assessment of automated records, rather than through a self-report. Although direct observations of pain behavior outcomes is sometimes impractical, measures sufficiently sensitive to detect the effects of treatment interventions are available for all the classes of pain behavior described here.9.10
SOCIAL ROLES
 Global pain-related disability (e.g., disability days, pain interference) may be assessed through a review of records or by a number of self-reporting approaches.11,12  A disability scale specific to activities of the orofacial region that may be impaired in TMD is also available,13 although experience with this scale is limited. Quality of life measures have been applied to populations of TMD patients over time;14 however, the effects of specific management approaches on quality of life have not been assessed systematically.
PATIENT SATISFACTON
 In addition to pain outcomes, patient satisfaction with TMD treatment is frequently measured in clinical studies. However, the approaches to assessing patient satisfaction have varied widely and have not generally been systematic across studies. Development of common patient satisfaction measures for use across treatment domains, as well as across pain conditions, would be a contribution to this field.
MULTIDIMENSIONAL MEASURES
 Several assessment approaches are available that tap multiple levels of pain assessment. These include some scales used for a number of pain conditions (e.g., the McGill Pain Questionnaire15 the Multidimensional Pain Inventory12) as well as some specific to TMD (e.g., the TMJ Scale.)16 Recently, standardized research diagnostic criteria for various subtypes of temporomandibular disorders have been formulated17 and accepted by experts from a number of institutions as a working set of common measures. This dual axis system involves both a clinical diagnosis and a psychosocial assessment. The psychosocial assessment by and large involves use of standardized measures with know psychometric properties. Work on the reliability and validity of the clinical diagnostic criteria.
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and their utility as treatment outcome measures is just beginning, and further research in this area is required.
ISSUES IN REGION DESIGN
 In evaluating physical or behavioral outcomes, randomized trials with appropriate control groups (i.e., persons receiving no treatment or a standard treatment) are needed to determine whether changes in pain and interference after treatment are attributable to the effects of the experimental treatment. Randomized trials, rather than observational studies, are necessary for two reasons: (1) Since TMD pain is frequently an episodic condition, improvement after receiving a specific treatment may be attributed to the effects of the treatment intervention when, in fact, it could be largely a result of the natural history of the pain condition.18 (2) It is difficult to drawn firm conclusions about treatment effectiveness based on a nonrandomized comparison because differences in outcomes may be due to preexisting differences in prognosis that are unmeasured at baseline.19  Adequate sample size is also a necessity, since small studies are likely to product inconclusive results.20  An additional design consideration is the timing of measurement to include appropriate baseline evaluation, as well as sufficient followup periods to assess the long-term effects of treatment for these pain conditions that are likely to run a concurrent course.
REFERENCES
  1.  Dworkin SF, Von Korff MR, LeResche L. Epidemiologic studies of chronic pain: a dynamic-ecologic perspective. Ann Behav Med 1992;14:3-11.
  2.  Dworkin SF, LeResche L, DeRouen T. Reliability of clinical measurements in temporomandibular disorders. Clin J Pain 4 1988;89-99.
3.  Goulet JP, Clark GT, Clinical TMJ examination methods. J Calif Dent Assoc 1990;18:25-33.
  4.  Widmer CG. Physical characteristics associated with temporomandibular disorders. In: Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular disorders and related pain conditions. Seattle: IASP Press, 1995;161-74.
5.  Jensen MP, Karoly P. Self-report scales and procedures for assessing pain in adults. In: Turk DC, Melzack R, eds. Handbook of pain assessment. New York: Guilford Press, 1992;135-51.
  6.  Price DD, Harkins SW. Psychophysical approaches to pain measurement and assessment. In: Turk DC, Melzack R, eds. Handbook of pain assessment. New York: Guilford Press, 1992;11-34.
  7.  Rosenstiel AK, Keefe FJ. The use of coping strategies in chronic low back pain patients: relationship to patient characteristics and current adjustment. Pain 1983;17:33-40.
8.  Brown GK, Nicassio PM. Development of a questionnaire for the assessment of active and passive coping strategies in chronic pain patients. Pain 1987;31:53-64.
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  9.  Fordyce WE. Behavioral methods in chronic pain and illness. St. Louis: C.V. Mosby Co., 1976.
  10. Keefe FJ, Dolan E. Pain behavior and pain coping strategies in low back pain and myofascial pain dysfunction syndrome patients. Pain 1986;24:49-56
  11. Von Korff M, Ormel J. Keefe FJ, Dworkin SF. Grading the severity of chronic pain. 1992;50:133-49.
  12. Kerns RD, Turk DC, Rudy TE. The West Haven-Yale Multidimensional Pain Inventory (WHYMPI). Pain 1985;23:345-56.
  13. Stegenga R. Temporomandibular joint osteoarthrosis and internal derangement: diagnostic and therapeutic outcome assessment. Thesis, University of Groningen, 1991.
  14. Reisine ST, Weber J. The effects of temporomandibular joint disorders on patients' quality of life. Community Dent Health 1989;6:257-70.
  15. Melzack R, Katz J. The McGill Pain Questionnaire: appraisal and current status. In: Turk DC, Melzack R, eds. Handbook of pain assessment. New York: Guilford Press, 1992;152-68.
  16. Levitt SR, Lundeen TF, McKinney MW. The TMJ scale manual. Durham (NC): Pain Resource Center, 1994.
17. Dworkin SF, LeResche L. eds. Research diagnostic criteria for temporomandibular disorders: Review, criteria, examinations and specifications, critique. J Craniomand Disord Facial Oral Pain 1992;6:301-55.
  18. Whitney C, Von Korff M. Magnitude of regression to the mean in before-after treatment comparisons of chronic pain. Pain 1992;50: 281-5.
  19. Von Korff M. Health services research and temporomandibular pain. In: Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular disorders and related pain conditions. Seattle: IASP Press 1995;227-36.
  20. DeRouen TA. Statistical and methodological issues in temporomandibular disorders. In: Sessle BJ, Bryant PS, Dionne RA, eds. Temporomandibular disorders and related pain conditions. Seattle: IASP Press, 1995;459-65.
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Occlusal Adjustment
Pentti Kirveskari, D.D.S., Ph.D.

 In the present context, occlusal adjustment refers to the reshaping of the occluding surfaces of teeth to redistribute the functional loading and (1) achieve axial load at least on the teeth posterior to the canine when biting down to guided and unguided centric positions and (2) eliminate tooth guidance (contacts on inclined planes) from the posterior teeth in all jaw excursions from the centric positions.
 The controversy over occlusal adjustment involves two separate questions: etiology and therapy of temporomandibular disorders (TMD). The role of occlusal factors in the etiology of various TMDs is denied by some, considered minor at best by others, and major by still others. Although a lack of any causal role in the etiology would not necessarily disqualify occlusal adjustment as a treatment modality, a causal role proven beyond reasonable doubt is likely to have a bearing on the choice between alternative treatment modalities.
 When evaluating epidemiologic studies and clinical trials on the relationship between occlusion and TMD, assumptions concerning the distribution of the variables studied in the population at large should be considered as well as the nature of the presumed causal relationship.1-3
 The majority of studies on occlusion do not seem to consider the possibility that the presumed risk from occlusion can be practically universal. In the light of evolutionary biology, such an assumption is not unrealistic. Moreover, the dose-response is likely to be low when the risk is quantified by conventional methods in clinical dentistry.
 Causal inference from epidemiological studies is not simple.4 We are testing the hypothesis that the presumed risk from occlusion is a nonsufficient cause of TMD. In practice, studies of such a risk factor need to be longitudinal and, if the factor is universal, to involve an intervention.
 We have conducted two double-bind clinical trials on healthy volunteers, and a third one is in its final stage. The basic design has been similar in all of them. In the first one, prophylactic occlusal adjustment or mock adjustment was performed on first- and second-year dental students who were considered not to have manifest TMD. Two years later, the students answered questions concerning symptoms of TMD, and they clinically examined. Increase in symptoms and signs was greater in the students who underwent mock grinding than in the students who received the real adjustment.5
 In the second study, a similar intervention involving limited occlusal adjustment or mock adjustment in 5-,10-, and 15-year old children was made. The occlusal adjustment and the mock adjustment were repeated once every 12 months with followup times of 5 years in the younger groups and of 2 years in the oldest group. Initially, occlusal interferences and clinical signs of TMD were unassociated, but after 2 years a consistent and statistically significant association could be observed,6,7,
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 Our ongoing study on nonpatient adolescents and young adults8 is designed to test the hypothesis that the elimination of or decrease in the presumed occlusal risk will reduce the incidence of TMD. We define a "case" operatively as a subject spontaneously demanding treatment for symptoms of TMD with simultaneous clinical muscle and/or joint signs. To date, the demand for treatment of TMD has almost exclusively come from the placebo group, yielding a statistically significant difference.
 We have also tested occlusal adjustment in patients suffering from TMD, from chronic headaches, and from chronic neck and shoulder pain.
 A group of workers suffering from TMD and granted sick leave for head and/or neck pain underwent occlusal adjustment. Significant reductions were observed in the utilization of sick leave and in its length during the posttrreatment year when compared with nontreatment control patients suffering from TMD.9
 Forssell et al. conducted a double-blind clinical trial on headache patients initially examined by a neurologist, who also grouped the patients into three categories: those with tension headache, classical migraine, and combination headache.10  The patients were then randomly assigned to a treatment group receiving occlusal adjustment, amended in a few cases with an occlusal splint, and to a placebo control group receiving mock grinding. The observation period was on average 4 months in the placebo group and approximately 8 months in the treatment group.
 The patients suffering from classical migraine responded equally well in both groups. The intensity of tension headache and combination headache was significantly lower in the treatment group than in the placebo group. Also, the frequency of headaches was significantly lower in the treatment group when the classical migraine group was excluded from the calculation.
      Karppinen's double-blind study design involved 20 carefully matched pairs of patients seeking treatment for chronic neck and shoulder pain.11  Prior to the trial, all of them received ordinary dental treatment for caries and periodontal disease to exclude possible confounding effects. All patients received routine medical treatment for their condition: physiotherapy and instructions for home exercise. In addition, one patient in each pair received occlusal adjustment and the other mock grinding. The response was evaluated by the patients on a VAS-scale, by physiotherapists, and by a dentist. Also electromyography (EMG)-recordings were made of masseter, temporalis, sternomastoid, and trapezius muscles.
 At 6 weeks after treatment the response was very good regardless of the type of treatment. However, at 12 months significant differences in several variables emerged because of reoccurrence of symptoms in the placebo group. Practically all variables used to measure the response favored the treatment group. At 60 months the difference between the groups still remained, but was statistically significant for the overall VAS-score, and in the 14 pairs that were available for examination, for neck pain and stiffness on movement. Remarkably, there was a significant correlation between the number of contacts on light clenching at centric occlusion and the VAS-score in the treatment group.
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 In conclusion, failure to recognize the universal nature of occlusal risk factors and incorrect causal inference appear to explain past deficiences in epidemiologic as well as treatment studies. Our results contradict the contentions that occlusion plays at best a minor role in the etiology of TMD, and that occlusal adjustment is at best only as effective as the so-called reversible treatment modalities. Instead, occlusal adjustment according to Dawson's principles appears to be safe and to have long-lasting effects in treating TMD patients. 12  It is therefore an essential part of the treatment regimen. In view of the probable cause role of occlusal factors there is an urgent need for an evaluation of possible detrimental long-term effects of all occlusal restorative work. A systematic search for variables sufficiently sensitive and specific to be useful in identifying risk groups, and cost-efficiency studies of occlusal adjustment are called for.
REFERENCES
1.  Alanen P, Kirveskari P. Disorders in TMJ research. J Craniomand Disord Facial Oral Pain 1990;4:223-7.
  2.  Kireveskari P, Alanen P. Scientific evidence of occlusion and craniomandibular disorders. J Orofacial Pain 1993;7:235-40.
  3.  Kireveskari P, Alanen P. Odds ratio in the estimation of the significance of occlusal factors in craniomandibular disorders. J Oral Rehabil 1995;22:581-4.
  4.  Susser M. What is a cause and how do we know one? A grammar for pragmatic epidemiology. Am J Epidemiol 1991;133:635-47.
  5.  Kireveskari P, Le Bell Y, Salonen M, Forssel H, Grans L. Effect of elimination of occlusal interferences on signs and symptoms of craniomandibular disorder in young adults. J Oral Rehabil 1989b;16:21-
6.  Kirveskari P, Alanen P, Jamsa T. Association between craniomandibular disorder and occlusal interferences. J Prosthet Dent 1989a;62:66-9.
  7.  Kirveskari P, Alanen P, Jamsa T. Association between craniomandibular disorders and occlusal interferences in children. J Prosthet Dent    1992;67:692-6.
   8.  Kirveskari P. The role of occlusal interferences in the etiology of CMD. Paper presented at the 1996 Annual Meeting of the American Equilibration Society, Chicago, 1996.
  9.  Kirveskari P, Alanen P. Effect of occlusal treatment on sick leaves in TMJ dysfunction patients with head and neck symptoms. Comm Dent Oral Epidemiol 1984;12:78-81.
  10. Forssell H, Kirveskari P, Kangasniemi P. Changes in headache after treatment of mandibular dysfunction. Cephalagia 1985;5:229-36.
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11. Karppinen K. Purennan hoito osana kroonisten paa-, ja hariakipujen hoitoa. Annales Universitatis Turkuensis, Ser C TOM, 114, 1995 ("Occlusal treatment as a part of treatment of chronic head, neck and shoulder pain," summary in English).
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The Role of Bioelectronic Instrumentation in the Documentation and Management of Temporomandibular Disorders
Barry C. Cooper, D.D.S.

THE STRUCTURAL/PHYSICAL BASIS OF TEMPOROMANDIBULAR DISORDERS
 To understand how the management of temporomandibular disorders (TMD) can be improved by the use of electronic quantification of masticatory function, it is necessary to first understand the essential pathophysiology of TMD. Temporomandibular disorders comprise a group of disorders involving hard and soft tissues associated with mandibular and masticatory function. Commonly, TMDs coexist with other musculoskeletal disorders within the head and neck area. The total management of these composite, multifaceted, and multicausal conditions may require the diagnostic and therapeutic intervention of a multidisciplinary team of health care providers.
 The reason for dentists' becoming involved on this team underscores the need to measure and quantify masticatory function objectively. TMD is a musculoskeletal disorder that affects alterations in the structure and/or function of the temporomandibular joints (TMJs), the dentition and its supporting structures, and its complex neuromuscular system. The basis of TMD is a physical or structural problem arising from an imbalance in the delicate working relationship of the mandible and skull with the muscles that posture and move the mandible into dental occlusion. This imbalance can result in muscle fatigue, spasm and/or joint dysfunction, and changes in the dentition.
 Psychosocial factors may contribute to the exacerbation or perpetuation of TMD; however, an underlying physical or structural predisposition or disorder must be present. If a patient has a healthy masticatory apparatus involving joint function, muscle function, and occlusion, the same stress would most likely produce effects in the human body other than TMD. Few data support those who believe TMD is principally a psychosocial disorder.
THE DIAGNOSIS AND TREATMENT DECISION
 Each TMD patient possesses a unique set of symptoms, clinical presentation, and history. The disorder may principally involve the TMJ or the masticatory muscles or both. The initial diagnosis of TMD and decision to institute treatment must be based on a comprehensive history, a clinical examination, and the clinical judgment of the health care provider.
 Once a clinical decision to institute treatment is made, the therapeutic plan must be based on an evaluation of the physical characteristics of the patient's illness specific to that patient. This process is greatly enhanced by the utilization of techniques that permit objective measurements of mandibular and masticatory function. This reduces the reliance on subjective assessment of clinically observed phenomenon and improvement, which are inaccurate, unreliable, and not reproducible. Objective measurements also aid in monitoring treatment results in a quantifiable manner and in gauging final outcome.
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THE ROLE OF OBJECTIVE ELECTRONIC MEASUREMENTS
 TMD involves three primary components: dental occlusion, mandibular movement, and masticatory muscle/TMJ function. Objective data are obtained of the patient's current masticatory function or dysfunctional before treatment. A therapeutic plan can then be created to effects the needed changes and to analyze the outcome of treatment for efficacy. Electronic instrumentation provides the reproducible objective data needed for this task.1  The specific therapeutic appliance fabricated remains the decision of the dentist, but it is now based not only on the nature of the patient's condition and the philosophy of treatment but also on this objective information. The ability to measure thus transcends treatment philosophies and becomes a common language for clinicians to compare different patient management strategies.
 The function of the electronic instruments if described followed by a specific treatment application  to demonstrate the utility of this measurement capability.
 Electronic mandibular tracking records the quality and nature of mandibular movement during function, the rest position of the mandible, and the movement of the jaw from rest to occlusion.2
 Surface/electromyography permits evaluation of resting muscle activity at presentation, after relaxation, and after a treatment intervention. Antagonistic muscle groups, the mandibular elevators and depressors, can be simultaneously monitored. In addition, functional activity can be evaluated to determine effectiveness of function and the symmetry of function of various occlusal relationships, including the presenting habitual occlusion as well as any therapeutically corrected occlusion.3
 The combination of recordings can be employed to evaluate muscle status at various habitual and therapeutically induced rest and functional positions. This enables the dentist to scrutinize the patient as treatment decisions are being continuously made throughout treatment.
 Electrosonography is used to record sound vibrations emanating from the TMJ at presentation and after therapeutic intervention. The electronic recording of joint sounds is more sensitive than that observed by auscultation with a stethoscope. This analysis aids in determining the presence of conditions within the TMJ that produce vibration associated with the specific points in opening and closing and help determine the need for more expensive and sometimes more invasive diagnostic and therapeutic procedures.4
 A fourth electronic instrument is a TENS neuromuscular stimulator. Employing low frequency, low voltage, transcutaneous electrical neural stimulation (TENS) effectively relaxes hyperactive masticatory muscles commonly found in TMD patients.5  TENS is valuable in achieving a true rest position of the mandible; this position can serve as a reference point for the evaluation of occlusion and for therapeutic intervention employing orthotic appliances.
 The instruments described above do not comprise all the diagnostic instruments and procedures employed. The various imaging techniques, psychometric testing, and arthroscopic examination that are frequently employed will not be discussed.
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THE GOAL OF TREATMENT
 The goal of therapy for the physical component of a TMD is to establish a healthy functioning relationship between teeth, TMJ, and the neuromusculature involved in mandibular function. When this relationship can be objectively and reliably measured, the doctor can confirm and refine clinical impressions. Throughout the treatment period during which these instruments are used, the dentist objectively measures the muscle function associated with a targeted therapeutic occlusion position. These measurements are used to decide what treatments should be employed and when they should be modified and discontinued. Thus, the clinician can separate the effects of the therapeutic physical intervention from psychosocial component of the disorder that may be present.
NEUROMUSCULAR TREATMENT POSITION
The position of occlusion arrived by a TENS-stimulated mandibular movement originating at a resting mandibular position is called a neuromuscular occlusal position. A therapeutic jaw position can be selected beginning with the rest position of the mandible, achieved by TENS stimulation and recorded by composite electromyography and electronic jaw tracking. Then a therapeutic mandibular orthosis with a precise anatomic surface can be fabricated and tested for accuracy of position and muscular function.6  The selection of this treatment position will be illustrated by a representative case.
 Selected data from research studies employing TENS, electromyography, computerized jaw tracking, and neuromuscular therapeutic occlusion will be presented. These data will illustrate the efficacy of TENS stimulation in relaxing musculature and the utility of electronic instrumentation in obtaining a durable, stable, and effective therapeutic occlusion.
CONCLUSION
 Bioelectronic measurements can be used to create objective milestones in planning and implementing a treatment plan and evaluating the outcome of treatment. Although the specific protocol illustrated reflects the neuromuscular occlusion treatment philosophy, different protocols can be tailored to provide relevant data for other treatment strategies. The challenge is to develop protocols in which each specific tests adds to or refines the treatment plan. Objective measurement of mandibular and masticatory muscle function provides information essential in establishing the status of patients before TMD therapy is instituted by providing quantification and documentation of key elements of their illness.
REFERENCES
  1. Cooper BC. The role of bioelectronic instruments in the management of TMD. NY State Dent J 1995 Nov;48-53
  2.  Cooper B. Alleva M, Cooper D, Lucente F. Myofacial pain dysfunction: analysis of 476 patients. Laryngoscope 1986;96(10):1099-1106.
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  3.  Cooper B, Cooper D, Lucente F, Electromyography of masticatory muscles in craniomandibular disorders. Laryngoscope 1991;101(2):150-7.
  4.  Ishigaki S, Bessette R, Maruyama T. A clinical study of temporomandibular (TMJ) vibration in TMJ dysfunction patients. J Craniomand Pract 1993;11(1):7-13.
  5.  Thomas NR. The effect of fatigue and TENS on the EMG mean power frequency. In: Bergamini M, ed. Pathophysiology of head and neck musculoskeletal disorders. Front oral physiology. Vol. 7. Basil: Karger, 1990;7:162-70.
6.  Hickman D, Cramer R, Stauber, W. The effect of four jaw relations on electromyographic activity in human masticatory muscles. Arch Oral Biol 1993;38(3):261-4.
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Modern Concepts of Occlusal Disease and the Efficacy of Occusal Therapy
Glenn T. Clark, D.D.S.,M.S.; Yoshihiro Tsukiyama, D.D.S., Ph.D.; and Michael Simmons, D.D.S.

 The request from the National Institute of Dental Research (NIDR) steering committee regarding this conference was to "review the efficacy of occlusal therapy for the management of TM disorders." Although we will respond to this charge, it also seems more logical to "review the efficacy of occlusal therapy for the management of occlusal disorders." This modified charge would first require that a set of modern definitions for these clinical problems be established. This is important because the traditional way that occlusal disorders are described tends to be based strictly upon structural deviation from ideal form--a concept of disease that is too limited. Second, most of the modern descriptions for temporomandibular disorders (TMD) no longer include occlusal disorders within their domain. As the concepts of TMD have evolved over the last three decades, those patient complaints which were largely centered around the occlusion (e.g. uncomfortable bite, sore teeth, unstable occlusions, etc.) have not been relegated to the status of ancillary symptoms. Despite this trend toward the exclusion of occlusal disorders from the TMD domain, the historical linkages between TMD and occlusal therapy are very strong. In fact, if everyone agreed that occlusal disorders were nonexistent entities, there would be no need for any presentations on occlusion at this conference. However, such an agreement is unlikely and clearly inappropriate, since many patients have substantial complaints about an uncomfortable bite, sore teeth, or an unstable occlusion that need to be addressed.
 After establishing the parameters of the problem, the main focus of this review article is to discuss and critically review the available treatment literature on occlusal disorder detection techniques and occlusal therapy procedures. It is necessary to examine both the diagnostic and therapeutic aspects of the issue, since a problem must be defined before it can be treated. Second, it does not hold that because we agree that a problem exists, we automatically know its best treatment. By looking at the "pro and con" efficacy evidence for the largely biomechanical procedures that comprise occlusal therapy and how they interface with those conditions defined previously as occlusal disorders and TMD, conclusions can be drawn about which treatments are logical and appropriate.
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Orthodontic Treatment and Tempormandibular Disorders
James A. McNamara, Jr., D.D.S., Ph.D.

     This paper addresses the relationships between orthodontic treatment and temporomandibular disorders (TMD). Although long recognized by orthodontists as a clinical problem, the diagnosis and treatment of TMD were not emphasized within the specialty until about the mid-1980's. Traditionally, scant mention was made of TMD treatment in the curricula of graduate programs in orthodontics, and only cursory examinations of the temporomandibular joint region were conducted in routine orthodontic clinical examinations. The interest of the orthodontic community in TMD, however, was awakened abruptly in the late 1980's following litigation that alleged that orthodontic treatment was the proximal cause of TMD in orthodontic patients, with substantial monetary judgments being awarded to several plaintiffs. The outcome of these court cases resulted in an heightened interest in TMD among orthodontists, as well as among other dental professionals, and in a burst of research activity investigating the relationship of orthodontic intervention to TMD.
 Prior to the mid-1980's, surprisingly few methodologically sound clinical studies regarding the relationship between orthodontic treatment and the TMD had been published. In a comprehensive review of the literature on this subject published between 1966 and 1988, Reynders1  separated 91 publications into three categories: viewpoints articles, case reports, and sample studies. The most numerous were viewpoint articles (n=55), publications that usually were anecdotal in nature, stating the opinion of the author regarding the orthodontic-TMD relationship. Few (or, more commonly, no) data were presented to support the opinion. The second most frequent type of article (n=30) was the case report, a category of publication that described the influence of certain orthodontic treatment modalities used in one or more patients on the signs and symptoms of temporomandibular dysfunction. the least numerous (n=6) were in the third category of sample studies, investigations that reported data from large sample groups. These studies were of variable quality, often having minor or major methodologic problems and limitations. Since 1988, however, a substantial number of clinical investigations have considered the association of orthodontics and TMD.
 Viewpoint articles, of course, are not suitable for critical evaluation of associations between two entities such as orthodontic treatment and TMD; they are, however, useful in identifying questions that may be worthy of scientific investigation. Some of these questions are considered below.
What is the Prevalence of Signs and Symptoms of TMD in Orthodontically Treated Populations?
 Numerous epidemiologic studies have examined the prevalence of signs and symptoms associated with TMD in a wide variety of subject populations (see McNamara et al.2 for a review). The prevalence has been shown to be of significance, with an average of 32 percent reporting at least one symptom of TMD, and an average of 55 percent demonstrating at least one clinical sign.
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 Cross-sectional epidemiologic studies of specific adult nonpatient populations indicate that at any given time, between 40 and 75 percent have at least one sign and about one-third report at least one symptom of TMD. The point prevalence of symptoms in children and teenagers is lower, about 12-20 percent.
 Because of the longitudinal nature of orthodontic treatment (e.g. 2-3 years for adolescents; 5-7 years for patients starting a two-phase treatment protocol in the early mixed dentition), an understanding of the changes in the signs and symptoms of TMD in a healthy population is essential. Several investigators have noted that signs and symptoms of TMD generally increase in frequency and severity, beginning in the second decade of life. Others have noted that the incidence of joint sounds in young adults in their late teens can be as high as 17.5 percent over a 2-year period. Thus, the occurrence of joint sounds during orthodontic treatment must be considered within the context of longitudinal changes in a comparable untreated population studied during the same interval.
Does Orthodontic Treatment Lead to a Greater Incidence of TMD?
 Two of the first investigations sponsored by the National Institutes of Health to consider the relationship between orthodontics and TMD3,4 considered the prevalence of TMD in large groups of subjects who had undergone orthodontic treatment at least 10 years previously. The results of these two studies provide evidence in support of the concept that orthodontic treatment performed during adolescence generally does not increase or decrease the risk of developing TMD later in life. Other studies of the long-term effects of orthodontic5-7 concluded that a relationship could not be established between orthodontic treatment in their patient population and either the onset or the change in severity of TMD signs and symptoms.
 Relatively few prospective studies have examined the relationship of orthodontics to TMD. The two major investigations have been conducted at the University of Gronigen in the Netherlands 8,9 and at the University of Iowa.10  In the latter study, Kremenak and coworkers10 reported no significant differences between mean pretreatment and posttreatment Helkimo scores for any of the various groupings. Ninety percent of the patients had Helkimo scores that remained the same or improved, and 10 percent had scores that worsened. Kremenak and colleagues concluded that the orthodontic treatment experienced by their sample was not an important etiologic factor for TMD.
Does the Type of Appliance (e.g. fixed vs. functional; orthodontic vs. orthopedic) Make a Difference?
 In the other major longitudinal study of this subject, Dibbets and colleagues 8,9 followed 171 patients treated with Begg, activator or chin cup therapy. The pretreatment documentation revealed a strong dependence of the prevalence of signs and symptoms on age: from 10 percent at age 10 years, sign increased to 30 percent, whereas symptoms increased to over 40 percent at age 15. The investigators also noted that at the end of treatment, the fixed appliance group had a higher percentage of objective symptoms than did the functional group, but no difference existed at the 20-year followup.9  A lack of association between orthodontic treatment and TMD also was noted by Janson and Hasund11 in a study of patients 5 years posttreatment.
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Does the Removal of Teeth as Part of an Orthodontic Protocol Lead to a Greater Incidence of TMD?
 Viewpoint articles and texts, publications that are long on opinion and short on data, have strongly associated the extraction of premolars with the occurrence of TMD in orthodontic patients. The clinical studies8-10,12 that have dealt with this issue, however, have not show a relationship between premolar extraction and TMD. The findings of these investigations do not indicate a progression of signs and symptoms to more serious problems during treatment. Also, no increase in the risk of developing joint sounds was reported regardless of whether teeth were removed or not.
 The long-term effects of extraction and nonextraction edgewise treatments were compared in a group of patients with Class II, division 1 malocclusions who were identified by discriminant analysis as being equally susceptible to the two treatment strategies.13,14  In terms of a menu of 62 signs and symptoms (e.g., muscle palpation, joint function) that are commonly thought to be characteristic of TMD, there were no differences between extraction and nonextraction samples. A followup study15 that examined an additional sample of "clear-cut" patients (those in the tail of the distribution) also noted that both extraction and nonextraction samples demonstrated similar findings.
 The longitudinal studies at Iowa also have addressed this question. Kremenak and colleagues10 followed three groups of patients: Patients treated by nonextraction (40 percent), patients with four premolars extracted (38 percent), and patients with two upper premolars extracted (22 percent). No significant intergroup differences between mean pretreatment or posttreatment Helkimo scores were noted. A small but statistically significant improvement in Helkimo scores was observed posttreatment in both the nonextraction group and the four premolar extraction group.
 Dibbets and van der Weele8.9 followed 111 of the original 172 orthodontic patients in the Gronigen study over a 20-yer period. In this group, a nonextraction approach was used in 34 percent of the patients, four premolars were extracted in 29 percent, and other extraction patterns were used in the remaining 37 percent. Functional appliances were used in 39 percent, fixed appliances (Begg) were used in 44 percent, and chin cups were used in 17 percent of the patients. Symptoms increased from 20 to 62 percent; signs of clicking and crepitus increased from 23 to 36 percent after 4 years and then stabilized. In contrast to the findings from the first 10 years, during which was no difference between the three treatment groups with regard to clicking, after 15 years this symptom was seen more often in the premolar extraction group.8 The authors noted, however, the clicking was higher in the premolar extraction group before treatment was started and concluded that the original growth pattern, rather than the extraction protocol, was the most likely factor responsible for the TMD complaints seen many years posttreatment. These investigators also noted that for a substantial number of patients, signs and symptoms of TMD appeared and disappeared during the course of study. At the 20-year followup, the difference between groups had disappeared completely.9 They also noted that even though the overall incidence of symptoms increased with time, many previously symptomatic children were found to have become asymptomatic at the time of subsequent evaluation.
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Can Orthodontic Treatment Lead to a Posterior Displacement of the Mandibular Condyle?
 A number of viewpoint articles have asserted that a wide variety of traditional orthodontic procedures (e.g., premolar extraction, extraoral traction, retraction of upper anterior teeth) cause TMD symptoms by producing  a distal displacement of the condyle. Gianelly et al.16 used corrected tomograms to evaluate condylar position in both extraction and nonextraction patients. No differences in condylar positions were noted between groups. Luecke and Johnston 17 evaluated the pretreatment and posttreatment cephalograms of patients treated with fixed appliances in conjunction with the removal of two upper premolars. The results of this study indicated that the majority of patients (about 70 percent) undergo a forward mandibular displacement and a slight opening rotation of the mandible. The remainder of the sample had distal movement of the condyle. Incisor changes were essentially unrelated to condylar displacement during treatment. Recall studies13,15 also reported no differences between groups with regard to TMD signs and symptoms.
Should the Occlusions of Orthodontic Patients be Treated to Specific Gnathologic Standards?
 Several viewpoint articles have maintained that TMD may result from a failure to treat orthodontic patients to gnathologic standards that include the establishment of a "mutually protected occlusion" and proper seating of the mandibular condyle within the glenoid fossa (in contrast to the more anterior position of the condyle advocated by the so-called "functional orthodontists"). The gnathologists claim that nonfunctional occlusal contacts, when introduced through orthodontic treatment, can lead to signs and symptoms of TMD. Pullinger and coworkers18  reported that small occlusal slides, mostly under 1 mm., are common in asymptomatic subjects as well as TMD patients. Only when a slide between retruded cuspal position and intercuspal position becomes extreme (5mm or greater) does the odds ratio for disease increased. Thus, a modest slide following orthodontic treatment typically is within the adaptive capabilities of most patients. Sadowsky and BeGole3 and Sadowsky and Polson4 evaluated the prevalence of nonfunctional occlusal contacts in patients at least 10 years postorthodontic treatment. They noted a high incidence of such occlusal contacts in both orthodontic and control groups.
Does Orthodontic Treatment Prevent TMD?
 This last topic probably is the most difficult to investigate, given the prevalence of signs and symptoms of TMD in healthy individuals and the many types of orthodontic treatment philosophies, goals, and techniques in existence today. The question of whether orthodontic treatment can prevent TMD is complicated further by many of the unsubstantiated viewpoint articles that claim preventive capabilities of nonextraction treatment, functional appliances, and some of the more nontraditional orthodontic treatment protocols (e.g., second-molar extraction and third-molar replacement) that have been advocated vigorously.
 Most studies have compared treated and untreated populations have found no difference between groups in the occurrence of TMD signs and symptoms. One of the few investigations that found improved TMD health in a treated group was the sample studied by Egermark and Thilander.19 About one-third of the sample had received orthodontic treatment at the end of the final examination
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period. Bruxism awareness and subjective symptoms of TMD increased in all age groups, with symptoms slightly more pronounced in untreated individuals. The investigators also noted that clicking recorded at the first examination sometimes disappeared at subsequent examinations and that clicking sometimes appeared at subsequent intervals, regardless of whether or not the subject underwent orthodontic treatment. The Helkimo clinical dysfunction index outcome was lower in those undergoing orthodontic treatment than those who had not.
Summary
 The findings of current research on the relationship of orthodontic treatment to TMD can be summarized as follows:
Signs and symptoms of TMD occur in healthy individuals.
Signs and symptoms of TMD increase with age, particularly during adolescence. Thus, TMD that originate during treatment may not be related to the treatment.
Orthodontic treatment performed during adolescence generally does not increase or decrease the odds of developing TMD later in life.
The extraction of teeth as part of an orthodontic treatment plan does not increase the risk of TMD.
There is no increased risk for TMD associated with any particular type of orthodontic mechanics.
Although a stable occlusion is a reasonable orthodontic treatment goal, not achieving a specific gnathologic ideal occlusion does not result in TMD signs and symptoms.
No method of TMJ disorder prevention has been demonstrated.
REFERENCES
 1.  Reynders RM. Orthodontics and temporomandibular disorders: a review of the literature (1966-1988). Am J Orthod Dentofacial Orthop 1990;97:463-71.
2.  McNamara JA Jr, Seligman DA, Okeson JP. Occlusion, orthodontic treatment and temporomandibular disorders: a review. J Orofac Pain 1995;9:73-90.
 3.  Sadowsky C, Begole EA. Long-term status of temporomandibular joint function and functional occlusion after orthodontic treatment. Am J Orthod 1980;78:201-12.
 4.  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.
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 5.  Larrson E, Ronnerman A. Mandibular dysfunction symptoms in orthodontically treated patients ten years after completion of treatment. Eur J Orthod 1981;3:89-94.
 6.  Dahl BL, Krogstad BO, Ogaard B, Eckersberg T. Signs and symptoms of craniomandibular disorders in two groups of 19-year old individuals, one treated orthodontically and the other not. Acta Odontol Scand 1988;46:89-93.
          7.  Rendell JD, Norton LA, Gay T. Orthodontic treatment and temporomandibular disorders. Am J Orthod Dentofacial Orthop. 1992;101:84-7.
 8.  Dibbets JHM, van der Weele LT. Extraction, orthodontic treatment and craniomandibular dysfunction. Am J Orthod Dentofacial Orthop 1991;99:210-9.
 9.  Dibbets JHM, van der Weele LT. Long-term effects of orthodontic treatment, including extractions, on signs and symptoms attributed to CMD. Eur J Orthod 1992;14:16-20.
           10. Kremenak CR, Kinser DD, Harman HA. Menard CC, Jakobsen JR. Orthodontic risk factors for temporomandibular disorders (TMD). Am J Orthod Dentofacial Orthop 1992;101:13-20-,21-7.
 11. Janson M, Hasund A. Functional problems in orthodontic patients out of retention. Eur J Orthod 1981;3:173-9.
 12. Sadowsky C, Theisen TA, Sakols EI. Orthodontic treatment and temporomandibular joint sounds; a longitudinal study. Am J Orthod Dentofacial Orthop 1991;99:441-7.
 13. Paquette De, Beattie JR, Johnston LE Jr. A long-term comparison of non-extraction and bicuspid-extraction edgewise therapy in "borderline" Class II patients. Am J Orthod Dentofacial Orthop 1992;102:1-14.
 14. Beattie JR, Paquette DE, Johnston LE Jr. The functional impact of extraction and non-extraction treatments: a long-term comparison in "borderline," equally-susceptible Class II patients. Am J Orthod Dentofacial Orthop 1994;105:444-9.
 15. Luppanapornlarp S, Johnson LE Jr. The effects of premolar-extraction: a long-term comparison of outcomes in "clear-cut" extraction and nonextraction Class II patients. Angle Orthod 1993;63:257-72.
 16. Gianelly AA, Hughes HM, Wolgemuth P, Glidea G. Condylar positions and extraction treatment. Am J Orthod Dentofacial Orthop 1988;93:201-5.
 17. Luecke PE, Johnston LE Jr. The effect of maxillary first premolar extraction and incisor retraction on mandibular position: testing the central dogma of "functional orthodontics." Am J Orthod Dentofacial Orthop 1992;101:4-12.
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 18. Pullinger AG, Seligman DA, Gornbein JA. A multiple regression analysis of the risk and relative odds of temporomandibular disorders as a function of common occlusal features. J Dent Res 1993;72:968-79.
 19. Egermark I, Thilander B. Craniomandibular disorders with special reference to orthodontic treatment: an evaluation from childhood to adulthood. Am J Orthod Dentofacial Orthop 1992;102:28-34.
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Physical Medicine Modalities and Trigger Point Injections in the Management of Temporomandibular Disorders
Gerald J. Murphy, D.D.S.

           The use of physical medicine modalities and trigger point injections in the clinical management of orthopedic, musculoskeletal, and neurologic disorders has a long and successful history of application in the field of health care, Because the problems encountered in temporomandibular disorders (TMD) are within the framework of the pathologic entities and because TMDs are classified by the International Headache Society (IHS) under the 11th major classification of headache,1 the introduction and successful applications of these modalities and injections in dentistry have become routine.
           In addition to discussing trigger point injections, this presentation focuses on five physical medicine modalities: (1) high voltage stimulation (high voltage electrogalvanic stimulation, electrogalvanic stimulation, (2) transcutaneous electrical nerve stimulation (TENS), (3) iontophoresis, (4) ultrasound, and (5) manipulative therapy. A valid and reliable method of assessing treatment outcome is also described.
 Although these therapeutic modalities may be used as the sole treatment, they are typically part of a combination therapeutic routine. This routine may include such modalities as orthotic therapy, pharmacologic management, moist heat and/or cryotherapy, exercise therapy, and relaxation and/or behavioral management.2,3  When a combined approach is used, more rapid symptom relief, decreased treatment time, and overall superior therapeutic outcome result.5,6
HIGH VOLTAGE STIMULATIONS
 High voltage stimulators deliver a monophasic, twin peak waveform. Because of the short pulse, duration twin peak wave, high voltages with a high peak current but low average current can be achieved. These characteristics provide for patient comfort and safety in application. In addition, in contrast to low voltage direct current devices. thermal and galvanic effects are minimized.4,13,29
 High voltage stimulators have shown to be effective in reducing or eliminating muscle spasm and soft tissue edema, improving muscle re-education and trigger point therapy, and increasing blood flow to tissues with decreased circulation.4-12,29-31,72,74
TRANSCUTANEOUS ELECTRIC NERVE STIMULATION
 Transcutaneous electrical nerve stimulation (TENS), which was first introduced in the early 1950's, was used to determine the suitability of pain patients as candidates for the implantation of dorsal column electrodes. From this experience, researchers first discovered the effectiveness of the modality as a noninvasive pain reduction device.15
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 TENS units classically deliver an asymmetrical biphasic wave of 100-500 milliseconds pulse duration. TENS may be applied for extended periods, and the biphasic waveform eliminates undesirable chemical changes at the electrode placement sites.9.16.24
 Two modes of action are theorized for the efficacy of this modality. The first is based on the gate theory of pain first introduced by Melzac and Wall in their paper "Pain Mechanisms: A New Therapy"  in 1965. Based on this theory, electrical stimulation of the large myelinated A-alpha fibers inhibits the transmission of the smaller pain transmitting unmyelinated C-fibers and myelinated A-delta fibers. This inhibition takes place primarily in the substantia gelatinosa of the dorsal horn of the spinal column. These large A-fibers have a low threshold for stimulation and therefore are easily activated by TENS.9,16,29  The second theory is based on the body's production of endogenous opiates when subjected to certain types of electrical stimulation. 9.16.29
        TENS has shown to be effective in the management of both acute and chronic pain, 31 including pain of myofascial, neurologic, and articular origin.2, 15  Although TENS has more traditionally been used outside of the temporomandibular complex, application techniques for temporomandibular/cervical pain have been described. 14,16,17
IONTOPHORESIS
 Iontophoresis is a process for delivering medications to tissues by means of a low amperage direct current.2,4,5,9,18  When salts are dissolved, ionized, or charged, particles are formed in an aqueous solution; this process is called dissociation or ionization.9,18
 Ionized medications or chemicals do not ordinarily penetrate tissues. If they do, it is not normally at a rate rapid enough to achieve therapeutic levels.18  This problem can be overcome by providing a direct current energy source that provides for penetration and transport.9,18  Based on the electrical principle that like charges repel whereas unlike attract,  negatively charged ions are repelled from a negative electrode and attracted toward the positive and positive ions are repelled from the positive electrode and attracted toward the negative.9, 18
 The application of iontophoresis in the treatment of TMD has proven to be a valuable treatment modality. Delivery of local anesthetics and anti-inflammatory agents, as well as vasoconstrictive agents to maintain medicament concentration, to the temporomandibular joint (TMJ) and associated musculature as well as ligaments, tendons, and nerve tissue has proven to be of therapeutic benefit.2,4,5,9,18-22,74,76,77,79
ULTRASOUND
 Ultrasound is acoustic energy in the ultrasonic range.9,23  This form of mechanical energy has application in diagnosis and treatment.23  Therapeutic ultrasound produces thermal and mechanical changes within tissues in the ultrasound field.9,23,24
 The thermal effects are seen as deep heating in the tissue, and the mechanical effects of cavitation and protoplasmic streaming are noted.9,23-27,29
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 Therapeutic ultrasound finds application in the treatment of TMD because of its ability to increase joint range of motion, increase tissue healing, increase extensibility of collagen tissue, reduce muscle spasm,  relieve pain, and help resolve chronic inflammation.2,5,9,23,29,30,72,74-80.  In addition, therapeutic ultrasound enhances transdermal delivery of medications through a phenomenon termed phonophoresis.2,5,9,23,25,28,29,72,74-80  The medication (i.e., anti-inflammatory is applied topically to the area to be treated, and the ultrasound field is applied to the area.
MANIPULATIVE THERAPY
 Manipulative or manual therapy is an adjunctive therapy that may be used as a singular modality or in combination with other therapeutic modalities used in the treatment of TMD. It is typically used to improve function between articulating surfaces of joints, eliminate soft tissue contracture, restore resting length of muscles, or improve the function of joints and soft tissue. Commonly employed approaches include massage, manual mobilization, and spray and stretch.2,5,9,72-75,77-79
 Massage increases mobility of soft tissue, improves blood and lymph flow, and reduces pain.5,33  Manual mobilization is used to improve the function of the TMJ and is particularly useful when contractures are present after surgery.5,9,30,31  Spray and stretch is a commonly used procedure for deactivating and eliminating trigger points and restore muscle resting length.5,30,34-37,73-75,77-79
 Numerous specific manipulative techniques have been developed to address specific problems, but most can be classified under the general areas mentioned. When dysfunction is present in osseous articulating surfaces or in soft tissue, manual therapy proves to be invaluable.
TRIGGER POINT INJECTION
 A trigger point is a focus of hyperirritability in a tissue that, when compressed, is locally tender and, if sufficiently hypersensitive, gives rise to referred pain and tenderness and sometimes to referred autonomic phenomena and distortion of proprioception.34
 According to Popelianskii, myofascial trigger points begin as neuromuscular dysfunction but may develop into a histologically demonstrable dystrophic phase.34  Trigger points are common in those soft tissues involved with TMD.38-53
 Trigger point development has been associated with direct trauma, sustained contraction (i.e., muscle spasm or prolonged splinting), and acute strain, to name a few causes.34
 Once formed, trigger points are self-perpetuating. Although they may cycle between active and latent, they are typically not self-resolving. Physical medicine modalities, as previously discussed, are frequently successful at eliminating trigger points. Some, however, respond only to localized needling, typically with the introduction of a local anesthetic and/or inflammatory agent.73    When the trigger point is entered, there is a typically a local twitch response of the muscle34 and a demonstration of the characteristic pain referral pattern. This method of trigger point deactivation has been shown to have high clinical success.
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ASSESSING TREATMENT OUTCOME
 The methodologically sound and statistically consistent assessment of treatment outcomes has become crucial to the field of TMD. Although subjective evaluation of symptom change has been the norm in the past, more sophisticated symptom assessment tools are now available and are being widely used.
 Various tests have been introduced over the last several years. One such test, the "TMJ Scale,"  is a validated psychometric assessment tool supported by a large body of published validation data,54-63,65-67 including three independent university studies. 63,66,71  This test assesses clusters of physical (joint dysfunction, pain, range of motion limitation and psychosocial (stress, psychological distress) symptoms and predicts overall clinical significance of a TMD. It is the only TMD diagnostic modality "accepted" by the American Dental Association that makes a direct prediction regarding the presence or absence of TMD. The TMJ Scale's published sensitivity and specificity in recent research is near or over 90 percent.68,70
 Recently published research on TMD efficacy64,68-70  employed "control" or "comparison" groups to determine relative changes in symptomology. These studies showed that statistically and clinically significant improvements resulted from several commonly used treatment protocols (including physical medicine modalities and mandibular repositioning). Matched control groups, on the other hand, manifested unchanged symptomology.
 The availability of a well-documented treatment outcome tool allows the scientific measurement of the effectiveness of the treatment modalities outlined above. Five such studies have now been published.64,68-71  As more become available, many of the issues facing this meeting may be resolved.
REFERENCES
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2.  Friction JR, Kroening RJ, Hathaway KM, TMJ and craniofacial pain: diagnosis and management. St. Louis: Ishiyaku EuroAmerica., 1988.
  3.  Gelb H. Clinical management of head, neck and TMJ pain and dysfunction. Philadelphia: WB Saunders, 1977.
  4.  Wolf SL. Electrotherapy: clinics in physical therapy. New York: Churchill Livingstone, 1981.
  5.  Okeson JP. Management of temporomandibular disorders and occlusion. St. Louis: C.V. Mosby Co., 1993.
  6.  Friedman MH, Weisberg J. Temporomandibular joint disorders: diagnosis and treatment. Chicago: Quintessence Publishing Co., Inc., 1985.
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  7.  Talley RL, Murphy GJ, et al. Standards for the history, examination, diagnosis and treatment of temporomandibular disorders (TMD): a position paper. J Craniomand Pract 1990;1:60-70.
  8.  McNeill C. Temporomandibular disorders: guidelines for classification, assessment and management. Chicago: Quintessence Publishing Co., Inc., 1993.
  9.  Coy RE. Anthology of craniomandibular orthopedics. Vol. 2. Seattle: International College of Craniomandibular Orthopedics, 1993.
10. Bettany JA, Fish DR, Mendel FC. Influence of high voltage pulsed direct current on edema formation following impact injury. Phys Ther 1988;4:219-24.
  11. Reed BV. Effect of high voltage pulsed electrical stimulation on microvascular permeability to plasma proteins. Phys Ther 1988;4:491-5.
  12. Sohn N, Weinstein MA, Robbins RD. The levator syndrome and its treatment with high-voltage electrogalvanic stimulation. Am J Surg 1982 Nov:580-2.
   13. Nelson RM, Currier DD. Clinical electrotherapy. Norwalk (CT): Appleton & Lang, 1987;166-82.
14. Holt CR, Finney JW, Wall CL. The use of transcutaneous electric nerve stimulation (TENS) in the treatment of facial pain. Ann Acad Med Singapore 1995;24(1).
  15. Dhero JC, Raj PP, McDonald JS. Transcutaneous electrical nerve stimulation and myoneural therapy for the management of chronic myofascial pain. Dent Clin North Am 1987;31(4):703-23.
16. Murphy GJ, Utilization of transcutaneous electrical nerve stimulation in managing craniofacial pain. Clin J Pain 1990a;6:64-69.
17. Murphy GJ. Management of craniofacial pain with transcutaneous electrical nerve stimulation: a clinical protocol. J Pain Symptom Manage 1990b;1:41-3.
  18. Gangarosa LP. Iontophoresis in dental practice. Chicago: Quintessence Publishing Co., Inc. 1982.
  19. Lark MR, Gangarosa LP. Iontophoresis: an effective modality for the treatment of inflammatory disorders of the temporomandibular joint and myofascial pain. J Craniomand Pract 1990;2:108-19.
  20. Gangarosa LP, et al. Treatment of post herpetic neuralgia by iontophoresis. Pain: 3rd International Dental Congress on Modern Pain Control, 1985.
  21. Gangarosa LP. Defining a practical solution for iontophoretic local anesthetic of skin. Methods Find Exp Clin Pharmacol 1981;3(2):83-94.
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  22. Costello CT, Jeske AH. Iontophoresis: application in transdermal medication delivery. Phys Ther 1995;6:104-13.
  23. Hartley A. Ultrasound, a monograph. Chattanooga: Chattanooga Group, 1991.
24. Lehman JF. Therapeutic heat and cold. Baltimore: Williams and Wilkins, 1982.
  25. Bly N. The use of ultrasound as an enhancer for transcutaneous drug deliver: phonophoresis. Phys Ther 1995;6:89-103.
  26. Dyson M. Non-thermal cellular effects of ultrasound. Br J Cancer 1982;45(5 suppl):165-71.
  27. Nyborg WL. Ultrasonic microstreaming and related phenomena. Br J Cancer 1982;45(5 Suppl):156-60.
  28. Davick JP, Martin RK, Albright JP. Distribution and deposition of tritiated cortisol using phonophoresis. Phys Ther 1988;11:1672-5.
29. Murphy GJ. Electrical physical therapy in treating TMJ patients. J Craniomand Pract 1983;2:67-73.
  30. Clark GT, Adachi NY, Dorman RM. Physical medicine procedures affect temporomandibular disorders: a review. J Am Dent Assoc 1990 Jul:151-60.
  31. Barrett NVJ, Martin JW, Jacob RF, King GE. Physical therapy techniques in treating head and neck patients. J Prosthet Dent 1988;3:343-46.
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37. Murphy, GJ. Myofascial trigger points. J Clin Ortho 1989;9.
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  57. Lundeen TF, Levitt SR, McKinney Mw. Evaluation of temporomandibular joint disorders by clinician ratings. J Prosthet Dent 1988;2:202-11.
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  63. Procock PR. Mamandras AH, Bellamy N. Evaluation of an anamnestic questionnaire as an instrument for investigating potential relationships between orthodontic therapy and temporomandibular disorders. Am J Dentofacial Orthop 1992;3:239-43.
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  65. Levitt SR, McKinney MW. Validating the TMJ scale in a national sample of 10,000 patients: demographic and epidemiologic characteristics. J Orofacial Pain 1994;1:25-35.
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  68. Brown DT, Gaudet EL. Outcome measurement for treated and untreated TMD patients using the TMJ scale. J Craniomand Pract 1994;4:216-21.
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  70. Wexler GB, McKinney MW. Assessing treatment outcomes in two TMD diagnostic categories employing a validated psychometric test. J Craniomand Pract 1995;4:256-63.
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  71. Simmons HC, Gibbs SJ. Recapture of temporomandibular disks using anterior repositioning appliances. J Craniomand Pract 1995;4:228-37.
  72. Rocabado M, Iglarsh ZA. Musculoskeletal approach to maxillofacial pain. Philadelphia: JB Lippincott Co., 1991.
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  74. Pertes RA, Gross SG. Clinical management of temporomandibular disorders and orofacial pain. Chicago: Quintessence Publishing Co., Inc., 1995.
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Physical Therapy: A Critique
Jocelyne S. Feine, D.D.S.,M.S.,H.D.R.;
C.G. Widmer, D.D.S., Ph.D.,
and J.P. Lund, B.D.S., Ph.D.

INTRODUCTION
 This paper is based on a Medline search of data from 1976 to 1996. The disease domains chosen were "musculoskeletal diseases" (n= 260,852) or "myofascial pain syndromes" (n=2,997) or "temporomandibular joint diseases (TMD)" (n=6,043). The search of the total data bank was refined using key words "physical therapy" (n=4,697) or "alternative medicine" (n=2,211), plus "controlled" or "randomized" or placebo" or "blind" or "trial" (n=700).  An additional search of TMD was made using several subcategories of physical therapy and alternative medicine (electrical stimulation, ultrasound, massage, etc.) All publications using human subjects and written in English or French were accepted. Duplications were eliminated, as well as studies that did not include an appropriate control group or conditions. In addition, relevant references cited in selected articles were included .Review papers were also included. This abstract presents the results of a review of approximately 140 publications that have been evaluated so far.
THE USE OF PHYSICAL THERAPY
       The results of a general survey of American dentists1 shows that some forms of physical therapy are used relatively frequently in both general and specialist practice for the treatment of trigeminal myofascial pain. Both groups report prescribing thermal packs for 27 percent and 28 percent of patients respectively, while "physiotherapy" (undefined) was recommended for 10 percent of patients by generalists and 17 percent by specialists. The only other physical modality mentioned by the authors, ultrasound, was used only by specialists for 7 percent of cases. Another survey of members of the American Equilibration Society showed that thermal packs were also used frequently by both the general practitioners and specialists (39 percent and 28 percent). Vapocoolants and physiotherapy were prescribed frequently by generalists (33 percent and 32 percent respectively), while specialists often used transcutaneous electrical nerve stimulation (TENS) (27 percent)2.  No surveys were found that report on the opinions of dentist regarding the value of physical medicine for TMD, but the great majority of physicians surveyed do seem to be convinced that certain of these treatments are of value for similar conditions elsewhere in the body.3,4
MUSCULOSKELETAL PAIN OF THE BACK, NECK, AND LIMBS
 However, several recent analysis of the efficacy of physical modalities, manipulation and exercise in the treatment of painful disorders of the limbs or spinal column did not lend much support to these beliefs. Chapman reviewed the evidence that cold, heat, ultrasound, diathermy, and low intensity laser are effective in reducing pain and associated symptoms.5 A major problem that she and other reviewers encountered was that most studies compared different forms of treatment; few used placebo or waiting list controls. Moreover, most treatments included several forms of intervention, making
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interpretation a risky business. Her conclusion was that there is little evidence to support the use of these modalities in long-term control.
 A Dutch group has conducted a series of blinded meta-analyses of randomized clinical trials that tested physical modalities and physiotherapy for back and neck pain, shoulder pain, and disorders of the knee were recently summasized.6  In each of five studies, the authors began by assigning scores to each trial, based on an analysis of the methods used; few of the 180 trials were judged to be of high quality, and most were very poor. The general conclusions were that, although some forms of therapy appeared promising, no definite conclusions could be drawn because of the overall low quality of the trial designs. The group believes that the disappointing results were due to the heterogeneity of the study populations, mixed treatment regimens, and small sample sizes in many of the studies that had negative outcomes. However, the tendency for small clinical trials to be published more frequently if the results are positive than if they are negative7 could mean that negative results are actually under-represented.
 This Dutch group designed its own trial to compare therapy by three groups of practitioners who deal with chronic lower back and neck pain in Holland: physical therapists, manual therapists, and general medical practitioners (GPs).8-10  A placebo group that was treated with detuned shortwave diathermy and detuned ultrasound was included. Although they designed a trial that avoided many of the weaknesses of their earlier studies, it suffered from some of its own: huge between-group differences in time spent with the therapist, mixed treatments, and unvalidated or inappropriate outcome measures. Nevertheless, the differences between the groups were almost all insignificant. The biggest difference occurred in patient reports of perceived effect: GPs rated lower than the other two therapists, which is not surprising since the patients usually paid a single visit to the GP and spent several hours with the others. They did better with frequent placebo physical therapy than with the GP! They concluded that a substantial part of any treatment success must be assigned to placebo effects.
 However, a trial by Timm11 did show that various forms of exercise may be efficacious, although he has not reported any followup data. He compared "low-tech" and "high-tech" exercise with physical agents (hot packs, ultrasound and TENS) and joint manipulation in the treatment of chronic lower back pain (CLBP).  A nontreatment control group was also included and the sample size was relatively large (50/group). At the end of an 8-week session, there was no improvement in the control and physical modality groups. The joint manipulation group had a slight improvement in mobility, while the exercise groups did significantly better than even the manipulation group in functional measures and also in a composite disability score. When coupled with earlier studies by Deyo et al.12 and Manniche et al.13, it does seem then that some form of exercise program will probably turn out to be the best way of improving CLBP. This was also the conclusion of the two task forces.14,15
TEMPOROMANDIBULAR DISORDERS
As with the general medical literature, studies designed to measure the efficacy of physical therapies used in the management of TMD suffered from a lack of controls, improper randomization, inadequate sample size, and inappropriate outcome measures. Furthermore, most trials reported on only the immediate posttreatment ratings. This information is of little help when assessing the efficacy
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of treatment for a chronic condition. An even more problematic issue is the fact that chronic pain is highly variable, changing in intensity from one day to the next and even during the same day. Results that are based on one-off posttreatment assessments must therefore be interpreted with caution.

 A summary of the better papers on each topic follows.
ULTRASOUND
 Like Mohl et al.,16 we have been unable to find a study of ultrasound vs. an ultrasound placebo as a single therapy for chronic TMD. (However, see Gray et al.17)
ELECTRICAL STIMULATION
 We found four studies that evaluated electrical stimulation of various types on TMD. One tested an "inferential current" stimulator vs. a placebo in subjects (n=20/group) with chronic uni- or bilateral jaw pain over a 3-9 day period.18  Pain decreased over time, but no between group differences were detected for pain or for maximum opening. Block and Laskin19 reported no significant between-group differences (TENS vs. placebo) after 3-6 weeks of treatment. Linde et al.20 compared TENS to occlusal splints in subjects (N=16 TENS, n=15 Splint) with internal derangements and pain complaints. Pain ratings decreased over time, and the incidence and intensity of pain was significantly less in the splint group than in the TENS group. One study suggesting that there may be some beneficial effect of TENS comes from Graff-Radford et al., 21 who applied four different forms of TENS to "active" trigger points of TMD subjects (n=12/group). Pain ratings were gathered before and after ten minutes of treatment. Pain decreased for all groups, and post-treatment pain was significantly less in three of the TENS treatment groups than in the placebo and the fourth TENS group. This small amount of information is consistent with conclusions that have been drawn for TENS treatment of other musculoskeletal conditions: that any diminution of pain is of very short duration.
MIXED THERAPIES
 Gray et al.17 compared shortwave diathermy (SWD), pulsed SWD, ultrasound, laser and mixed placebo delivered over a 4-week period in a between-group blinded trial. Posttreatment clinical assessments were made after treatment (at 4 weeks) and at a 3-month recall. Patients were classified as "improved" or "not improved."  They found no between-treatment differences at the end of the trial. However, 3 months later, the percent of treated patients that were improved had remained the same, while the percentage of improved placebo patients had fallen significantly. Burgess et al.22 compared cold (ethyl chloride spray and home ice packs) and stretch to passive resistance exercises and a no-treatment control group in subjects with TMD. They found that pain was significantly less for the two treatment groups immediately after the first session. At the second session (3 weeks later), the group assigned to the cold and stretch regime had significantly less pain than did the other two groups.
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SUMMARY
 Most authors of large-scale reviews of treatments of chronic pain conditions, including TMD,23 conclude that there is a remarkable similarity in the apparent efficacy of the various forms of nonmedical or nonsurgical treatments. Malone and Strube24 concluded that, because of a uniform efficacy of treatments, the effectiveness of treatments is probably attributable not to their differences, but to their similarities. Eight years later, we see no reason to challenge their conclusions.
REFERENCES
1.  Glass EG, Glaros AG, McGlynn FD. Myofascial pain dysfunction: treatments by ADA members. Cranio 1993;11:25-9.
2.  Glass EG, McGlynn FD, Glaros AG. A survey of treatments for myofascial pain dysfunction. J Craniomand Pract 1991;9: 165-8.
  3.  Knipschild J, Kleijen J, Ter Riet G. Belief in the efficacy of alternative medicine among general practitioners in the Netherlands. Soc Sci Med 1990;31:625-6.
4.  Rush PJ, Shore A. Physicians' perceptions of the value of physical modalities in the treatment of musculoskeletal disease. Br J Rheumatol 1994;33.
  5.  Chapman CE. Can the use of physical modalities for pain control be rationalized by the research evidence? Can J Physiol Pharmacol 1991;69:704-12.
  6.  Beckerman H, Bouter LM, Van Der Heijden GJMG, De Bie RA, Koes BW. Efficacy of physiotherapy for musculoskeletal disorders: what can we learn from research? Br J Gen Pract 1993;43:73-7.
  7.  Dickersin K. The existence of publication bias and risk factors for its occurrence. JAMA 1990;263:1385-9.
8.  Koes BW, Bouter LM van Mameren H, et al. The effectiveness of manual therapy, physiotherapy and treatment by the general practitioner for non-specific back and neck complaints: a randomized clinical trial. Spine 1992a;17:29-35.
  9.  Koes BW, Bouter LM, van Mameren H, et al. A blinded randomized clinical trial of manual therapy and physiotherapy for chronic back and neck complaints: physical outcome measures. J Manipulative Physiol Ther 1992b;15:16-23.
10. Koes, BW, Bouter LM, van Mameren H, et al. Randomized clinical trial of manual therapy and physiotherapy for persistent back and neck complaints: results of one year follow-up. BMJ 1992;304:601-5.
  11. Timm KE. A randomized-control study of active and passive treatments for chronic low back pain following L5 laminectomy. JOSPT 1994;20:276-86.
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  12. Deyo RA. Conservative therapy for low back pain. Distinguishing useful from useless therapy. JAMA 1983;250:1057-62.
  13. Manniche C, Hesselsue G, Bentzen L, Christensen I, Lundberg E. Clinical trial of intensive muscle training for chronic low back pain. Lancet 1988;2(8626-7), 1473-6.
  14. Spitzer W, LeBlanc F, et al. Scientific approach to assessment and management of activity-related spinal disorders: report of the Quebec Task Force on Spinal Disorders. Spine 1987;12:7S(European ed., Suppl.1) S1-59.
  15. Fordyce FE. Back pain in the work place. Management of disability in nonspecific conditions. IASP Press, 1995.
  16. Mohl ND, Ohrbach RK, Crow HC, Gross AJ. Devices for the diagnosis and treatment of temporomandibular disorder part III: thermography, ultrasound, electrical stimulation, and electromyographic biofeedback. J Prosthet Dent 1990;63(4):472-7.
  17. Gray RJM, Quayle AA, Hall CA, Schofield MA. Physiotherapy in the treatment of temporomandibular joint disorder: a comparative study of four treatment methods. Br Dent J 1994;176:257-61.
  18. Taylor K, Newton RA, Personius WJ, Bush FM. Effects of interferential current stimulation for treatment of subjects with recurrent jaw pain. Phys Ther 1987;67:346-50.
  19. Block and Laskin (1980).
  20. Linde C, Isacsson G, Jonsson BG. Outcome of a 6-week treatment with transcutaneous electric nerve stimulation compared with splint on symptomatic temporomandibular joint disk displacement without reduction. Acta Odontol Scand 1995;53:92-8.
  21. Graff-Radford SB, Reeves JL, Baker RL, Chiu D. Effects of transcutaneous electrical nerve stimulation on myofascial pain and trigger point sensitivity. Pain 1989;37:1-5.
  22. Burgess JA, Sommers EE, Truelove EL, Dworkin SF. Short-term effect of two therapeutic methods on myofascial pain and dysfunction of the masticatory system. J Prosthet Dent 1988;60:606-10.
  23. Dahlstrom L. Conservative treatment methods in craniomandibular disorder. Swed Dent J 1992;16:217-30.
  24. Malone MD, Strube MJ. Meta-analysis of non-medical treatments for chronic pain. Pain 1988;34:231-44.
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Behavioral and Educational Modalities
Samuel F. Dworkin, D.D.S., Ph.D.

 General agreement has emerged in the scientific literature that behavioral and educational modalities are useful and effective in the management of chronic pain conditions, although gains achieved are often modest and factors contributing to the efficacy of such modalities remain to be more precisely defined.1-3  Behavioral and educational treatment modalities constitute a component of virtually every reported chronic pain treatment program.4  While the majority of studies establishing the efficacy of psychologically based treatments for chronic pain have focused on the two most common chronic pain conditions, namely back pain and headache, it has been demonstrated that management of temporomandibular disorders (TMD) has benefited from such behavioral interventions as well.5
 The label "biobehavioral" has gained acceptance as a collective term that refers to treatment approaches for chronic pain derived from applying behavioral science theory and methods to changing the perception of pain and ameliorating or eliminating the personal suffering and psychosocial dysfunction that often accompanies persistent pain conditions.4  These biobehavioral interventions are viewed as safe, reversible, and noninvasive and, for the most part, emphasize strategies under the patient's control. A large collection of treatment modalities is subsumed under the label of biobehavioral treatments, and the most commonly studied of these include biofeedback, relaxation, hypnosis, and education.3,6-8  The biobehavioral pain modalities are drawn from the field of psychotherapy, and those methods that have been scientifically validated are derived most heavily from cognitive-
behavioral and behavioral psychotherapeutic approaches; the efficacy of pschodynamic and psychoanalytic treatment approaches for management of chronic pain have not yet been scientifically validated. Overwhelmingly these methods emphasize as their common objective self-management and the acquisition of self-control over not only pain symptoms but also cognitive attributions or meanings given to those symptoms and, most importantly, to maintaining a productive level of psychosocial function, even if pain is not totally absent.2,3
       A recent NIH Technology Assessment Conference entitled "Integration of Behavioral and Relaxation Approaches Into the Treatment of Chronic Pain and Insomnia" provides the best available summary of the state-of-the-art concerning the suitability of biobehavioral methods are useful approaches to ameliorating chronic pain and its debilitating psychosocial sequelae.5  With regard to TMD, reference is made to specific studies establishing efficacy of relaxation, biofeedback, hypnosis and cognitive-behavioral approaches in the management of temporomandibular disorder.
 The use of educational approaches to modify TMD-related pain and dysfunction had not been studied extensively, and no comprehensive review of such approaches is available. One clinical trial of a psychoeducational group intervention conducted early in treatment for TMD demonstrated a modest effect in reducing TMD pain-related interference in psychosocial function, compared with usual treatment, and the benefits gained continued to be present at a 1-year followup. Educational methods have been demonstrated efficacious in the self-management of headache and back pain, using both group and individual approaches to deliver the educational interventions.9,10
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 When biobehavioral treatments are employed in the management of TMD, the effects are virtually always positive and beneficial, though they are often moderate in size. However, these biobehavioral methods, especially those subsumed under the label "cognitive-behavioral" appear to have the potential for producing long-lasting benefits when compared with usual clinical treatment for TMD. Increasingly, it should be noted, conservative, noninvasive approaches to TMD management are being advocated as the preferred overall treatment approach for this hard-to-understand chronic pain problem.11  These so-called "conservative" treatments" generally incorporated many of the same elements, i.e., relaxation, stress-education, habit behavioral modification, etc., found in cognitive-behavioral and behavioral therapies for TMD. Thus, both usual clinical treatment for TMD and biobehavioral treatment employ multimodal approaches, and it does not yet appear possible to determine which of the multiple therapeutic components are most efficacious. If one method had to be singled out, relaxation seems to emerge consistently as an effective method for chronic pain management across a wide variety of pain conditions and over a wide variety of clinical settings. In any event, the combined biobehavioral methods commonly used in clinical practice and in research have yet as failed to establish one modality as superior to another. It is important to note that the same situation holds true with regard to biomedically based TMD treatments. Little is known about the superiority of any one of the multiple methods commonly employed for the biomedical management of TMD--there is no strong scientific evidence to substantiate invasive versus noninvasive treatments of pharmacologic treatments emphasizing analgesics versus those stressing antidepressants or muscle relaxants. The absence of compelling evidence to the contrary has compelled many clinical researchers to advocate conservative, reversible therapies for the largest majority of TMD patients.
 A great deal more research is needed to adequately evaluate how biobehavioral interventions achieve their desired effects and which components of the multimodal approaches now in common use are most potent. Perhaps of greatest interest is the need to develop treatment approaches tailored to both the physical and the behavioral status of the patient. Typically, treatment of TMD seems driven largely by the physical diagnosis alone, without addressing the personal or psychosocial impact of TMD pain or the patterns of coping with TMD used by TMD patients. Although TMD is regarded by many as a condition in which psychosocial factors influence its course,12 little attention has been paid in clinical research to assessing how psychological or psychological or psychosocial factors influence treatment outcome and whether successful clinical outcome is associated with improved psychosocial function. It seems fair to say that outcome assessment for TMD, except for assessing self-report of pain, is focused almost exclusively on assessment of physical factors (range of jaw motion, joint sound, etc.).
 Recent interest has been shown in developing biobehavioral treatment approaches that differ according to the differing levels of psychosocial functioning and/or level of cognitive or emotional disturbance exhibited by specific TMD patients or by groups of TMD patients clustered by psychological and psychosocial level of adaptation to their chronic pain condition.13,14  Such an approach would involve development of clinical decision-making criteria that engaged physical and psychosocial variables and treatment outcome measures capable of assessing change along both physical and psychosocial dimensions.15
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REFERENCES
  1.  Osterweis M, Kleinman A, Mechanic D. Pain and disability: Clinical, behavioral and public policy perspectives. Washington, DC National Academy Press, 1987.
  2.  Turk DC, Meichenbaum D. A cognitive behavioral approach to pain management. In: Wall PD, Melzack R, eds. Textbook of pain (Second Edition). London: Churchill Livingstone, 1989:1001-9.
  3.  Turner JA, Clancy S, McQuade KJ, Cardenas DD. Effectiveness of behavioral therapy for chronic low back pain: a component analysis. J Consult Clin Psychol 1990;58:573-9.
  4.  Gallagher RM. The comprehensive pain clinic. A biobehavioral approach to pain management and rehabilitation [abstract]. In: Program and abstract book on integration of behavioral and relaxation approaches into the treatment of chronic pain and insomnia; NIH Technology Assessment Conference; 1995 Oct 16-18; Bethesda (MD): National Institutes of Health; 1995. p.55-8.
  5.  Integration of behavioral and relaxation approaches into the treatment of chronic pain and insomnia {Program and Abstracts]. NIH Technology Assessment Conference; 1995 Oct 16-18; Bethesda. Bethesda (MD): National Institutes of Health; 1995. 104 p.
6.  Dworkin SF, Turner JA, Wilson L, Massoth DL, Whitney C, Huggins KH, Sommers E, Truelove E. Brief cognitive-behavioral intervention for temporomandibular disorders. Pain 1994 Nov; 59(2):175-87.
  7.  Flor H, Biraumer N. Comparison of the efficacy of electromyographic biofeedback, cognitive behavioral therapy, and conservative interventions in the treatment of chronic musculoskeletal pain. J Consult Clin Psychol 1993;61:653-8.
  8.  Rugh J. Psychological management of the orofacial pain patient. In: Cranio-facial Growth Series Ann Arbor: University of Michigan Press, 1993:121-33.
  9.  Barsky AJ, Geringer E, Wool CA. A cognitive educational treatment for hypochondriasis. Gen Hosp Psychiatry 1988;10:1-6
10. Blanchard EB, Andrasik F, Appelbaum KA, Evans DD, Jurish SE, Teders SJ. The efficacy and cost-effectiveness of minimal-therapist-contact non-drug treatments of chronic migraine and tension headache. Headache 1985;25:214-20.
11. Clark GT, Seligman DA, Solberg WK, Pullinger AG. Guidelines for the treatment of temporomandibular disorders. J Craniomand Disord 1990;4:80-8.
  12. Marbach JJ, Lennon MC, Dohrenwend BP. Candidate risk factors for temporomandibular pain and dysfunction syndrome: Psychosocial, health behavior, physical illness and injury. Pain 1988;34:139-51.
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  13. McGlynn FD, Gale EN, Glaros AG, LeResche L, Massoth DL, Weiffenbach JM. Biobehavioral research in dentistry: Some research directions for the 1990's. Ann Behav Med 1990;12:133-140.
14. Rudy TE, Turk DC, Kubinski JA, Zaki-Hussein S. Differential treatment responses of TMD patients as a function of psychological characteristics. Pain 1995;6:103-12.
  15. Turk DC. Customizing treatment for chronic pain patients: Who what, why. Clin J Pain 1990;6:255-70.
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Pharmacologic Modalities
Raymond A. Dionne, D.D.S., Ph.D.

 Pharmacologic intervention in the management of chronic orofacial pain is usually considered adjunctive, on the assumption that more definitive treatments will eventually correct the underlying pathophysiologic process. Many putative therapies, however, have not withstood the scientific scrutiny of controlled clinical trials. Additionally, the possible adverse effects of long-term use of drugs for chronic pain may be less harmful than the iatrogenic effects of failed dental or surgical procedures. Drug therapy can often be the primary approach to treating depression associated with chronic pain or for inhibiting inflammatory processes that may contribute to temporomandibular disorders (TMD). This presentation reviews the scientific basis for the use of drugs both adjunctively and as the primary treatment in the management of TMD.
 A wide variety of drug classes have been described for chronic orofacial pain, ranging from short-term treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants for pain of muscular origin to chronic administration of antidepressants for less well-characterized pain. In general, enthusiastic claims of efficacy based on clinical observations are superseded by equivocal findings of efficacy and belated recognition of adverse effects of toxicity associated with long-term administration, e.g., elevated incidence of renal failure with chronic NSAID use.1  The use of a drug for chronic orofacial pain should be based on documented therapeutic efficacy in one or more well-controlled clinical trials, an acceptable side effect liability, and minimal potential for systemic toxicity with chronic administration.
 Antidepressant drugs have been used for more than 30 years for management of pain from a wide variety of conditions, including chronic orofacial pain. A consensus is emerging that the analgesic effects are largely independent of antidepressant activity, can be differentiated from placebo, are seen at dosages lower that those usually effective in depression, and are effective in patients who are not depressed.2,3  Although approximately 40 placebo-controlled studies have been identified in the literature regarding the use of antidepressants for chronic pain, only three evaluated their use for chronic orofacial pain, one of which was published nearly 30 years ago. More clinical research is needed to determine prognostic factors in this patient population predictive of analgesic responsiveness to antidepressants and to determine which drugs have the most favorable balance of analgesia and side-effect liability.
          Drugs of the benzodiazepine class frequently are administered to chronic pain patients, often for prolonged periods, despite long-standing professional concern over their ability to produce dependence. The few studies that have evaluated the use of benzodiazepines for TMD provide evidence of therapeutic efficacy, but the small sample sizes limit generalization of the findings.4,5 Similarly, muscle relaxants are often prescribed for chronic muscular pain to help prevent or alleviate the increased muscle activity attributed to some forms of TMD. Limited clinical data support the effectiveness of cyclobenzaprine in some chronic musculoskeletal disorders,6 but it is not clear whether this can be generalized to chronic orofacial pain. Further studies are needed to demonstrate efficacy
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greater than remission of symptoms over time and to differentiate effects due to muscle relaxation rather than nonspecific central nervous system sedation.
        Nonopoid analgesics (aspirin, acetaminophen, NSAIDs) are often recommended in standard texts and summaries of expert opinion,7 but their use is not well supported in the scientific literature. Administration of ibuprofen at a dosage of up to 2400 mg/day for 4 weeks, for example, could not be differentiated from placebo in a group of patients with chronic orofacial pain.5  A dosage of 20 mg/day of piroxican for TMD pain compared with placebo also failed to demonstrate any therapeutic advantage for the NSAID.8  The lack of clinical studies to support the efficacy of NSAIDs for TMD becomes more important when contrasted with the growing body of evidence on the serious toxic effects of NSAIDs when administered chronically. Retrospective studies have established an association between ingestion of aspirin or NSAIDs and increased risk of upper GI bleeding.9.10  NSAIDs also alter renal blood flow, leading to an estimated 500,000 cases of abnormalities in renal function.  Retrospective analysis of patients with end-stage renal disease requiring hemodialysis demonstrated an association between chronic NSAID use (defined as more than 5000 pills  over the lifetime) and a ninefold increased risk of renal disease.1  A lack of clinical evidence of a therapeutic effect for nonopioid analgesics in the symptomatic treatment of chronic orofacial pain must be weighed against this potential for serious toxicity with chronic use.
 Review of the drug classes most commonly used for TMD does not reveal a wealth of data upon which to base therapy. A need exists for well-controlled studies of drugs in the chronic orofacial pain population, for periods that approximate their use clinically, with appropriate indices of therapeutic efficacy and toxicity, and in comparison to a group receiving placebo medication to control for cyclic fluctuations in symptomology. Future therapeutic progress, however, may require intervention in pathophysiologic processes with novel drugs acting by nontraditional mechanisms.
REFERENCES
  1. Perneger TV, Whelton PK, Klag MJ. Risk of kidney failure associated with the use of acetaminophen, aspirin, and non-steroidal anti-inflammatory drugs. N Engl J Med 1994;331:1675-9.
  2. Egbunike IG, Chaffee BJ. Antidepressants in the management of chronic pain syndromes. Pharmacology 1990;10:262-70.
  3.  Onghena P, Van Houdenhove B. Antidepressant-induced analgesia in chronic non-malignant: a meta-analysis of 39 placebo-controlled studies. Pain 1992;49:205-19.
  4.  Harkins S, et al. Administration of clonazepam in the treatment of TMD and associated myofascial pain. J Craniomand Disord 1991;5:179-86.
  5.  Singer EJ, Sharav Y, Dubner R, Dionne RA. The efficacy of diazepam and ibuprofen in the treatment of chronic myofascial orofacial pain (abstract:. Pain S83. 1987.
  6.  Elenbaus JK. Centrally acting oral skeletal muscle relaxants. Am J Hosp Pharm 1980;37:131-2.
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  7.  McNeill C. Temporomandibular disorders. Chicago: Quintessence Publishing Co., 1993, p. 87.
  8.  Gordon SM, Montgomery MT, Jones LE. Comparative efficacy of piroxicam versus placebo for temporomandibular pain (abstract). J Dent Res 1990;69:218.
  9.  Holvoet J. et al. Relationship of upper gastrointestinal bleeding to non-steroidal anti-inflammatory drugs and aspirin: a case-control study. Gut 1991;32: 730-4.
10. Kaufman DW, et al. Non-steroidal anti-inflammatory drug use in relation to major upper gastrointestinal bleeding. Clin Pharmacol Ther 1993;53:485-94.
  11. Whelton A, Hamilton CW. Nonsteroidal anti-inflammatory drugs: effects on kidney function. J Clin Pharmacol 1991;31:588-98.
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Temporomandibular Joint Devices: Treatment Factors and Outcome
Larry M. Wolford, D.D.S.

INTRODUCTION
 Temporomandibular joint (TMJ) devices have been used for many years as (1) endosseous implants to stabilize articular discs, (2) articular disc replacements, (3) condylar replacements, (4) fossa replacements or liners, and (5) total joint prostheses. Some of these devices have worked very well in the treatment of TMJ pathology, but others have created worse problems, at times leaving patients severely debilitated. Other factors that may affect patient outcomes include (1) connective tissue and autoimmune diseases, (2) hormonal imbalances, (3) thyroid disease, and (4) genetic predisposition to diseases or acquired diseases that affect the body's biological responses. This paper discusses information on these devices, factors affecting treatment outcomes, and the outcomes of the devices that have been studied.
ENDOSSEOUS IMPLANTS
 Endosseous implants can be placed in the condyle to aid in securing the articular disc in position. The Mitek Mini-Anchor (Mitek Inc., Norwood, MA) is the device most commonly used in the the TMJ,1 but the Statak anchor (Sharpoint, Reading, PA) has also been used. The Mitek mini-anchor is placed in the posterior head of the condyle, with artificial ligaments (O-Ethibond suture, Ethicon, Inc., Somerville, NJ) attached to it that are then secured to the articular disc to stabilize the disc in position. Wolford et al.2 studied 61 patients (Group 1) for an average followup of 12.2 months (range=8 to 16 months), with 11 unilateral and 50 bilateral copies. Group 2 consisted of 32 patients followed for an average of 25.5 months (range=18 to 36 months) with 8 unilateral and 24 bilateral cases. In Group, 1 59 of 61 patients (98.5 percent) had significant reduction of pain, with an average decrease of 4.2 points on a 0 to 10 visual analog scale. In Group 2, 29 of 32 patients (90.7 percent) had significant reduction in pain, with an average of 4.0 points on a 0 to 10 visual analog scale. All implants remain in place. Studies are being conducted to determine condylar response to these devices.
Fields et al.3 studied the pull-out strength of Mitek-Mini Anchors inserted in 20 human cadaver condyles, demonstrating an average load of 16.0 points (range=8.5-28.4 lbs.) with the bone failing in 18 of the 20 specimens, the suture failing 2 specimens, and no failure of the anchor.
TEMPOROMANDIBULAR JOINT ARTICULAR DISC REPLACEMENT
 Alloplastic replacement of the TMJ articular disc was a popular technique in the 1970's and 1980's. The two materials most commonly used as Interpositional Implants (IPI) to replace the articular disc were Proplast/Teflon (PT-Vitek, Inc., Houston, TX) and Silastic (Dow Corning, Midland, MO). These materials fragment under loading and functional conditions, creating microscopic particles. The human body cannot degrade these polymers, and severe local and systemic reactions can occur. PT and silastic TMJ implants have resulted in numerous complications, including
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fragmentation, foreign body giant cell reaction, particle migration, pain lymphadenopathy, severe osteoarthritis, bone resorption into the middle cranial fossa, and immunological dysfunction.4-9
Henry and Wolford 10 evaluated 107 patients with Proplast-Teflon implants. Patients were reconstructed using autogenous tissues, including temporal fascia and muscle grafts, dermal grafts, conchal cartilage grafts, costochondral grafts, and sternoclavicular grafts, with a success rate of the various grafts ranging from 8 to 31 percent. Failures with these autogenous tissues were primarily secondary to pain and ankylosis, created by foreign body giant cell reaction and reactive bone. Even multiple debridements of the TMJ will demonstrate the continued presence of a foreign body giant cell reaction, with as many as 4 to 5 TMJ surgical debridements. Patients who have had previous Proplast-Teflon implants reconstructed with the Techmedica total joint prosthesis that uses materials well proven in orthopedics had functional and occlusal stability in 84 percent of the cases.
CONDYLE, FOSSA, AND TOTAL JOINT REPLACEMENT
 Materials used in partial and total JTMJ reconstruction included Proplast/Teflon, polymethylmethacrylate (PMMA), dense ultra-high molecular weight polyethylene, and various metals. Several companies have made TMJ total joint prostheses, including Vitek, Inc. (these devices included PT as a component material and are no longer available); Osteomed (Dallas, TX); Techmedica, Inc. (Camarillo, CA); TMJ, Inc. (Golden, CO) which makes the Christensen prosthesis; and Morgan prosthesis (The Temporomandibular Research Foundation, Los Angeles, CA) The Food and Drug Administration (FDA) has stopped the companies from making TMJ prostheses, except for the Christensen and Morgan devices which are "Grandfathered," since they fall within the FDA preamendment for implanted devices, making them available for patients although not FDA approved. The materials used in their standard prostheses include PMMA in the articulating surface, which is not used for articulation in any orthopedically approved device. This material has poor wear characteristics. However, Chase et al.11 reported on 69 patients with either just the metal (Chromium-Cobalt alloy) fossa implant or the total joint prosthesis with the PMMA condylar head. The study stated that the fossa implant with retention of the articular disc resulted in 100 percent of the patients having decreased pain, 82 percent having improved ability to eat, and 77 percent having increased incisal opening. With the fossa implant without the articular disc, 100 percent of patients had decreased pain, 96 percent had increased eating ability, and 86 percent had increased incisal opening. With the total joint prosthesis with the PMMA condylar head, 95 percent had decreased pain, 86 percent had increased eating ability, and 9 percent had increased incisal opening.
 The Techmedica total joint prosthesis used materials well proven in orthopedics for joint replacement. The devices have been tracked for up to 6 years with very good results, but the FDA refuses to accept this data, and has developed TMJ criteria far more stringent than for any other joint in the body. Therefore, no company has been able to provide an FDA-approved TMJ total joint prosthesis. Wolford et al.12 published data on 100 consecutive Techmedica joint prostheses placed in 56 patients with an 86 percent success rate with 16 to 46 month followup. In their study, 49 percent of the joints had previous PT implants. Patient outcomes were effected by the number of previous surgeries. Fourteen patients had one or no previous surgeries and had significant improvement relative
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to pain and function, while 19 percent of the remaining 42 patients with two or more previous surgeries had unfavorable outcomes, related primarily to pain.
 A common problem with total joint prostheses, particularly in patients with previous PT or Silastic implants is the recurrent development of foreign body giant cell reaction and reactive bone, causing pain and limited jaw function. Wolford and Karras13 have presented a technique of harvesting abdominal fat and packing it around the Techmedica total joint prostheses to prevent these unwanted tissues from developing. Prior to using these fat grafts, 35 percent of 20 patients (37 joints) required additional TMJ debridement surgeries. Since beginning this fat graft procedure 3 years ago, not one of the 15 patients (22) joints has had to return to surgery for additional joint debridement.
 For complex, multiply operated TMJ patients, with previously failed alloplasts, a total joint prosthesis using materials with proven safety and efficacy in orthopedic use may be the only option available to predictably improve quality of life.
HUMAN LEUKOCYTE ANTIGEN STUDIES
 The association of certain arthropathies with an increased incidence of specific human leukocyte antigens (HLA) has been demonstrated in well-controlled human studies. We have performed HLA typing on 25 patients with TMJ dysfunction and failed PT implants to determine if an increased incidence of HLA markers associated with a predisposition to connective tissue and autoimmune diseases could be demonstrated. Most of the patients were experiencing chronic pain and dysfunction.  Medical histories of the 24 female patients also included the following findings: 58 percent with fibrocystic breast disease; 50 percent with hypersensitivity to metals; and 35 percent with endometriosis. Results showed that 10 of 25 patients (40 percent) had HLA-B locus antigens associated with psoriasis or psoriatic arthritis, versus 17.6 percent of 125 controls. Other patients demonstrated antigens associated with juvenile rheumatoid arthritis or sarcoidosis, ankylosing spondylitis, Rieter's syndrome, and/or systemic lupus erythematosus. If these findings are considered, then 20 of 25 patients (80 percent) have antigenic associations with various connective tissue diseases, which may have predisposed them to immune dysfunction and treatment failure.
IMMUNOLOGICAL STUDIES
 We have performed a preliminary study evaluating immunological response to Proplast-Teflon implants in 12 patients. The total lymphocyte count was calculated and immune response assessed by immunophenotyping peripheral blood lymphocytes IA, CD2, CD3, CD4, CD8, CD4:CD8 ratio, CD20, CD56, and surface Ig positive cells. The IA subset was below controls in 73 percent of patients, and the CD4:CD8 ratio was decreased significantly below the normal range. By contrast, the CD56 subset was elevated in 60 percent of patients. An in vitro lymphocyte activation assay was used with six patients to determine the presence of activated T-cells. Lymphocytic activation was present in four of six patients. The activated T-cell response was greater in those patients experiencing more severe symptoms. The immunologic consequences of the activated T-cell response remains to be investigated.
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 A small study followed four patients who had a significant decrease in their immunodefiency panel prior to removal of the PT implant. Three of the patients who had reconstruction with Techmedica custom-made total joint prosthesis demonstrated a significant improvement toward normal values at 1 year postsurgery.
SYSTEMIC DISEASES
          Clinical observations suggest that some patients may have developed connective tissue diseases that may have promoted or exacerbated by TMJ implant materials. Some conditions that have been recorded in TMJ patients with PT, Silastic, and PMMA implants include chronic fatigue syndrome, chronic pain, impaired cognition, short-term memory loss, lupus, psoriasis, psoriatic arthritis, sarcoidosis, polyarthritis, fibromyalgia, human adjuvent disease, sclerderma, Sjogren's syndrome, rheumatoid arthritis, visual disturbances, localized and distant muscular disease, neurologic dysfunction, chronic low-grade fever, generalized synovitis, and significant hormonal imbalances. Undifferentiated or mixed connective tissue disease may be a common finding. Problems associated with these conditions, especially chronic pain, physical limitations, and diminished mentation often render these patients partially or totally disabled. Foreign body giant cell granulomas have been found in the TMJ, masticatory muscles, parotid and submandibular glands, regional lymph nodes, on the roof of the orbit, within the orbit, in the lung, and in breast biopsies. The extent of systemic involvement with alloplastic materials remains unclear and requires further investigation.
HISOPATHOLOGIC DIFFERENCE OF ALLOPLASTIC TEMPOROMANDIUBULAR JOINT IMPLANTS
          Our series of patients suggests that foreign body giant cell reaction to PT implants is proliferative and worsens with time, as more PT particles are generated. Cartilage and bone degeneration and resorption occur. Heterotopic bone formation and/or reactive neo-ossification can develop. It is unknown what effect the aluminum oxide used in some PT implants has in the pathological process.
 Silastic and PMMA particles appear to create a less proliferative foreign body giant cell reaction. Cartilage and bone resorption can occur. Particle size may be larger than the PT particles, resulting in fibrosis, sometimes with reactive cartilage, neo-ossification, and/or heterotopic bone formation. Local tissues may be affected by direct contact with the material or leaching of monomer from the PMMA. Local reactions may in part be chemically mediated from the polymers, from cells releasing substances in an effort to degrade the polymers or upon cell death and lysis. Goldblum et al.14 identified antibodies to silicone. Unidentified antibodies may exist for other polymers.
CONCLUSIONS
 The local and systemic effects of Proplast-Teflon, Silastic, and other polymeric implants undergo fragmentation and formation of particulate debris are not clearly understood. Further studies will be necessary to identify the effects of these materials, particularly in patients who may have a predisposition to connective tissue and autoimmune disease, and to develop treatment modalities that will predictably help the unfortunate patients afflicted with these diseases.
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 The evidence also demonstrates that the use of custom-made total joint prostheses, utilizing materials that are well proven and used as the standards for orthopedic joint devices, work very well in patients with TMJ pathology. It is the only predictable alternative for thousands of patients. The unavailability of these types of devices due to excessive stringent requirements is forcing thousands of patients to remain in a state of chronic pain, dysfunction, and ill health.
REFERENCES
  1.  Wolford LM, Cottrell DA, Karras SC. Mitek mini-anchor in maxillofacial surgery: proceedings of SMST-94. The First International Conference on Shape Memory and Superelastic Technologies. Monterey, CA: MIAS, 1995.
2.  Wolford LM, Cottrell DA, Karras SC, Cardenas L. Mitek-mini-anchor for TMJ articular disc stabilization. J Oral Maxillofac Surg. Forthcoming.
  3.  Fields TR, Cardenas L, Wolford LM. The pullout strength of mitek mini- and micro-anchors in human mandibular condyles. Abstract presented at the 77th AAOMS Annual Meeting, Toronto, 1995.
  4.  Timmis DP, Aragon SB, Van Sickels JE, Aufdenmorte TB. Comparative study of alloplastic material for temporomandibular joint disc replacement in rabbits. J Oral Maxillofac Surg 1986;44:541-54.
  5.  Heffez L, Mafee MF, Rosenberg H, Langer B. CT evaluation of TMJ disc replacement with a proplast-teflon laminate. J Oral Maxillofac Surg 1987;44:657-65.
  6.  Ryan DE. Alloplastic implants in the temporomandibular joint. Oral Maxillofac Surg Clin North Am 1989;1:427-41.
  7.  Yih WY, Merrill RG. Pathology of alloplastic interpositional implants in the temporomandibular joint. Oral Maxillofacial Surg Clin North Am 1989;1:415-26.
  8.  Wagner JD, Mosby EL. Assessment of proplast-Teflon disc replacements. J Oral Maxillofac Surg 1990;48:1140-4.
  9.  Wolford LM, Henry CH, Nikaein A, Newman JT, Namey TC. The temporomandibular joint alloplastic implant problem. In: Sessle BJ, Bryant PS, Dionne RA, eds. Progress in pain research and management. Seattle: IASP Press; 1995.
  10. Henry CH, Wolford LM. Treatment outcomes of temporomandibular joint reconstruction after proplast-teflon implant failure. J Oral Maxillofac Surg 1993;51:352-8.
  11. Chase DC, Hudson JW, et al. The Christiansen prosthesis: a retrospective clinical study. Oral Surg Oral Med Oral Pathol Oral Radial Endo 1995;80:273-8.
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  12. Wolford LM, Cottrell DA, Henry CH. Temporomandibular joint reconstruction of the complex patient with the techmedica custom-made total joint prosthesis. J Oral Maxillofac Surg 1994;52:2-10.
  13. Wolford LM, Karras SC. Autologous fat transplantation around TMJ total joint prostheses: treatment outcomes. Abstract presented at 77th AAOMS Annual Meeting, Toronto, 1995.
  14.  Goldblum RM, Pelley RP, O'Donnell AA, Pyron D, Heggers JP. Antibodies to silicone elastomers and reactions to ventriculoperitoneal shunts. Lancet 1992;340:510-3.
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Temporomandibular Joint Surgery for Internal Derangement
M. Franklin Dolwick, D.M.D., Ph.D.

            Although approximately 5 percent of all patients being treated for temporomandibular disorders undergo surgery; controversy continues to surround the role of surgery in the management of temporomandibular joint (TMJ) pain and dysfunction. The role of surgery has increased since the idea of internal derangement gathered momentum during the 1970's. During this time, renewed interest was focused on the importance of disc displacement and deformity as the cause of TMJ pain and dysfunction. As a result, numerous open joint procedures were developed to reposition and reshape the displaced or deformed disc. With the introduction of new and less invasive techniques, the success of simpler procedures such as lavage and lysis has raised important questions about the central pathosis of internal derangement.
 The undisputed application of surgery is found in the management of the least common TMJ disorders such as ankylosis, growth disorders, recurrent dislocation, and neoplasia. Unfortunately, for the more common disorders such as internal derangement and osteoarthritis, the indications for surgery are less clear and often dependent on the patient's ability to accurately report their symptoms as well as the surgeon's ability to interpret the often confusing clinical signs. Although TMJ arthrography and magnetic resonance imaging have proven to be of value in depicting disc displacement, the clinic symptoms often fail to correlate with the findings of these studies. Overreliance on the diagnostic value of imaging may lead to overdiagnosis of internal derangement and hence to overtreatment. Therefore, it is essential that the clinician emphasize the history and clinical examinations rather than the results of imaging. Clinical indications for TMJ surgery are relative rather than absolute and the following general guidelines are recommended. TMJ pain and dysfunction refractory to appropriate nonsurgical therapies and which constitutes a significant impairment to the patient in his/her day to day activities. It must be emphasized that the criterion is not simply refractory pain specifically localized to the TMJ.
  A spectrum of surgical procedures are currently used for the treatment of internal derangement, ranging from simple arthrocentesis and lavage to the most complex open joint operations. The success of surgery is largely dependent on appropriate case selection. With the increased surgical options available to surgeons, it seems prudent that selection of the surgical procedure with the highest probability of success and the least morbidity should be the ultimate objective. Unfortunately, few techniques have gained universal acceptance. This is a reflection of the continued poor understanding of the complex behavioral influences of the patient which more often than not tend to make the true etiology and pathology of this disorder. Surgical treatment of TMJ internal derangement has proven effective for reducing pain and increasing range of motion in about 80 percent of patients, regardless of operative technique, based on retrospective studies. Unfortunately, long-term randomized prospective studies are lacking.
 Surgery of the TMJ continues to have a small, but nonetheless, important role in the management of TMJ pain and dysfunction. It is best undertaken by surgeons who maintain the philosophy that surgery should aim to avoid further harm to the joint itself and err on the side of more conservative.
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surgical procedures. The surgeon's enthusiasm for successful outcomes must always be tempered by his/her concern for the unsuccessful outcomes and their consequences to the patient.
 Further research should be focused on the following areas: (1) defining the TMJ pathology and its relationship to pain and dysfunction, (2) identifying its etiology, (3) development of objective criteria for surgical intervention, and (4) long-term randomized prospective studies of TMJ surgical procedures.
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FAILED IMPLANTS AND MULTIPLE OPERATIONS
Stephen B. Milam, D.D.S., Ph.D.
Rationale for the Use of Alloplastic Materials to Reconstruct the Temporomandibular Joint

 The temporomandibular joint (TMJ), site of articulation between the mandible and cranial base, is a complex compound joint capable of both hinge and sliding movements. The major structural components of the TMJ are the mandibular condyle and the glenoid fossa of the temporal bone. These articular structures are separated by an interposing articular disk that is chiefly composed of type 1 collagen, proteoglycans, and a sparse population of fibroblast-like cells.1-6
 Several functions have been ascribed for the articular disk of the TMJ, including (1) distribution of contact stresses over a broad area, (2) creation of two joint compartments allowing for extended complex movements, and (3) providing additional lubricated surfaces allowing for smooth joint movements. Although the exact function(s) of the articular disk of the TMJ is unknown, it is apparent from both animal7-9 and clinical10-13 studies that displacement or loss (i.e., surgical removal) of the articular disk typically is associated with, or promotes, morphological changes involving the mandibular condyle and temporal bone.
 A majority of clinicians have held the belief that restoration of "normal" mandibular condyle-articular disk-temporal bone structural relationships were vitally important to sustained health of the joint. Modifications of articular surfaces resulting from the functional loss of the articular disk have been interpreted to represent a progressive, pathological process evoked by altered load dynamics. However, this belief is founded on inadequately tested models of degenerative TMJ disease.14  At the present time, there is little convincing evidence that these "normal" structural relationships are essential requirements for normal joint function. Furthermore, the notion that progressive degenerative joint disease is inevitable consequence of the functional loss of the articular disk has recently been challenged by investigators who argue that the observed structural changes associated with loss of the articular disk represent adaptive remodeling. This latter view is supported by observations from long-term clinical studies of individuals who underwent TMJ discectomy, but maintained adequate functional use of the mandible for up to 30 years.15,16  Despite the fact that neither view is totally supported by scientific study, the prevailing attitude is that the articular disk of the TMJ provides a
vital function for joint health. Likewise, it is believed by many treating clinicians that articular disk replacement strategies should be considered when the articular disk is surgically removed.
 Several surgical methods have been devised in an attempt to restore "normal" structural and functional relationships in the TMJ following discectomy. Autologous grafting procedures employing dermis, articular (ear) cartilage, fat and temporalis muscle have been used to provide some interposing tissue between the mandibular condyle and the temporal bone. Allogeneic materials, including fresh frozen cartilage, lyophyilized cartilage, and lyophilized dura, have also been used to reconstruct the TMJ following discectomy. Enthusiasm for allogeneic materials has been dampened by
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concerns of host responses against these materials, a limited availability of materials, and transmission of infectious diseases to recipients.
ALLOPLASTIC MATERIALS USED TO RECONSTRUCT THE TEMPOROMANDIBULAR JOINT
 Alloplastic materials used as medical devices have traditionally been viewed as biologically inert substances that can be designed to reproducible specifications with desirable mechanical properties. Furthermore, the use of an alloplastic material eliminates the need for tissue harvesting, an additional surgical procedure required when autogenous tissues are used for TMJ reconstruction. Therefore, donor site morbidity can be avoided when alloplastic materials are used.
 Alloplastic devices have been used as interpositional materials to replace the articular disk of the TMJ following discectomy17-25 or to replace the mandibular condyle and articular fossa26 affected by advanced degenerative disease or ankylosis. Silicone rubber and Proplast/Teflon implants were the most commonly used devices in TMJ reconstructive surgery in the 1980's.
SILICONE RUBBER
 Silicone rubber (Silastic, Dow Corning) was first used to reconstruct the TMJ in 1969.27,28  Since then, either silicone rubber or Dacron-reinforced silicone rubber has been used as a permanent or temporary interpositional (i.e., placed between the mandibular condyle and the temporal bone) material in TMJ reconstructive surgery. Early reported experiences with these materials were favorable. Short-term success rates were reported from 87 to 91 percent, although the criteria used to determine successful outcomes in these clinical reports were generally vague.29
 Animal studies subsequently revealed that silicone rubber implants placed into the TMJ following discectomy are typically encapsulated by a fibrous  reactive tissue that has been characterized superficially by histological studies.30  It has been suggested that this tissue can function as a disk replacement material that may prevent or minimize responses of articular tissues to altered biomechanics induced by discectomy. On the basis of this assumption, Dacron-reinforced silicone rubber has been used as a temporary implant to elicit the formation of this reactive tissue in TMJ after discectomy. The implant is typically placed for less than 6 months and then removed, leaving the fibrous capsule interposed between the mandibular condyle and temporal bone. Preliminary animal studies indicate that this approach may be valid.30  However, to date, no clinical studies that are adequately designed to assess the efficacy of this technique have been conducted.
PROPLAST-TEFLON (P/T)
 Implants composed primarily of carbon fiber and polytetrafluoroethylene (Proplast/Teflon 1), were introduced in the mid-1970's as devices to reconstruct the TMJ following discectomy. Later, the composition of this material was altered to produce a polytetrafluoroethylene and aluminum oxide composite material. Early successes with the use of these materials (Proplast/Teflon 1 and II interpositional implants; Vitek, Inc., Houston, TX.) were reported, and specific advantages of these materials over silicone over rubber-based devices were noted.18. 19  The perceived advantages of these materials included greater implant stability afforded by tissue ingrowth into the more porous P/T
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implants. In addition, the handling properties of the P/T implants were superior to the silicone rubber materials. In 1985, P/T implants were favored 3 to 1 over silicone rubber implants by surveyed oral surgeons.31  The peak use of these materials is thought to have occurred in the mid-1980's.32
FAILURE RATES AND ESTIMATES OF THE NUMBER OF SURGICAL PROCEDURES PERFORMED IN THE UNITED STATES
 Reliable statistics concerning (1) the actual number of implants placed, (2) the percentage of patients requiring multiple surgical interventions to manage complications associated with implant placement, or (3) the number of patients experiencing protracted difficulties as a result of surgical reconstruction of the TMJ with alloplastic materials do not exist at the present time. It has been estimated that over 20,000 TMJs have been reconstructed with P/T devices.33  However, this figure is not based on epidemiologic data. The figure merely represents an estimate based on the number of P/T implants produced (i.e., approximately 26,000).
 The only published relevant data indicate that, in 1985, approximately 17,000 TMJ arthroplasties were performed in the United States.32   The same publication indicates that, from 1973 to 1993, more than 170,000 procedures were performed. More recent estimates suggest that the number of surgeries has sharply declined in recent years. The National Center for Health Statistics (NCHS) estimates that 5,000 TMJ arthroplasties were performed in the United States in nongovernment hospitals in 1993.34  (Interestingly, this estimate is inconsistent with that reported for the same year by Mendenhall32 (i.e., approximately 14,000 cases)). Statistics provided by the American Association of Oral and Maxillofacial Surgeons concerning case numbers reported by training programs in the United States provide further evidence of a declining trend in the number of TMJ arthroplasties performed in the United States over the past 5 years (personal communication, 3/11/96). These data indicate that the total number of surgical procedures performed at 108 training centers declined from 9,338 surgeries during the period 1991 to 1992 to 2,939 surgeries from 1994 to 1995. Reliable data for the period 1980 to 1990 are not available from any source. It should be noted that the figures mentioned above represent all the TMJ arthroplasties and do not necessarily reflect those procedures employing alloplastic implants. Furthermore, these data do not allow for accurate estimates of patients who have undergone multiple TMJ surgeries.
FAILURE RATES FOR SURGICAL PROCEDURES EMPLOYING ALLOPLASTIC IMPLANTS
 P/T implants specifically have been shown to be vulnerable to repeated mechanical stresses encountered in the TMJ with functional movements of the jaw. In vitro wear data have predicted an in vivo service life of 1 to 3 years for P/T implants used to reconstruct human TMJs.35  Clinical experiences are in general agreement with this estimate. Failure rates ranging from 50 to 100 percent have been reported.29,31,36-38  P/T implant failures have been observed as early as 3 months following their placement into the TMJ. Animal studies indicate that the cellular responses directed against P/T implant debris created by wear are similar to those observed in response to particulate silicone rubber.39  However, the foreign body response to P/T debris may be more intense with greater damage to articular tissue.39  The reason for this difference is not readily apparent, but may be due to differences in particle size generated from implant failure and the presence of other noxious chemical substances (i.e., aluminum oxide).
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ADVERSE TISSUE RESPONSES TO ALLOPLASTIC MATERIALS IN THE TEMPOROMANDIBULAR JOINT
 In 1984, Dolwick et al. reported results from histological studies of biopsy specimens obtained from a human TMJ previously reconstructed with a silicone rubber implant.40  These investigators observed a foreign body response directed against particulate silicone generated by excessive wear of the implant. Many multinucleated giant cells were observed in the specimens examined. One year later, evidence that implant debris could be disseminated outside the TMJ by phagocytic cell populations was provided when silicone rubber particles were observed in an ipsilateral cervical lymph node in a patient who had previously received a silicone rubber implant for TMJ reconstruction.41 The cellular response to the observed particulate silicone rubber in this lymphoid tissue was histologically similar to the silicone lymphadenopathy resulting from implant failure in the hand42 as observed 8 years earlier by Christie et al.
          Eriksson and Westesson found that 55 percent of the silicone rubber implants from TMJ after 1 to 19 months of service were cracked or fragmented.43  Degeneration of articular tissues of the TMJ and subsequent failure of autologous grafts used to reconstruct joints following removal of failed silicone rubber or P/T implants are believed to result from a chronic inflammatory condition produced by cellular responses to microparticulate implant debris.44  Malocclusions have resulted from a progressive loss of structural support provided by the mandibular condyle secondary to resorption in some patients. However, in other individuals, heterotopic bone formation may be observed in TMJs previously reconstructed with alloplastic implants. In extreme cases, a resultant fibro-osseous ankylosis can severely restrict jaw movements and may necessitate additional surgery.
 Perforations of the glenoid fossa with exposure of dura are commonly observed during retrieval of failed TMJ implants.45,46  Defects as large as 2.5cm in diameter have been reported.46  In one case, a cerebrospinal fluid leak was observed indicating violation of the dura in a patient with a failed P/T implant.46  On the basis of these observations, there is some concern regarding the potential involvement of the CNS in isolated cases. However, to date there have been no reported cases of direct injury to the brain as a result of complications from implant failure.
 It is also apparent that some individuals with failed TMJ implants do not manifest any apparent  untoward physiologic effects. At the present time, it is not clear why these individuals remain virtually unaffected by the implant failure, while others seem to manifest signs and symptoms of a progressively debilitating condition. These clinical observations suggest that several host factors influence local tissue responses to surgical reconstruction with alloplastic implants.
CHRONIC PAIN
 Perhaps the most troublesome aspect of failed surgical therapy for TMJ disorders is the frequently observed complaint of chronic pain. The pain is frequently localized to the preauricular region. However, many patients described a more diffuse painful condition perceived in distant regions of the head, neck, upper back, and upper extremities. In most cases, the pain complaint persists in the face of therapeutic interventions.
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 Some patients who have undergone multiple temporomandibular surgeries experience a marked allodynia with cold intolerance in the preauricular region overlying the affected joint. Pain experienced by these patients is typically described as a constant, burning pain. Furthermore, some patients suffering from this condition have experienced relief of pain following either phentolamine administration or stellate ganglion blockade, suggesting a sympathetically maintained pain component.
 That relationship between persistent pain and the foreign body response to failed implant debris has not been firmly established. Similar symptoms of equal intensity are also described by patients who have failed multiple TMJ surgeries, but have not received any alloplastic devices as part of the joint reconstruction. It appears that chronic painful conditions observed in the multiply operated TMJ patient may be secondary to the effects of repeated surgical trauma of the region. Alternatively, these painful conditions could be the result of a continuation of a pre-existing condition that was either not recognized or ineffectively treated.
SYSTEMIC ABNORMALITIES IN PATIENTS WHO HAVE RECEIVED ALLOPLASTIC IMPLANTS FOR RECONSTRUCTION OF THE TEMPOROMANDIBULAR JOINT
 Some patients who have received alloplastic TMJ implants also appear to manifest signs and symptoms of systemic abnormalities. Recurrent low grade fevers, malaise, polyarthralgia, polymyalgia, generalized muscle weakness, reflex sympathetic dystrophy, increased sensitivity to chemicals or odors, and food intolerances are occasionally reported by patients. At the present time, it is not clear whether these additional signs and symptoms are coincidental, related to a previously unidentified systemic disorder that predisposed the patient to an adverse surgical response, or was triggered by a foreign body response to the implant. Concurrent diseases including rheumatoid arthritis, scleroderma, multiple sclerosis, and Sjogren's disease have also been observed in some patients who have received alloplastic implants for TMJ reconstruction. No relationship can be established from existing clinical data between the co-existence of these conditions and the foreign body response directed against either silicone rubber or P/T implants.
CONCLUSION
The use of alloplastic implants for reconstruction of the TMJ was based on the widely held belief that ankylosis, degenerative changes, and/or occlusal instability would likely occur if an interpositional material was not used in the reconstruction of TMJ following discectomy. An undetermined number of patients received these devices during the 1970's and 1980's.
Silicone rubber and Proplast-Teflon implants were used to reconstruct the TMJ as interpositional materials. However, the materials were insufficiently designed to withstand contact stresses generated during functional movements of the jaw.
A foreign body response directed against implant debris, characterized by the formation of multinucleated giant cells, has been consistently observed in tissue specimens obtained from biopsy of human and animal TMJs implanted with these alloplastic devices.
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A variable response to failed TMJ implants is observed clinically. An undetermined percentage of patients appear to manifest severe de-generative changes in affected joints, as determined by a rapid and progressive loss of articular structure. Another undetermined percentage of patients appear to form excessive bone (i.e., heterotopic bone) in affected TMJs. Other patients do no appear to experience serious adverse responses to failed implants.
Failure to effectively manage chronic pain is a primary concern of both patients and treating clinicians.
Although co-existing systemic illnesses have been observed in patients manifesting signs of an aggressive foreign body response to implant debris, the nature of this relationship, if any, has not been established.
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3.  Fujita S. Hoshino K. Histochemical and immunohistochemical studies on the articular disk of the temporomandibular joint in rats. Acta Anatomica 1989;134:26.
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10. Westesson PL, Rohlin M. Internal derangement related to osteoarthritis in temporomandibular joint autopsy specimens. Oral Surg Oral Med Oral Pathol 1984;57:17.
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12. Westesson PL. Structural hard-tissue changes in temporomandibular joints with internal derangement. Oral Surg Oral Med Oral Path 1985;59:220.
13. de Bont LGB, Boering G. Liem RSB, et al. Osteoarthritis and internal derangement of the temporomandibular joint: a light microscopic study. J Oral Maxillofac Surg 1986;44:634.
  14. Wilkes CH. Internal derangments of the temporomandibular joint. Arch Otolaryngol Head Neck Surg 1989;115:469.
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  16. Tolvanen M, Oikarinen VJ, Wolf J. A 30-year follow-up study of temporomandibular joint meniscectomies: a report on five patients. Br J Oral Maxillofac Surg 1988;26:311.
  17. Kent JN, Homsy CA, Hinds EC. Proplast in dental facial reconstruction. Oral Surg Oral Med Oral Path 1975;39:347.
  18. Farrell CD, Kent JN. Clinical application of Proplast in oral and maxillofacial surgery. Alpha Omegan 1975.
  19. Gallagher DM, Wolford LM. Comparison of Silastic and Proplast implants in the temporomandibular joint after condylectomy for osteoarthritis. J Oral Maxillofac Surg 1982;40:627.
  20. Moriconi ES. Popowich LD, Guernsey LH. Alloplastic reconstruction of the temporomandibular joint. Dent Clin North Am 1986;30:307.
  21. Dattilo DJ, Granick MS, Soteranos GS. Alloplastic reconstruction of the temporomandibular joint. Dent Clin North Am 1986;30:307.
  22. Kalamch S, Walker RV. Silastic implant as part of temporomandibular joint arthroplasty: evaluation of its efficacy Br J Oral Maxillofac Surg 1987;25:222.
  23. Blauth W, Hassenpflug J. Prosthetic replacement of the condylar head for temporomandibular joint disease. Plast Reconst Surg 1987;80:536.
  24. Posnick JC, Jacobs JS, Magee WJ. Prosthetic replacement of the condylar head for temporomandibular joint disease. Plast Reconst Surg 1987;80:536.
  25. Morgan DH. Evaluation of alloplastic TMJ implants. Cranio 1988;6:224.
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  26. van Loon J-P, deBont LGM, Boering G. Evaluation of temporomandibular joint prostheses: review of the literature from 1946 to 1994 and implications for future prosthesis designs. J Oral Maxillofac Surg 1995;53:984.
  27. Hansen WC, Deshazo BW. Silastic reconstruction of temporomandibular joint meniscus. Plast Reconst Surg 1969;43:388.
  28. Henny FA. Surgical treatment of the painful temporomandibular joint. J Am Dent Assoc 1969;79:171.
  29. Ryan DE. Alloplastic implants in the temporomandibular joint. In: Merrill RG, ed. Oral Maxillofac Surg Clinics North Am. Vol. 1. Philadelphia: WB Saunders Co., 1989. p427.
  30. Tucker MR, Burkes EJ. Temporary Silastic implantation following diskectomy in the primate temporomandibular joint. J Oral Maxillofac Surg 1989;47:1290.
  31. Yih WY, Merrill RG. Pathology of alloplastic interpositional implants in the temporomandibular joint. In: Merrill RG, ed. Oral Maxillofac Surg Clin North Amer. Vol 1. Philadelphia: WB Saunders Co., 1989. p.415.
  32.  Mendenhall S. TMJ implants: lessons for all of us. Orthop Network News 1995:6:1.
  33. Spagnoli D, Kent JN. Multicenter evaluation of temporomandibular joint Proplast-Teflon disk implant. Oral Surg Oral Med Oral Pathol 1992;74:411.
  34. CDC. Detailed Diagnoses and Procedures. National Hospital Discharge Survey, 1993. 1995:122.
  35. Fontenot MG, Kent JN, In vitro wear performance of Proplast TMJ disc implants. J Oral Maxillofac Surg 1992;50:133.
  36. Heffez L, Mafee MF, Rosenberg H, et al. CT evaluation of TMJ disc replacement with a Proplast-Teflon laminate. J Oral Maxillofac Surg 1987:45:657.
37. Valentine JJ, Reiman BE, Beuttenmuller EA, et al. Light and electron microscopic evaluation of Proplast II TMJ disc implants. J Oral Maxillofac Surg 1989;47:689.
  38. Schellhas KP, Wilkes CH, el DM, et al. Permanent Proplast temporomandibular joint implants: MR imaging of destructive complications. Ajr Am J Roentgenol 1988;151:731.
  39. Timmis DP, Aragon SB, Van SJ, et al. Comparative study of alloplastic materials for temporomandibular joint disc replacement in rabbits. J Oral Maxillofac Surg 1986;44:541.
  40. Dolwick MF, Aufdemorte TB, Cornelius JD. Histopathologic findings internal temporomandibular joint derangements. J Dent Res 1984;63:267.
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  41. Dolwick MF, Aufdemorte TB. Silicone-induced foreign body reaction and lymphadenopathy after temporomandibular joint arthroplasty. Oral Surg 1985;59:449.
  42. Christie A, Weinberger K, Dietrich M. Silicone lymphadenopathy and synovitis. JAMA 1977;237:1463.
  43. Eriksson L, Westesson P-L. Deterioration of temporary silicone implant in the temporomandibular joints: a clinical and arthroscopic follow-up study. Oral Surg Oral Med Oral Pathol 1986;62:2.
  44. Henry CH, Wolford LM. Treatment outcomes for temporomandibular joint reconstruction after Proplast-Teflon implant failure. J Oral Maxillofac Surg 1993;51:352.
45. Berarducci JP, Thompson DA, Scheffer RB, Perforation into middle cranial fossa as a sequel to use of a Proplast-Teflon implant for temporomandibular joint reconstruction. J Oral Maxillofac Surg 1990;48:496.
  46. Choung R, Piper MA, Cerebrospinal fluid leak associated with proplast implant removal from the temporomandibular joint. Oral Surg Med Oral Pathol 1992;74:422.
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Neuroendocrine and Immune Considerations
Kenneth M. Hargreaves, D.D.S., Ph.D., and Lois Kehl, D.D.S.
 
     Numerous physiologic systems are activated in response to tissue injury, degeneration, and repair. A list of these responses includes the central, peripheral, and autonomic nervous systems, as well as activation of neuroendocrine, endocrine, and paracrine systems.  However, not all responses can be considered adaptive. Indeed, many forms of chronic inflammation/injury are characterized by a substantial immunological component directed against host tissue.1,2  The collective action of these pathophysiologic responses modulates the progression of temporomandibular disorders (TMD) and the clinical response of the patient to treatment.
     In contrast to a transient pain-producing stimulus (e.g., electric pulp test, venipuncture, etc.), pain related to inflammation or injury is associated with a prolonged period of hyperalgesia. Hyperalgesia can be characterized as spontaneous pain, a decrease in pain threshold, and an increase in responsiveness to suprathreshold stimule.3  Hyperalgesia is a common response to tissue injury and appears to be a response to combined peripheral and central mechanisms.4
     In general, inflammatory mediators have two main effects on the peripheral nociceptive nerve ending. Mediators activate and/or sensitive certain peipheral nerve terminals and, as described below, also evoke peripheral release of neuropeptides such as substance P or calcitonin gene-related peptide.3,5-10  The sensory fibers that innervate skin, muscle, and joints can also become sensitized. During inflammation in joints, the spontaneous electrical activity of C- and A-delta fibers more than doubles, and their responses to nonnoxious joint movements increases twofold to sevenfold.11,12
     The actual biochemical substances that mediate peripheal sensitization are unknown but probably vary depending on the tissue examined, intervention employed, and dependent measure evaluated. For example, prostaglandins, leukotrienes, bradykinin, histamine, serotonin, acetylcholine, potassium, interleukin-1 and hydrogen ions (e.g., low pH) all activate or sensitize primary afferent fibers located in skin, muscle, or joint.9,11-15  Collectively, these results suggest that these various biochemical mediators can produce hyperalgesia with differential efficacy and time courses. Thus, simultaneous measure of multiple inflammatory mediators may be required to assess factors modulating the activity of peripheral nociceptors. The resulting activation and sensitization of certain primary afferent neurons is thought to contribute to hyperalgesia at the site of injury.3,5  This sustained peripheral response may also induce plasticity changes within the central nervous system (CNS) and activate central mechanisms of hyperalgesia.
     In the CNS, a number of changes are now known to occur in response to tissue inflammation. A potentially important implication of central hyperalgesia is the proposal that relatively long-lasting changes may occur in the CNS in response to the afferent barrage that occurs during injury. It has been proposed that persistent CNS component of hyperalgesia may contribute to some forms  of chronic pain and that this CNS component may persist even in the absence of continued peripheral nociceptor input.16,17 According to this hypothesis, certain proposed mechanisms of CNS hyperalgesia (e.g., those secondary to cell death) may prove refractory to therapeutic approaches designed solely to
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 reduce peipheral afferent input. A corollary to this hypothesis is that therapeutic interventions for certain TMD may have only limited efficacy because of an inability to reverse cell death.
     A substantial amount of research in the last 20 years has focused on local (e.g., paracrine) mediators that act to alter tissue responses to injury, inflammation, and repair. It is beyond the scope of this review to provide extensive detail on this burgeoning field; indeed, numerous symposia have been held on only one class of these paracrine factors (i.e., the cytokines). A greater understanding of the paracrine response and its regulation is important in elucidating tissue response to injury, degeneration, and repair.
     Considerable research has focused on determining the actions and identifying tissue levels of arachidonic acid metabolites in joint inflammation. Levels of immunoreactive, PGE2 and LTB4 are increased or correlated with symptoms in synovial fluid collected from the temporomandibular and other joints.18-20  Cells isolated from synovium, or macrophages collected from patients with inflamed joints, have enhanced the ability to synthesize prostanoids such as PGE2.21-23  These biochemical studies, together with studies demonstrating the anti-inflammatory efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs), are consistent with the hypothesis that certain eicosanoids may contribute to sustained joint inflammation.
     A number of studies have implicated immune modulation of joint disease. Several animal models of joint inflammation indicate that both T-and B-cell responses can modulate the development of inflammation.2,24-27  Additional studies have pointed to the possible roles that macrophages or neutrophils may play in the development of joint inflammation28,29 and pain.30  Several clinical studies have demonstrated increased levels of cytokines in synovial tissues or fluid collected from inflamed joints. For example, IL-1, IL-6, and leukemia inhibitory factor have been reported to be increased during joint inflammation. 31-33
     Growth factors such as nerve growth factor (NGF) may also contribute to chronic pain. NGF is increased after tissue injury34,35 and induces hyperalgesia when injected into either skin or muscle of rats.36,37  Interestingly, injection of NGF into the muscle of rats produces a long-lasting hyperalgesia to movement.37 In addition, injection of NGF into humans produces a persistent hyperalgesia, which has lasted up to 7 weeks following a single injection.38  Increased levels of NGF are found in the synovium of pain patients39 and were reportedly detected in the sera of pain patients.40  NGF and perhaps other growth factors may serve as a molecular switch for altering the phenotype of peripheral nociceptors. This is a new and potentially important area of research for chronic pain.
CLINICAL RELEVANCE
     The heterogeneous population of conditions that chronic orofacial pain has rendered accurate diagnosis and effective treatment problematic issues. Recent research on peripheral pain mechanisms offers new information on possible etiologies for activation of peripheral nociceptors and central neurons which may contribute to chronic pain. Together with the newly developed microdialysis method,4 it is now possible to conduct biochemically based clinical and animal studies to evaluate the role of potential peripheral pain mechanisms that may contribute to various chronic orofacial pain conditions.
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      This approach is clinically significant, since it offers the possibility of developing biochemically diagnostic tests for including (or excluding) various peripheral etiologies contributing to a specific patient's chronic orofacial pain. This diagnostic information may allow the clinician to systematically elucidate the possible factors contributing to the pain state and provide some insight into the specific peripheral biochemical mechanisms contributing to the chronic pain condition. An additional opportunity afforded by this method is the development of improved therapeutic approaches for the management of the pain. Knowledge of basal levels of inflammatory mediators may permit a more rational selection of pharmacologic and nonpharmacologic treatments. Knowledge of post-treatment levels of inflammatory mediators may be equally important for evaluating treatment efficacy and optimizing patient care. Moreover, this approach may ultimately provide prognostic information for developing a unified approach for management of chronic orofacial pain. Moreover, identification of growth factors such as NGF that evoke persistent pain following a single injection may lead to studies directly testing the role of NGF and other mediators in contributing to temporomandibular disorders.
REFERENCES
  1.  Birkedahl-Hansen H. Role of cytokines and inflammatory mediators in tissue destruction. J Periodont Res 1993;28:500-10.
  2.  Van Eden W. Holoshitz J, Nevo Z, Frenkel A, Klajman A, Cohen I. Arthritis induced by a T-lymphocyte clone that responds to Mycobacterium tuberculosis and to cartilage proteoglycans. Proc Nat Acad Sci USA 1985;82:5117-20.
  3.  Willis, W. The pain system. Basel: Karger 1985.
  4. Hargreaves KM, Roszkowski M, Jackson D, Bowles W, Richardson JD, Swift JQ. Neuroendocrine and immune responses to injury, degeneration and repair. In: Sessle B. Dionne R, Bryant P, eds. Temporomandibular disorders and related pain conditions. Seattle (WA): IASP Press, 1995;273-92.
  5.  Dubner R, Bennett G. Spinal, and trigeminal mechanisms of nociception. Ann Rev Neurosci 1983:6:381-418.
  6.  Jackson D, Garry M, Engelstad M, Geier H, Hargreaves K. Evaluation of iCGRP secretion from dental pulp in response to inflammatory mediators. Abs Soc Neurosci 1992;18:689.
  7.  Jackson D, Aanonsen L, Richardson JD, Wiski B, Groves N, Hargreaves KM. Binding sites and actions of excitatory amino acids in bovine dental pulp (abstract). J Dent Res 1990;73.
  8.  Light AR, The initial processing of pain and its descending control: spinal and trigeminal systems. Basel: Karger, 1992.
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  9. Martin H, Basbaum A. Kwiat G, Goetzl E, Levine J. Leukotriene and prostaglandin sensitization of cutaneous high-threshold C-and A-delta mechanoreceptors in the hairy skin of rat hindlimbs. Neuroscience
1987;22;651-9.
  10. Sessle B. Neurophysiology of orofacial pain. Dent Clin North Am 1987;31:595-614.
  11. Schaible H, Schmidt R. Discharge characteristics of receptors with fine afferents from normal and inflamed joints: influence of analgesics and prostaglandins. Agents Actions (Suppl) 1986;19:99-117.
  12.  Schaible H, Grubb D. Afferent and spinal mechanisms of joint pain. Pain 1993;55:5-54.
  13.  Mense S. Nervous outflow from skeletal muscle following chemical noxious stimulation. J Neurophysiol 1977;267:75-88.
14.  O'Byrne E, Blancuzzi V, Wilson D, Wong M, Jeng A. Elevated substance P and accelerated cartilage degradation in rabbit knees injected with interleukin-1 and tumor necrosis factor. Arthritis Rheum 1990;33:1023-7.
  15.  Steen KH, Reeh PW, Anton F, Handwerker HO. Protons selectively induce lasting excitation and sensitization to mechanical stimulation of nociceptors in rat skin in vitro. J Neurosci 1992:21:86-95.
  16.  Coderre, T, Melzack, R. The contribution of excitatory amino acids to central sensitization and persistent nociception after formalin-induced tissue-injury. J Neurosci 1992;12:3665-70.
  17.  Dubner R, Ruda MA. Activity-dependent neuronal plasticity following tissue injury and inflammation. Trends Neurosci 1992;15:96-102.
  18.  Quinn JH, Bazan NG. Identification of Prostaglandin E2 and Leukotriene B4 in the synovial fluid of painful, dysfunctional temporomandibular joints. J Oral Maxillofac Surg 1990;48:968-71.
  19.  Atik OS. Leukotriene B4 and prostaglandin E2-like activity in synovial fluid in osteoarthritis. Prostaglandins Leukot Essent Fatty Acids 1990:39:253-4.
  20.  Trang LE, Granstrom L, Lovgren L. Levels of prostaglandins F2 and E2 and thromboxane B2 in joint fluid in rheumatoid arthritis. Scand J Rheumatol 1977;6:151-4.
  21.  Moilanen E. Effects of diclofenac, indomethacin, toldenamic acid and hydrocortisone on prostanoid production in healthy and rheumatic synovial cells. Agents Actions 1989;26:342-7.
  22.  Seitz M, Hunstein W. Enhanced prostanoid release from monocytes of patients with rhematoid arthritis and active systemic lupus erythematosus. Ann Rheum Dis 1985;44:438-45.
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  23.  Wittenberg RH, Willburger RE, Kleemeyer KS, Peskar BA. In vitro release of prostaglandins and leukotrienes from synovial tissue, cartilage, and bone in degenerative joint diseases. Arthritis Rheum 1993;36:1444-50.
  24.  Buchan G, Barrett T, Fujita T, Taniguchi T, Maini, R, Feldmann, M. Detection of activated T cell products in the rheumatoid joint using cDNA probes to Interleukin-2(IL-2) (IL-2) IL-2 receptor and IFN-y. Clin Exp Immunol 1988;71:295-301.
  25.  Brauer R, Thoss K, Henzgen S, Waldmann G. Significance of cell-mediated and humoral immunity in the acute and chronic phase of antigen-induced arthritis in rabbits. Exp Pathol 1988;34:197-206.
  26.  Haynes BF, Grover BJ, Whichard LP, Hale LP, Nunley JA, McCollu DE, Singer KH. Synovial microenvironment-T cell interactions. Arthritis Rheum 1988;31:947-53.
  27.  Holmdahl R, Klareskog L, Rubin K, Bjork J, Smedegarde G, Jonsson R. Role of T lymphocytes in murine collagen induced arthritis. Agents Actions 1986;19:295-303.
  28. Alwan WH, Dieppe PA, Elson CJ, Bradfield JW, Hydroxapatite and urate crystal induced cytokine release by macrophages. Ann Rheum Dis 1989;48:476-82.
  29.  Haas DA, Nakanishi O, MacMillan RE, Jordan RC, Hu JW. Development of an orofacial model of acute inflammation in the rat. Arch Oral Biol 1992:37:417-22.
  30.  Levine J, Lau W, Kwiat G, Goetzl E. Leukotriene B4 produces hyperalgesia that is dependent on ploymorphonuclear leukocytes. Science 1984: 225:743-5.
  31.  Feldmann M, Brennan FM, Chantry D, Haworth C, Turner M, Abney E, Buchan G, Barrett K, Barkley D, Chu A, Field M, Maini RN. Cytokine production in the rheumatoid joint: implications for treatment. Ann Rheum Dis 1990;49: 480-6
32.  Rosenbaum JT, Cugnini R, Tara DC, Hefeneider S, Ansel JC. Production and modulation of interleukin 6 synthesis by synoviocytes derived from patients with arthritic disease. Ann Rheum Dis 1992;51:198-202.
33.  Waring PM, Carroll GJ, Kandiah DA, Buirski G. Metcalf D. Increased levels of leukemia inhibitory factor in synovial fluid from patients with rheumatoid arthritis and other inflammatory arthritides. Arthritis Rheum 1993;36:911-5
  34.  Aloe L, Tuveri M, Levi-Montalcini R. Studies on carrageenan-induced arthritis in adult rats: presence of NGF and role of sympathetic innervation. Rheumatol Intl 1992a;12:213-6.
35.  Byers MR, Wheeler EF. Bothwell M. Altered expression of NGF and p75 NGF-receptor by fibroblasts of injured teeth  precedes sensory nerve sprouting. Growth Factors 1992;6:41-8.
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  36.  Lewin GR, Ritter AM, Mendell L. Nerve growth factor induced hyperalgesia in the neonatal and adult rat. J Neurosci 1993;13:2136-48.
  37.  Kehl L, Trempe T, Hargreaves KM, NGF enhances carrageenan-evoked muscle hyperalgesia in rats. Pain 1996 (submitted).
38.  Petty BG, Cornblath DR, Flexner C, Wachsman M, Sinicropi D, Burton L, Peroutka SJ. The effect of systemically administered recombinant human nerve growth factor in healthy human subjects. Ann Neurol 1994;36:244-6
  39.  Aloe L, Tuveri M, Carcassi U, Levi-Montalcini R. NGF in the synovial fluid of patients with chronic arthritis. Arthritis Rheum 1992b;35:351-5.
40.  Dicou E, Mason C, Jabbour W, Nerriere V. Increased frequency of NGF in sera of rheumatoid arthritis and systemic lupus erythematosus patients. Neuroreport 1993;5:321-4.
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Tissue Engineering
Joseph P. Vacanti, M.D.

     Disease of the temporomandibular joint (TMJ) has been a very difficult clinical problem. Current methodology for replacing joints has been ineffective in the management of this particular disease. Over the last 10 years, a new field called tissue engineering has emerged.1-3  It applies the principles of life sciences to engineering to develop new tissues to restore lost function. A significant amount of work has been performed creating new cartilage for both reconstructive and orthopaedic applications. Likewise, new bone has been created. In these applications, cells can be expanded directly from the patient, eliminating any problems of immune attack. Also, by creating normal autologous tissue and avoiding permanent foreign body, a permanent structure with the ability to grow and remodel is created.
     Several approaches have evolved in the field of tissue engineering through the years. Our approach has been to attach tissue-specific cells onto open, porous, degradable synthetic polymer systems in cell culture. After appropriate times in culture, these devices can then be surgically implanted. After implantation, angiogenesis, tissue remodeling, and permanent engraftment occur. Using this technique, we have been able to create highly complex cartilaginous tissues and repair joint defects. We have also created composite tissue consisting of bone and cartilage for potential joint replacement where erosion has caused bone resorption.
     One can hypothesize that attaching patients' own living tissue into the TMJ reconstruction will allow durability and remodeling to produce better long-term function.
REFERENCES
  1.  Langer R, Vacanti JP. Artificial organs. Sci Am 1995;273(3):130-3.
  2.  Langer R, Vacanti J. Tissue engineering. Science 1993;260:920-6.
  3.  Puclacher WC, Wisser J, Vacanti CA, Ferraro NF, Jaramillo D, Vacanti JP. Temporomandibular joint disk replacement made by tissue-engineered growth of cartilage. J Oral Maxillofac Surg 1994;52:1172-7.
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A Scientific Basis for the Biological Regeneration of Synovial Joints
Frank P. Luyten, M.D., Ph.D.

     Temporomandibular disorders (TMD) represent a group of conditions ranging from local disease processes, restricted to the temporomandibular joint (TMJ), to more generalized diseases such as polyarthritis. Therefore, the pathogenic mechanisms leading to TMD are diverse and the therapeutic approaches different, depending on the underlying process. However, regardless of the etiopathogensis, TMD may result in the partial or complete destruction of the different tissues in the synovial joints, including the disc, the articular surface, the underlying bone, and the ligamentous structures. Even in these instances where a polyarthritic process is brought into remission, it is clear that in many cases a degenerative process will lead to further joint reconstruction. Therefore, it is a major challenge for the biomedical community to develop new approaches to regenerate or repair joint associated tissues.
     We have been focusing on the biology of the formation and regeneration of skeletal and joint tissues. It is now widely accepted that the molecular processes underlying tissue formation are to a large extent recapitulated during tissue regeneration. Consequently, we have devoted most of our attention to the molecular signals and cells involved in skeletal development and joint morphogenesis in particular. Most diathrodial joints of the skeleton, including the temporomandibular joint develop from a mesenchymal cell population in the joint interzone between the chondrifying bone primordia. This tissue differentiates then further into cartilaginous layers at either end of the future joint in contact with the adjacent bone and a central layer of dense connective tissue. This central connective tissue gives rise to the distinct elements of the joint, including disci, menisci, ligaments, and the synovial tissue that will line the future joint cavity. A cavitation process will lead to the formation of vacuoles in the joint interzone and ultimately coalesce to form the synovial cavity. The morphogenesis of the TMJ has some distinct characteristics, which will be discussed in some detail. Briefly, in mammalian and human development, there is a sequential existence of both a primary and secondary TMJ. The secondary joint functions throughout life as a synovial joint.
     Recent scientific developments have provided us with new tools to study at the molecular level the mechanisms involved in early skeletal and joint development. The cartilage-derived morphogenetic proteins-1 and -2 (CDMP-1 and -2)1 are members of the TGF=DF superfamily and are most closely related to the bone morphogenetic proteins. Localization data indicate that CDMP-1 is predominantly expressed in the precartilaginous cores of the developing limbs, in the joint interzone at the time of early joint development, and subsequently in the cartilaginous cores of the developing long bones. Mutations in the CDMP-1 gene, resulting in a loss of function of the protein, have been associated with human acromesomelic chondrodysplasia.2  The affected individuals display skeletal abnormalities with short limbs and hypoplastic, dislocated limb joints. These data support a crucial role of CDMP-1 in early limb developed and joint morphogenesis. Interestingly, in the chondrodysplastic individuals, several joints are not or are only discretely affected, including the acromioclavicular, sternoclavicular, and temporomandibular joint, suggesting that molecular processes in the morphogenesis of these joints are distinct.
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     The human chondrodysplastic disease due to a mutation in the CDMP-1 gene provides insight into the physiologic role of this protein in development. The data indicate that this gene is certainly involved in chondrogenesis and chondrocyte maturation. We are further exploring the biologic functions of the CDMPs and their potential to induce or maintain specific skeletal tissues, including cartilage, bone, and ligaments in a variety of in vitro and in vivo models. The data indicate  that it might be possible, depending on the cells and the respective signals, to direct tissue-specific cell differentiation.
     One of the major challenges in the biologic regeneration of a joint is the articular surface. Recent evidence suggests that the developmental origin of this tissue is distinct from other cartilaginous tissues.3  In vivo studies using autologous articular chondrocytes, expanded in vitro, to repair defects in human knee joints suggested the importance of the proper "articular" chondrocyte.4  It is clear that additional rigorous preclinical studies are necessary to evaluate the data and establish the role of all the components including the "articular" chondrocyte in this protocol. However, these studies provide some evidence for the potential of biologic approaches in joint surface repair and additional motivation for the scientist and clinician to further pursue at the molecular level the processes guiding joint formation. Principals established from these studies will likely pave the way to develop more advanced approaches for the biological regeneration of joint surfaces, including the TMJ. Comparative studies between the TMJ and other joints will provide important clues to design joint specific procedures.
REFERENCES
  1.  Chang S, Hoang B, Thomas JT, Vukicevic S, Luyten FP, Ryba N, Kozak, CA, Reddi AH, Moos M. Cartilage-derived morphogenetic proteins: new members of the TGF=DF superfamily, predominantly expressed in long bones during human embryonic development. J Biol Chem 1994;269:28227-34.
  2.  Thomas JT, Lin K, Nandedkar M, McBride W, Camargo M, Cervenka J, Luyten FP. A human chondrodysplasia due to a mutation in a TGF=DF superfamily member. Nat Gen 1996;12:315-7.
  3.  Luyten FP. Cartilage-derived morphogenetic proteins: key regulators in chondrocyte differentiation? Acta Orthop Scand 1995;66:51-4.
  4.  Brittberg M, Lindahl A, Nilsson A, Ohlson C, Isaksson O, Peterson L. Treatment of deep cartilage defects in the knee with autologous chondrocyte transplantation. N Engl J Med 1994;331:889-95.
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Future Directions for Advancing Treatment of
Chronic Musculoskeletal Facial Pain
Joseph J. Marbach, D.D.S., and Karen G. Raphael, Ph.D.

     How should the NIH direct its limited resources to improve treatment for musculoskeletal facial pain?
     The assertion of what constitutes state-of-the-art treatment depends on who "controls the state."  Wide variation exists in the actual practice of treating musculoskeletal facial pain. Depending on the referral, musculoskeletal facial pain patients, presenting with virtually identical signs and symptoms, can, for example (1) undergo temporomandibular joint (TMJ) surgery, (2) receive psychotherapy,(3) be recommended for 3 years of orthodontic treatment, or (4) be fitted with a $600.00 intraoral appliance, or (5) any combination of the above, in no particular order.
     Glass et al. report that oral appliances are the most widely used form of treatment for musculoskeletal facial pain.1,2  Generally, the practitioner who provides an intraoral appliance for musculoskeletal facial pain patient feels confident that, at the very least, he or she is practicing state-of-the-art treatment.
     Why is the use and belief in the efficacy of these appliances so pervasive? Clinical observation and uncontrolled trials have convinced that vast majority of practitioners that appliances are effective. However, relatively well-designed controlled clinical trials have produced conflicting results.3-5  This suggests that effects seen in uncontrolled trials and clinical observation may be due to factors that are nonspecific to treatment. For example, the natural course of the disorder may dictate that some patients spontaneously remit over time. Regression toward the mean6,7 may mimic treatment effects. Placebo effects may account for improvement.8  Failure to consider treatment drop-out may distort conclusions. The clinician may assume mistakenly that patients who do not return for treatment have improved, just as the naive researcher  may assume that attriters had the same outcome as those who continue treatment. In addition, self-report of symptom remission is subject to distortion. Patients who seek the approval of the clinician may inform the clinician that they have improved, while seeking care elsewhere. In short, careful clinical observation, regardless of the number of patients observed, is no substitute for the randomized controlled clinical trial.
     Why has the traditional treatment approach asserted the appropriateness of intraoral appliances for musculoskeletal facial pain, given the equivocal findings from controlled clinical trials? First, the primacy of controlled clinical trials in evaluating treatments is not yet fully appreciated in clinical circles. And second, traditionally, dentists treat musculoskeletal facial pain and are trained to make appliances.
     Historically, physicians have relegated chronic musculoskeletal facial pain to the dental realm. Ostensibly, this decision is based on the notion that this problem requires special expertise outside the scope of traditional medical training. In 1934, Costen, an otolaryngologist, described a symptom.
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complex that became know as the temporomandibular joint syndrome or simply TMJ.9  Costen attributed the etiology of TMJ pain to the loss of posterior teeth and the resultant compression of nerve tissue in the TM joint and periarticular muscles of the face, head, and neck. Costen placed TMJ treatment squarely in the provenance of dentistry. This focus was maintained by generations of treatment models that evolved along dental lines. However, it does not follow that new treatment models should evolve along dental lines.
     The first author does not recommend intraoral appliances.
     The first author practices a biopsychosocial model for musculoskeletal facial pain treatment, one that incorporates the perspective of Engel. 10  The theory is derived from observations concerning which signs and symptoms patients perceive as deviations from health, what meanings they ascribe to these changes, and the action, or inaction of the patient in response to the sum of this information. Embedded in the biopsychosocial model is the notion that patients' behavior toward illness is motivated by psychological and social factors, in addition to biomedical considerations. By the time the clinician has collected the history and performed the physical examination, he or she should also have a knowledge of the biopsychosocial framework with which the patient is approaching his/her illness. It is often not enough to arrive at a diagnosis, correct as it may be, to achieve a successful therapeutic intervention with musculoskeletal facial pain patients.
     Does a biopsychosocial approach to treatment need to be adopted? The first author contends that he cannot yet recommend the approach that he practices daily until (1) he can develop a standardized 'biopsychosocial treatment approach' that can be implemented by any clinician (albeit, with training), and (2) he and his colleague(s) design and conduct multiple controlled clinical trials that test the efficacy of this approach.
     In this technology assessment conference, all the presenters should be especially sensitive to the fact that some variation in practice patterns is inevitable because of differences in available resources, clinician access to training, and patients' preferences. However, these variations should be small and explainable. Practice variation of the magnitude found for musculoskeletal facial pain is more likely to reflect uncertainty regarding how to treat.
     What can be done to remedy the confusion about appropriate treatment? Clinicians must change the way they assess appropriate treatment for musculoskeletal facial pain or, for that matter, any health condition. In a forthcoming chapter,11 the authors assert that treatment will inevitably be made more effective by applying a new modality for clinical decisionmaking labeled "Evidence-Based Medicine" (EBM). Medical practice in the late 20th century is in the early phase of a paradigmal shift that is about to radically alter clinical decisionmaking. Pain medicine will not escape this revolutionary change.
     The difference between EBM and the traditional treatment model is a shift in the source of authority on which to base treatment. EBM augments clinical training and experiences with critical synthesis of research evidence.
(118)
     To advance the treatment of musculoskeletal facial pain by adopting an EBM approach, the authors advocate the following:
  1.  Pain clinicians, regardless of research experience, must develop the skills necessary to critically evaluate the research literature pertaining to treatment.
  2.  Journal editors and reviewers have the responsibility to require authors to adhere to higher standards of research methodology and to prohibit unsubstaniated claims.
  3.  As researchers, we need to conduct (and as a shaping force, the National Institute of Dental Research (NIDR) should support) controlled clinical trials evaluating widely practice treatments. The impression that conservative treatments do no harm is an insufficient basis for deflecting research monies toward evaluation of invasive and radical treatments such as TMJ surgery. This is not to suggest that the consequences of surgery should not be investigated. Supporting trials of conservative treatments will have a greater impact on society, because conclusions from these trials will affect treatment of far more patients and the practice of far more clinicians.
  4.  In addition, we need to conduct trials of underutilized treatment modalities, e.g., narcotic analgesics, tender point injections. If such trials demonstrate efficacy, we need to understand psychosocial barriers to their widespread use by clinicians and patients.
  By training clinicians in an EBM approach, by raising the standards of our professional journals, and by supporting and conducting the necessary controlled clinical trials, it is inevitable that we will progress in improving treatment for chronic musculoskeletal facial pain.
REFERENCES
  1.  Glass EG. Glaros AG, McGlynn FD. Myofascial pain dysfunction: treatments used by ADA members. J Cranio Pract 1993;11:25-9.
2.  Glass EG, McGlynn FD, Glaros AG. A survey of treatment for myofacial pain dysfunction. J Cranio Pract 1991;9:165-8
  3.  Dao TT, Lavigne GJ, Charbonneau A, Feine JS, Lund JP. The efficacy of oral splints in the treatments of myofascial pain of the jaw muscles: a controlled clinical trial. Pain 1994;56:85-94.
  4.  Rubinoff MS, Gross A, McCall WD. Conventional and nonoccluding splint therapy compared with patients with myofascial pain dysfunction syndrome. Gen Dent 1987;35:502-6.
  5.  Turk DC, Zaki HS, Rudy TE. Effect of intraoral appliance and biofeedback/stress management alone and in combination in treating pain and depression in patients with temporomandibular disorders. J Prosthet Dent 1993;7-:158-64.
  6. Raphael KG, Marbach JJ. A year of chronic TMPDS: evaluating patient' pain patterns. J Am Dent Assoc 1992;123(11):53-8.
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  7.  Whitney, CW. Von Korff M. Regression to the mean in treated versus untreated chronic pain. Pain 1992;50:281-5.
8.  Laskin DM, Greene CS. Influence of the doctor-patient relationship on placebo therapy for patients with myofascial pain-dysfunction (MPD) syndrome. JADA 1972;85:892-4.
  9.  Costen JB. A syndrome of ear and sinus symptoms dependent upon disturbed function of the temporomandibular joint. Ann Otolaryngol 1934;43:1-15.
  10.  Engel. GL. The need for a new medical model: a challenge for biomedicine. Science 1977;196:129-.
  11. Marbach JJ, Raphael KG. An introduction to evidence-based treatment of orofacial pain disorders. In: Proceedings of the 8th World Congress of Pain, IASP Press (in press).
(120)
END

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WE ARE ANGELS UNITED TOGETHER ON TMJ! TMJD_SAFE_HAVEN_4_LIFE_ISSUES · TMJ SUPPORT GROUP This TMJD Support Group is intended to be a Safe Haven and provide a place where people with TMJ pain can come and offer and receive support from people who know what they are going through. This is not a medical group and we do not have medical degrees or medical backgrounds. However, with the variety of members in here, there is bound to be someone who has been there and done that and can answer your questions. This group is in memory of Debbie Ward whom suffered from TMJD & died of unknown causes. There are many types of members with TMJD. Some have been treated medically, some treated with various splint therapies and physical therapies as well as some with surgical treatments ranging from Arthroscopy to full jaw joint replacements. Everyone with any degree of TMJD or has a family member that deals with it is welcome to join and offer and receive support that we all so badly need to get through each day with the pain we have to live with. It is YOUR place to cry, scream or vent on the pain you are dealing with and how it is affecting your life and the lives of your loved ones. The group is MODERATED to avoid the unsolicited advertisements and spam. We are all in pain and do not need to have to deal with that too. TMJ SURGERY FAMILY!. A Great Place to Share Information! This site is for sharing and is not a substitute for the advise of your physician/oral surgeon. Please consult with your health care professional. Welcome to TMJ Surgery Chat Forums! A Great Place to Share Information! This site is for sharing and is not a substitute for the advise of your physician/oral surgeon. Please consult with your health care professional. TMJRealSupport-Information � TMJ Real Support & Information. A Special Place For Those Who Suffer From TMJ, Pain,and the many other diseases/disorders that acompany TMJ related health problems. Our hope is everyone can benefit from this group. This group is here for support and to exchange information and ideas openly.

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