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CLINICAL RESEARCH: LEARNING RIGHT FROM WRONG: Author's response
LETTERS someone unfamiliar with the hypotheses of the study (blind), not the chief investigator, performs the clinical examination. While not a perfect or the only solution, this method is preferable to the one employed. Why is this so? Not primarily because the subject is biased but because of the inherent bias of the investigator (Cohen P, Cohen J. The clinician’s illusion. Arch Gen Psychiatry 1984;41[12]:1178-82). Does anyone believe that Dr. Wright was unaware of his goal to identify referred pain patterns? In a recent popular movie, a youngster, and only he, sees ghosts. Since he is the only one who sees them, he is helpless to prove his unique power to anyone else. Finding referred pain patterns is analogous to identifying ghosts; only one person performed the examination and wrote the report. One cannot deny that Dr. Wright has special skills to identify referred pain patterns, but neither can he prove the validity of these skills. The study states that “patients with TMD often report referred craniofacial pain generated from head and neck palpation ... .” How does he know this without a control group? Perhaps anyone would respond with reports of pain at sites other than those palpated when Dr. Wright performs his examination. For example, maybe only depressed pain patients report referred pain. And since rates of depression, common in facial pain patients, were not reported, the reader just does not know. The list of absent variables is nearly endless, and one cannot expect Dr. Wright to include all of them. That is why researchers employ control groups. 1536
The appropriate selection of a control group, while not simple (Marbach JJ, Schwartz S, Link BG. The control group conundrum in chronic pain case/control studies. Clin J Pain 1992; 8[1]:39-43), is absolutely necessary in studies such as this one. Because no control group was used, we have, in fact, learned nothing about the relation between facial pain patients and referred pain patterns. The asymmetry makes it impossible to determine if differences detected are due to the presence of the disorder under investigation, or some other uncontrolled and unidentified variable. The lack of controls in the present study does not inform us about potential correlates of so-called TMD because the study did not compare patients with controls. One final point is important to mention. The paper includes a lengthy discussion of referred pain theories. Nevertheless, the data do not move forward our understanding of whether or not referred pain is a ghost or real. It does not tell us whether it is related to or—if it exists— is independent of facial pain. Remember, no hypothesis was presented, so it is not surprising that no problem was solved. For those who want to move knowledge forward, do not despair. However, before you undertake lengthy and time-consuming activities, spend some time thinking through the problem. Clinical researchers who are also child prodigies are rare indeed. Even among those who succeed, learning research techniques takes time. If you get stuck, find yourself a mentor; they are out there. Do the right thing. Joseph J. Marbach, D.D.S.
New Jersey Dental School, Department of Oral Pathology, Biology and Diagnostic Sciences New Jersey Medical School, Department of Psychiatry Newark, N.J. Author’s response: The research design used in this study is classified as descriptive (Babbie ER. The practice of social research. 6th ed. Belmont, Calif.: Wadsworth Pub. Co.; 1992:91), and the intent of the study was to describe the potential referred pain patterns of this population. In a descriptive study, a second population (that is, a control or other group) is not utilized unless the researcher desires to compare the populations (Norman GR, Streiner DL. PDQ statistics. St. Louis: Mosby; 1986:159-62). If a research design utilizes an intervention, then I strongly recommend a control group be utilized so the intervention group can be compared with the control group in order to determine whether the intervention group had a significantly better effect than the control group. Unfortunately, there is no objective method to identify referred pain (that is, cervicogenic headaches and the like) other than through patient reports. TMD pain (intensity, frequency and character) is similarly based on patient perception, with no objective technique available to measure the perceived pain. Probably the closest procedure we have is pressure algometer pain thresholds, which is also based on patient perception. I concur with Dr. Marbach that researchers need to be cognizant of the tendency for subjects to distort their perceptions
JADA, Vol. 131, November 2000 Copyright ©1998-2001 American Dental Association. All rights reserved.
LETTERS to please the examiner. During a study, subjects should observe an atmosphere in which the examiner is seeking the absolute truth and nothing less. I believe accurate study results are a product of the subject’s integrity as well as the integrity of the individuals running the study. I disagree with Dr. Marbach that utilizing an examiner unfamiliar with the hypotheses makes the individual blinded nor does it necessarily enable him or her to obtain more honest subject perceptions. In this article, I tried to convey that the results were collected with the greatest subject honesty possible. In the environment this study was conducted, I cannot believe a subject would have reported he or she felt pain in a distant location when he or she had not, and then fabricated a mythical location. My belief is supported by the comparison of our results with the Branch et al. study (Branch MA, Carlson CR, Okeson JP. Influence of biased clinical statements on patient report of referred pain. J Orofac Pain 2000;14[2]:120-7). If only Dr. Marbach had the experience of working with me, he would know that my integrity is not an issue that needs to be challenged. My objective for donating my time to research is to provide myself and our colleagues with information that enables us to better diagnose and treat TMD patients, not to provide disingenuous information that would be refuted by future studies. I concur with many of the points Dr. Marbach made. One central thrust is that readers need to critically evaluate the research they read to determine
whether the results can be generalized back to their patients. After reading Dr. Marbach’s comment, in hindsight, it would have been nice to evaluate subgroups (that is, more depressed subjects, subjects with greater pain chronicity and others) of this population for referred pain differences. I appreciate Dr. Marbach’s taking his time to review the important subject of research design. Edward F. Wright, D.D.S., M.S. San Antonio OCCLUSAL VS. NONOCCLUSAL ETIOLOGY
I read with interest Dr. Ronald Gilligan’s letter to the editor in March JADA, as well as Dr. Jeremy Shulman’s letter and Dr. Gilligan’s response in August JADA. Certainly, the occlusal vs. nonocclusal etiology of temporomandibular disorder and bruxism has raged on for years and will continue to do so until it is addressed in a fair forum by members of both sides of the issue and researched properly. What I find interesting and lacking in Dr. Gilligan’s response is the scientific evidence to show that introducing a slight prematurity into the dentition creates a change in a patient’s baseline muscle activity reading. To my knowledge, no research has shown this. To the contrary, what research is available was done in the past by doctors such as John Rugh, Chuck Green and Dan Laskin, showing that this has no effect. If occlusal prematurities are the cause of bruxism, then we should be able to create bruxism in a nonbruxist population by introducing them. If creating strong cuspid rise or deep bite
conditions causes a decrease in patient parafunctional activity, show me these studies. C. R. Hoopingarner, D.D.S. Houston Author’s response: I wholeheartedly agree that proper research and a “fair forum,” along with well-defined diagnoses, would go a long way toward resolving the differences that seem to cloud the TMD issue. I agree with Dr. Hoopingarner that occlusal prematurities do not cause bruxism. However, I believe working and balancing interferences starts a chain reaction that can cause muscular hyperactivity, which leads to excess force on teeth, bone, ligaments and temporomandibular joints as well as muscle fatigue and pain. That excess force is either mitigated by or exacerbated by host resistance and adaptability, behavior issues and a variety of other factors such as bruxism. Some of the original research demonstrating that occlusal discrepancies directly affect muscle activity was done by Ramfjord almost 40 years ago. Muscular activity has been repeatedly linked to occlusion. Dr. Sig Ramfjord’s EMG studies showed that a meticulous occlusal equilibration quelled disharmonious muscle activity patterns. When the teeth can be brought together with no deflection from centric relation to centric occlusion, muscle activity is harmonious (Ramfjord SP. Dysfunctional temporomandibular joint and muscle pain. J Prosthet Dent 1961;11[3-4]:353-74). Williamson and Lundquist proved that posterior disclusion is a solid scientific tenet. They
JADA, Vol. 131, November 2000 Copyright ©1998-2001 American Dental Association. All rights reserved.
1537
The appropriate selection of a control group, while not simple (Marbach JJ, Schwartz S, Link BG. The control group conundrum in chronic pain case/control studies. Clin J Pain 1992; 8[1]:39-43), is absolutely necessary in studies such as this one. Because no control group was used, we have, in fact, learned nothing about the relation between facial pain patients and referred pain patterns. The asymmetry makes it impossible to determine if differences detected are due to the presence of the disorder under investigation, or some other uncontrolled and unidentified variable. The lack of controls in the present study does not inform us about potential correlates of so-called TMD because the study did not compare patients with controls. One final point is important to mention. The paper includes a lengthy discussion of referred pain theories. Nevertheless, the data do not move forward our understanding of whether or not referred pain is a ghost or real. It does not tell us whether it is related to or—if it exists— is independent of facial pain. Remember, no hypothesis was presented, so it is not surprising that no problem was solved. For those who want to move knowledge forward, do not despair. However, before you undertake lengthy and time-consuming activities, spend some time thinking through the problem. Clinical researchers who are also child prodigies are rare indeed. Even among those who succeed, learning research techniques takes time. If you get stuck, find yourself a mentor; they are out there. Do the right thing. Joseph J. Marbach, D.D.S.
New Jersey Dental School, Department of Oral Pathology, Biology and Diagnostic Sciences New Jersey Medical School, Department of Psychiatry Newark, N.J. Author’s response: The research design used in this study is classified as descriptive (Babbie ER. The practice of social research. 6th ed. Belmont, Calif.: Wadsworth Pub. Co.; 1992:91), and the intent of the study was to describe the potential referred pain patterns of this population. In a descriptive study, a second population (that is, a control or other group) is not utilized unless the researcher desires to compare the populations (Norman GR, Streiner DL. PDQ statistics. St. Louis: Mosby; 1986:159-62). If a research design utilizes an intervention, then I strongly recommend a control group be utilized so the intervention group can be compared with the control group in order to determine whether the intervention group had a significantly better effect than the control group. Unfortunately, there is no objective method to identify referred pain (that is, cervicogenic headaches and the like) other than through patient reports. TMD pain (intensity, frequency and character) is similarly based on patient perception, with no objective technique available to measure the perceived pain. Probably the closest procedure we have is pressure algometer pain thresholds, which is also based on patient perception. I concur with Dr. Marbach that researchers need to be cognizant of the tendency for subjects to distort their perceptions
JADA, Vol. 131, November 2000 Copyright ©1998-2001 American Dental Association. All rights reserved.
LETTERS to please the examiner. During a study, subjects should observe an atmosphere in which the examiner is seeking the absolute truth and nothing less. I believe accurate study results are a product of the subject’s integrity as well as the integrity of the individuals running the study. I disagree with Dr. Marbach that utilizing an examiner unfamiliar with the hypotheses makes the individual blinded nor does it necessarily enable him or her to obtain more honest subject perceptions. In this article, I tried to convey that the results were collected with the greatest subject honesty possible. In the environment this study was conducted, I cannot believe a subject would have reported he or she felt pain in a distant location when he or she had not, and then fabricated a mythical location. My belief is supported by the comparison of our results with the Branch et al. study (Branch MA, Carlson CR, Okeson JP. Influence of biased clinical statements on patient report of referred pain. J Orofac Pain 2000;14[2]:120-7). If only Dr. Marbach had the experience of working with me, he would know that my integrity is not an issue that needs to be challenged. My objective for donating my time to research is to provide myself and our colleagues with information that enables us to better diagnose and treat TMD patients, not to provide disingenuous information that would be refuted by future studies. I concur with many of the points Dr. Marbach made. One central thrust is that readers need to critically evaluate the research they read to determine
whether the results can be generalized back to their patients. After reading Dr. Marbach’s comment, in hindsight, it would have been nice to evaluate subgroups (that is, more depressed subjects, subjects with greater pain chronicity and others) of this population for referred pain differences. I appreciate Dr. Marbach’s taking his time to review the important subject of research design. Edward F. Wright, D.D.S., M.S. San Antonio OCCLUSAL VS. NONOCCLUSAL ETIOLOGY
I read with interest Dr. Ronald Gilligan’s letter to the editor in March JADA, as well as Dr. Jeremy Shulman’s letter and Dr. Gilligan’s response in August JADA. Certainly, the occlusal vs. nonocclusal etiology of temporomandibular disorder and bruxism has raged on for years and will continue to do so until it is addressed in a fair forum by members of both sides of the issue and researched properly. What I find interesting and lacking in Dr. Gilligan’s response is the scientific evidence to show that introducing a slight prematurity into the dentition creates a change in a patient’s baseline muscle activity reading. To my knowledge, no research has shown this. To the contrary, what research is available was done in the past by doctors such as John Rugh, Chuck Green and Dan Laskin, showing that this has no effect. If occlusal prematurities are the cause of bruxism, then we should be able to create bruxism in a nonbruxist population by introducing them. If creating strong cuspid rise or deep bite
conditions causes a decrease in patient parafunctional activity, show me these studies. C. R. Hoopingarner, D.D.S. Houston Author’s response: I wholeheartedly agree that proper research and a “fair forum,” along with well-defined diagnoses, would go a long way toward resolving the differences that seem to cloud the TMD issue. I agree with Dr. Hoopingarner that occlusal prematurities do not cause bruxism. However, I believe working and balancing interferences starts a chain reaction that can cause muscular hyperactivity, which leads to excess force on teeth, bone, ligaments and temporomandibular joints as well as muscle fatigue and pain. That excess force is either mitigated by or exacerbated by host resistance and adaptability, behavior issues and a variety of other factors such as bruxism. Some of the original research demonstrating that occlusal discrepancies directly affect muscle activity was done by Ramfjord almost 40 years ago. Muscular activity has been repeatedly linked to occlusion. Dr. Sig Ramfjord’s EMG studies showed that a meticulous occlusal equilibration quelled disharmonious muscle activity patterns. When the teeth can be brought together with no deflection from centric relation to centric occlusion, muscle activity is harmonious (Ramfjord SP. Dysfunctional temporomandibular joint and muscle pain. J Prosthet Dent 1961;11[3-4]:353-74). Williamson and Lundquist proved that posterior disclusion is a solid scientific tenet. They
JADA, Vol. 131, November 2000 Copyright ©1998-2001 American Dental Association. All rights reserved.
1537