This candle signifies the light we wish to shine on the
knowledge needed, to continue our struggle against our
pain, suffering and injustices...Please, don't let the light go
PROGRAM AND ABSTRACTS
TMD
NIH TECHNOLOGY ASSESSMENT CONFERENCE
MANAGEMENT OF
TEMPOROMANDIBULAR DISORDERS
Office of the Director, National Institutes of Health (cover) NIH Technology Assessment Conference on Management of Temporomandibular Disorders -------------------------------------------------------------------------------------------------------------------------------------------
Sponsored by the National Institute of Dental Research and the NIH Office of Medical Applications of Research and cosponsored by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute of Neurological Disorders and Stroke, the National Institute of Nursing Research, and the NIH Office of Research on Women's Health.
Bethesda, Maryland Continuing Education Sponsorship National Institutes of Health Continuing Medical Education
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Contents
Agenda..........................................................................................................................3
Panel..............................................................................................................................7
Speakers.......................................................................................................................9
Planning Committee..................................................................................................11
Abstracts.....................................................................................................................13
I. Introduction and Overview
History and Evolution of Temporomandibular Disorder Concepts Charles McNeill, D.D.S...................................................................................15
II. Current Diagnostic Classification Schema and Assessment of Temporomandibular Disorder Patients Current Terminology and Diagnostic Classification Schema Jeffrey P. Okeson, D.M.D..............................................................................21
Psychological and Behavioral Assessment of Temporomandibular Disorder Patients Dennis C. Turk, Ph.D..................................................................................................27
III. Health Care Services, Epidemiology, and Natural Progression of Temporomandibular Disorders Health Care Services Issues Concerning Temporomandibular Disorders Michael R. Von Korff, Sc.D.......................................................................................29
Epidemiology and Natural Progression of Temporomandibular Joint Intra- Capsular and Arthritic Conditions Lambert G. M. de Bont, D.D.S., Ph.D.......................................................................33
Epidemiology and Natural Progression of Muscular Temporomandibular Disorder Conditions Charles S. Stohler, D.D.S., Ph. D., D.M.D..................................................................37
I. Current Management Approaches Assessing Physical and Behavioral Outcomes of Treatment Linda LeResche, Sc.D...............................................................................................41
Occlusal Adjustment Pentti Kirveskari, D.D.S., Ph.D.................................................................................47
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Modern Concepts of Occlusal Disease and the Efficacy Therapy Glenn T. Clark, D.D.S., M.S.; Yoshihiro Tsukiyama, D.D.S., Ph.D.; and Michael Simmons, D.D.S..........................................................................................55
Orthodontic Treatment and Temporomandibular Disorders James A. McNamara, Jr., D.D.S., Ph.D..................................................................57
Physical Modalities and Trigger Point Injections in the Management of Temporomandibular Disorders Gerald J. Murphy, D.D.S........................................................................................65
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.............................................................................................75
Behavioral and Education Modalities Samuel F. Dworkin, D.D.S., Ph.D............................................................................81
Pharmacologic Modalities Raymond A. Dionne, D.D.S., Ph.D..........................................................................85
Temporomandibular Joint Devices: Treatment Factors and Outcomes Larry M. Wolford, D.D.S..........................................................................................89
Temporomandibular Joint Surgery for Internal Derangement M. Franklin Dolwick, D.M.D., Ph.D........................................................................95
Failed Implants and Multiple Operations Stephen B. Milam, D.D.S., Ph.D.............................................................................97
Neuroendocrine and Immune Considerations Kenneth M. Hargreaves, D.D.S., Ph.D., and Lois Kehl, D.D.S...........................107
Tissue Engineering Joseph P. Vacanti, M.D........................................................................................113
A Scientific Basis for the Biological Regeneration of Synovial Joints Frank P. Luyten, M.D., Ph.D.................................................................................115
Future Directions for Advancing Treatment of Chronic Musculoskeletal Facial Pain Joseph J. Marbach, D.D.S., and Karen G. Raphael, Ph.D................................117
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Temporomandibular disorders (TMD), a group of often painful conditions that affect the temporomandibular joint and muscles of mastication confound and frustrate both patient and practitioners alike. Controversy surrounds virtually all aspects of TMD, from diagnosis and treatment to epidemiology and pathogenesis. Even agreement on which conditions comprise TMD has been elusive. The term has been used to characterize individuals with a wide variety of symptoms and signs, such as pain in the face, or jaw joint area; headaches, earaches, and dizziness; and clicking sounds in the jaw joint. A key issue to explore is the appropriateness of the label "TMD" for the numerous conditions now included under this rubric.
In the absence of universally accepted, scientifically based guidelines for diagnosing and managing TMD, diagnostic and treatment approaches of unproven value have proliferated in clinical practice. Concerns about the safety and efficacy of these approaches as well as potential for harm have arisen among clinicians and patients. There is a need to examine the rationale for and outcomes of a variety of treatments currently used in practice, such as behavioral and pharmacologic management, orthotics, surgery, occlusal therapy, orthodontics, physical therapy, and others. This conference will bring together specialists in pain management, cellular and molecular biology, epidemiology, immunology, behavioral and social sciences, tissue engineering, and clinical dentistry, medicine and surgery, as well as representatives from the public.
After 1-1/2 days of presentations and audience discussion, an independent, non-Federal technology assessment panel will weigh the scientific evidence and write a draft statement that it will present to the audience on the third day. The technology assessment statement will address the following key questions:
What clinical conditions are classified as temporomandibular disorders, and what occurs if these conditions are left untreated?
What types of symptoms, signs, and other assessments provide a basis for initiating therapeutic interventions? What are effective approaches to the initial management and treatment of patients with various TMD subtypes? What are effective approaches to management and treatment of patients with persistent TMD pain and dysfunction? What are the most productive directions for future research, and what types of new collaborations and partnerships should be developed for pursuing these directions?
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On the final day of the meeting, the conference and panel chairperson, Judith E. N. Albino, Ph.D., President Emerita and Professor of Psychiatry, University of Colorado Health Sciences Center will read the draft statement to the conference audience and invite comments and questions. A press conference will follow to allow the panel and chairperson to respond to questions from media representatives.
Conference sessions will be held in the Natcher Conference Center (Building 45), National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland. Sessions will run from 8:30 a. m. to 5:30 p.m. on Monday, 8:00 a.m. to 12:30 p.m. on Tuesday, and 9:00 a.m. to 2 p.m. on Wednesday. The telephone number for the message center is 301-496-9966.
CAFETERIA
The cafeteria is located on the lobby level and open daily from 7:00 a.m. to 3:00 p.m.
CONTINUING EDUCATION CREDIT
For Physicians
The National Institutes of Health by the Accreditation Council for Continuing Medical Education to sponsor continuing medical education for physicians.
The National Institutes of Health designates this continuing medical education activity for a maximum of 14 credit hours in Category 1 of the Physician's Recognition Award of the American Medical Association. For Dentists
Health professionals attending this conference may receive a certificate of attendance for up to 14 hours of Academy of General Dentistry fellowship/mastership continuing dental education credits through the U. S. Public Health Service. SPONSORS
The primary sponsors for this conference are the National Institute of Dental Research and the NIH Office of Medical Applications of Research. The Conference is cosponsored by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute of Neurological Disorders and Stroke, the National Institute of Nursing Research, and the NIH Office of Research on Women's Health. This is the 18th Technology Assessment Conference held by the NIH since the establishment of the Consensus Development Program in 1977.
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Agenda
Monday, April 29, 1996
8:30 a.m. Welcome Harold Slavkin
Director
National Institute
Dental Research
8:40 a. m. Charge to the Panel John H. Ferguson
Director
Office of Medical
Applications of Research
8:50 a.m. Conference Issues Judith E. N. Albino
Conference and Panel Chairperson I. INTRODUCTION AND OVERVIEW
9:00 a.m. History and Evolution of Charles McNeill Temporomandibular
Disorder Concepts
II. CURRENT DIAGNOSTIC CLASSIFI- CATION SCHEMA AND ASSESSMENT OF TEMPOROMANDIBULAR PATIENTS
9:20 a.m. Current Terminology and Diagnostic Jeffrey P. Okeson
Classification Schema
9:40 a.m. Psychosocial and Behavioral Dennis C. Turk
Assessment of Temporomandibular Disorder Patients 10:00 a.m. Discussion
III. HEALTH CARE SERVICES, EPIDEMIOLOGY, AND NATURAL PROGRESSION OF TEMPORO- MANDIBULAR DISORDERS
10:30 a.m. Health Care Services Issues Concerning Michael R Von Korff
(3) Monday, April 29, 1996 (continued)
10:50 a.m. Epidemiology and Natural Progression of Lambert GM deBont Temporomandibular Joint Intracapsular and Arthritic Conditions
11:10 a.m. Epidemiology and Natural Progression of Christian S. Stohler
Muscular Temporomandibular Disorder Condition
11:30 a.m. Discussion
12:00 p.m. Lunch
IV. CURRENT MANAGEMENT APPROACHES
1:00 p.m. Assessing Physical and Behavioral Linda LeResche
Outcomes of Treatment
1:20 p.m. Occlusal Adjustment Pentti Kirveskari
1:40 p.m. The Role of Bioelectronic Instrumentation Barry C. Cooper
in the Documentation and Management of Temporomandibular Disorders
2:00 p.m. Modern Concepts of Occlusal Disease and Glenn T. Clark the Efficacy of Occlusal Therapy
2:20 p.m. Discussion
2:50 p.m. Orthodontic Treatment and Temporo- James A McNamara andibular Disorders
3:10 p.m. Physical Modalities and Trigger Point Gerald J Murphy Injections in the Management of Temporomandibular Disorders
3:30 p.m. Physical Therapy: A Critique Jocelyne S Feine
3:50 p.m. Behavioral and Education Modalities Samuel F Dworkin
4:10 p.m. Pharmacologic Modalities Raymond A Dionne
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Monday, April 29, 1996 (continued)
4:30 p.m. Temporomandibular Joint Devices: Larry M. Wolford Treatment Factors and Outcomes
4:50 p.m. Discussion
5:30 p.m. Adjournment until Tuesday
Tuesday, April 30, 1996 IV. CURRENT MANAGEMENT APPROACHES (continued)
8:00 a.m. Temporomandibular Joint Surgery for M Franklin Dolwick Internal Derangement
8:20 a.m. Failed Implants and Multiple Operations Stephen B. Milam
8:40 a.m. Clinical Decision-Making Alexia Antczak-Bouckoms
9:00 a.m. Discussion
V. POSSIBLE FUTURE APPROACHES
9:30 a.m. Neuroendocrine and Immune Kenneth M Hargreaves
Considerations
9:50 a.m. Tissue Engineering Joseph P Vacanti
10:10 a.m. A Scientific Basis for the Biological Frank P Luyten
Regeneration of Synovial Joints
10:30 a.m. Future Directions for Advancing Treatment Joseph J Marbach of Chronic Musculoskeletal Facial Pain
10:50 a.m. Discussion
VI. PUBLIC PRESENTATIONS
11:30 a.m. Presentations by representatives of professional and patient groups
12:30 p.m. Adjournment
(5) Wednesday, May 1, 1996
9:00 a.m. Presentation of Technology Assessment Judith EN Albino Statement
9:30 a.m. Discussion
11:00 a.m. Panel Meets in Executive Session
1:00 p.m. Press Conference
2:00 p.m. Adjournment
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PANEL
Panel and Conference
Chairperson: Judith E. N. Albino, Ph.D. President Emerita and Professor of Psychiatry University of Colorado Health Sciences Center Denver, Colorado
James D. Beck, Ph.D. Marjorie Jeffcoat, D.M.D. Kenan Professor and Chair Rosen Professor and Chair Department of Dental Ecology Department of Periodontics School of Dentistry School of Dentistry University of North Carolina University of Alabama at Chapel Hill, North Carolina Birmingham Birmingham, Alabama
Karen J. Berkley, Ph.D. Thomas Jeter, D.D.S., M.D. McKenzie Professor Oral and Maxillofacial Surgeon Program in Neuroscience Private Practice Department of Psychology San Angelo, Texas Florida State University
Tallahassee, Florida Sonja M. McKinlay, Ph.D. President
James Campbell, M.D. New England Research
Professor of Neurosurgery Institutes John Hopkins Hospital Watertown, Massachusetts Baltimore, Maryland
Elizabeth J Narcessian, M.D. Clinical Chief, Pain Management
Program
Joel Edelman Kessler Institute for Executive Vice President Rehabilitation, Inc. Frontier Community Health Plans, Inc. East Orange, New Jersey
Englewood, Colorado Buddy D. Ratner, Ph.D. Professor
Edgar Haber, M.D. Department of Chemical Elkan R Blout Professor of Biological Engineering Sciences University of Washington
Director, Division of Biological Sciences Seattle, Washington
Harvard School of Public Health Boston, Massachusetts E. Dianne Rekow, D.D.S., Ph.D. Professor and Chair Department of Orthodontics
Donna L. Hammond, Ph.D. New Jersey Dental School Associate Professor of Anesthesia and Newark, New Jersey
Critical Care and The Committee on Neurobiology Department of Anesthesia and Critical Care University of Chicago Chicago, Illinois
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Lisa Tedesco, Ph.D. Stephen B. Towns, D.D.S. President, American Association of President Dental Schools National Dental Association Professor and Associate Dean for Chicago, Illinois
Academic Affairs School of Dentistry University of Michigan Ann Arbor, Michigan
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Alexia Antczak-Bouckoms,D.M.D., Ph.D. Samuel F Dworkin,D.D.S., Ph.D. D.M.Sc. Professor Farmington, Connecticut Departments of Oral Medicine, Psychiatry, and Behavioral Sciences Glenn T Clark, D.D.S., M.S. School of Dentistry
Associate Dean of Research University of Washington Section of Diagnostic Sciences and School of Medicine Orofacial Pain Seattle, Washington
Center for the Health Sciences School of Dentistry Jocelyne S Feine, University of California, Los Angeles D.D.S., M.S., H.D.R. Los Angeles, California Associate Professor McGill University Faculty of Dentistry
Barry C Cooper, D.D.S. Montreal, Quebec International President Canada
International College of Cranio- Mandibular Orthopedics Kenneth M Hargreaves, D.D.S., Lawrence, New York Ph.D. Division of Endodontics School of Dentistry
Lambert GM de Bont, D.D.S., Ph.D. University of Minnesota Chairman, Department of Oral and Minneapolis, Minnesota Maxillofacial Surgery
University Hospital, Gronigen Pentti Kirveskari, D.D.S., Ph.D. Gronigen, The Netherlands Institute of Dentistry University of Turku
Raymond A Dionne, D.D.S., Ph.D. Turku Chief, Clinical Pharmacology Unit Finland
Neurobiology and Anesthesiology Branch Division of Intramural Research Linda LeResche, Sc.D. National Institute of Dental Research Research Associate Professor National Institutes of Health Department of Oral Medicine Bethesda, Maryland Orofacial Pain Research Group
School of Dentistry
M Franklin Dolwick, D.M.D., Ph.D.
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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.
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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
(25)
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
(33)
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
(34)
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.
(35)
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.
(36)
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.
(37)
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
(38)
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.
(39)
(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:
(41)
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.
(42)
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.
(43)
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.
(44)
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.
(45)
(46) BLANK PAGE
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,
(47)
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.
(48)
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.
(49)
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).
(50)
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.
(51)
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.
(52)
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.
(53)
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.
(54)
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.
(55)
(56) BLANK PAGE
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.
(57)
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.
(58)
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.
(59)
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
(60)
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.
(61)
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.
(62)
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.
(63)
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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
(65)
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
(66)
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.
(67)
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.
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(73)
(74) BLANK PAGE
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
(75)
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
(76)
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.
(77)
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.
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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.
(93)
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.
(94)
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.
(95)
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.
(96)
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
(97)
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
(98)
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).
(99)
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.
(100)
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.
(101)
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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2. Nakano T, Scott PG. A quantitative chemical study of
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6. Berkovitz BK, Robertshaw H. Ultrastructural quantification
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7. Yaillen DM, Shapiro PA, Luschei ES, et al. Temporomandibular
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in macaca fascicularis. J Maxillofac Surg 1979;7:255.
8. Hinton RJ. Alterations in rat condylar cartilage following
discectomy. J Dent Res 1992;71:1292.
9. Lang TC, Zimny ML, Vijayagopal P. Experimental temporomandibular
joint disc perforation in the rabbit: a gross morphologic, biochemical,
and ultrastructual analysis. J Oral Maxillofac Surg 1993;51:1115.
10. Westesson PL, Rohlin M. Internal derangement related to osteoarthritis
in temporomandibular joint autopsy specimens. Oral Surg Oral Med Oral Pathol
1984;57:17.
(102)
11. Westesson PL, Bronstein SL, Liedberg J. Internal derangement
of the temporomandibular joint: morphologic description with correlation
to joint function. Oral Surg Oral Med Oral Path 1985;59:323.
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.
15. Eriksson L. Westesson PL. Long-term evaluation of meniscectomy
of the temporomandibular joint. J Oral Maxillofac Surg 1985:43:263.
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.
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20. Moriconi ES. Popowich LD, Guernsey LH. Alloplastic reconstruction
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21. Dattilo DJ, Granick MS, Soteranos GS. Alloplastic reconstruction
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22. Kalamch S, Walker RV. Silastic implant as part of temporomandibular
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study. Oral Surg Oral Med Oral Pathol 1986;62:2.
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(106) BLANK PAGE
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
(107)
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.
(108)
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.
(109)
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.
(110)
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.
(111)
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.
(112)
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.
(113)
(114) BLANK PAGE
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.
(115)
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.
(116)
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.
(117)
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.
(119)
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
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(120)
END
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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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