J Oral Maxillofac
Surg
50:427-428,1992
WHIPLASH AS A BASIS FOR TMJ DYSFUNCTION
background on which they base this statement. The practical implication of this article is a major problem. I can foresee attorneys for insurance companies citing it as a “scientific” paper refuting the mechanism of this injury. If the AAOMS is truly interested in trauma and this particular issue, perhaps research studies can be designed in cooperation with the National Safety Council to truly study this phenomenon. Good video studies of a mobile mandible during this mechanism of forced deceleration would offer visual proof one way or the other whether hyperextension injuries are possible during extension-flexion injuries. Crash studies of the past cannot be used as a good model because of the use of solid mannequin heads with no way of testing the supposed mechanism of TMJ hypertranslation during the deceleration phase and extension-flexion of the neck. This is the model on which this paper is based. Accurate, scientific data are long overdue. The implications for victims are far too great not to provide them.
Tb the Editor:-1 read with interest the clinical update aricle “Assessing Neck Extension-Flexion as a Basis for Temporomandibular Joint Dysfunction” (J Oral Maxillofac 3urg 49: 12 10, 199 1). This is one of the few articles in the literature that refutes an accepted mechanism of hyperextension injury to the TM joint. My concern about its pubication is that this article carries extreme medicolegal :onsequence for patients who have been injured in motor vehicle accidents. At best, it is anecdotal in its presentation, md the authors do not offer any evidence of testing their hypothesis or any laboratory data that supports their position other than Newton’s laws. Part of the problem with this article is that the authors do not allow for the concept of translation of the TM joint during injury. Review of the diagrams in this article show them to involve a solid mannequin head and a condyle/fossa relationship that does not translate. If the translatory glide sequence during rapid deceleration is ignored, then they may be correct in asserting that compression forces rather than tensile forces are generated during this type of injury. However, it is very questionable that this is what occurs in the human model. I am certainly not a physicist. However, I believe the application of Newton’s second law (F = MA) is entirely too simplistic in the argument that they try to make. Newton’s second law applies quite nicely to solid bodies in motion and to other experiments that provide data that are easily measurable. I would suspect that the conclusions drawn by the authors are suspect because they did not incorporate coefficients of elasticity of tissues, vectors of force, and a multitude of variable that must be considered in the human model. Their statement that “. . . myospasm produced by other factors such as stress, malocclusion problems, and bruxism may be a major cause of the factor in temporomandibular joints and myofascial pain syndromes” is very bothersome. In fact, this is the usual argument that counsels for insurance companies generally use to try to refute claims in court of patients who are injured. In the summary, they state: “Head accelerations produced by forces in the neck (extension-flexion motion) within the subthreshold range for cervical spine injury will generate forces in the temporomandibular joints that act in similar direction to, but are of substantially lower magnitude than, the forces encountered routinely in normal mastication.” This statement is somewhat dangerous in that it has no scientific data to support it. Only their drawings and Newton’s second law, and their application of this law, are the
WILLIAMS. KIRKJR, DDS
Charlotte. North Carolina
The authors reply:-Among the various concerns voiced in Dr William S. Kirk’s letter, the one point that actually addresses the validity of the diagramed physical mechanism of the temporomandibular joint during extension-flexion motion is the issue of translatory glide. The free-body diagram depicts the cranium and mandible as solid bodies, which, for the purpose of demonstrating the mechanical principles involved, seems reasonable. Although the mechanism depicted does not preclude translatory glide of the condyle within the joint, a review of the direction of forces existing at the joint through free-body analysis with translatory glide present confirms the forces to be compressive rather than tensile. The head would have to be prevented from rotating in order for tensile forces resulting from inertial loads to exist at the joint. Prevention of head rotation would preclude the extension-flexion motion. I am unable to address Dr Kirk’s concern regarding the failure to consider “coefficients of elasticity of tissues, vectors of force, and a multitude of variables” without his further definition of the quantitative effect these “variables” are thought to have on the conclusions drawn. His comment that the article is “anecdotal in its presentation” and relies on Newton’s laws, is puzzling. The analysis of a physical process using the laws of physics can hardly be termed anecdotal. Dr Kirk alludes to the triad of etiologies, malocclusion, bruxism, and stress, as a legal mechanism for claim refutation. In fact, these conditions are cited broadly in the medical and dental literature as components in the multifactorial etiology of temporomandibular joint disorders. Dr Kirk suggests that experimental testing should be conducted to study the phenomenon of extension-flexion effects on the mandible and temporomandibular joint. If the purpose of the testing is simply to determine whether significant tensile forces can be generated at the temporo-
427
Surg
50:427-428,1992
WHIPLASH AS A BASIS FOR TMJ DYSFUNCTION
background on which they base this statement. The practical implication of this article is a major problem. I can foresee attorneys for insurance companies citing it as a “scientific” paper refuting the mechanism of this injury. If the AAOMS is truly interested in trauma and this particular issue, perhaps research studies can be designed in cooperation with the National Safety Council to truly study this phenomenon. Good video studies of a mobile mandible during this mechanism of forced deceleration would offer visual proof one way or the other whether hyperextension injuries are possible during extension-flexion injuries. Crash studies of the past cannot be used as a good model because of the use of solid mannequin heads with no way of testing the supposed mechanism of TMJ hypertranslation during the deceleration phase and extension-flexion of the neck. This is the model on which this paper is based. Accurate, scientific data are long overdue. The implications for victims are far too great not to provide them.
Tb the Editor:-1 read with interest the clinical update aricle “Assessing Neck Extension-Flexion as a Basis for Temporomandibular Joint Dysfunction” (J Oral Maxillofac 3urg 49: 12 10, 199 1). This is one of the few articles in the literature that refutes an accepted mechanism of hyperextension injury to the TM joint. My concern about its pubication is that this article carries extreme medicolegal :onsequence for patients who have been injured in motor vehicle accidents. At best, it is anecdotal in its presentation, md the authors do not offer any evidence of testing their hypothesis or any laboratory data that supports their position other than Newton’s laws. Part of the problem with this article is that the authors do not allow for the concept of translation of the TM joint during injury. Review of the diagrams in this article show them to involve a solid mannequin head and a condyle/fossa relationship that does not translate. If the translatory glide sequence during rapid deceleration is ignored, then they may be correct in asserting that compression forces rather than tensile forces are generated during this type of injury. However, it is very questionable that this is what occurs in the human model. I am certainly not a physicist. However, I believe the application of Newton’s second law (F = MA) is entirely too simplistic in the argument that they try to make. Newton’s second law applies quite nicely to solid bodies in motion and to other experiments that provide data that are easily measurable. I would suspect that the conclusions drawn by the authors are suspect because they did not incorporate coefficients of elasticity of tissues, vectors of force, and a multitude of variable that must be considered in the human model. Their statement that “. . . myospasm produced by other factors such as stress, malocclusion problems, and bruxism may be a major cause of the factor in temporomandibular joints and myofascial pain syndromes” is very bothersome. In fact, this is the usual argument that counsels for insurance companies generally use to try to refute claims in court of patients who are injured. In the summary, they state: “Head accelerations produced by forces in the neck (extension-flexion motion) within the subthreshold range for cervical spine injury will generate forces in the temporomandibular joints that act in similar direction to, but are of substantially lower magnitude than, the forces encountered routinely in normal mastication.” This statement is somewhat dangerous in that it has no scientific data to support it. Only their drawings and Newton’s second law, and their application of this law, are the
WILLIAMS. KIRKJR, DDS
Charlotte. North Carolina
The authors reply:-Among the various concerns voiced in Dr William S. Kirk’s letter, the one point that actually addresses the validity of the diagramed physical mechanism of the temporomandibular joint during extension-flexion motion is the issue of translatory glide. The free-body diagram depicts the cranium and mandible as solid bodies, which, for the purpose of demonstrating the mechanical principles involved, seems reasonable. Although the mechanism depicted does not preclude translatory glide of the condyle within the joint, a review of the direction of forces existing at the joint through free-body analysis with translatory glide present confirms the forces to be compressive rather than tensile. The head would have to be prevented from rotating in order for tensile forces resulting from inertial loads to exist at the joint. Prevention of head rotation would preclude the extension-flexion motion. I am unable to address Dr Kirk’s concern regarding the failure to consider “coefficients of elasticity of tissues, vectors of force, and a multitude of variables” without his further definition of the quantitative effect these “variables” are thought to have on the conclusions drawn. His comment that the article is “anecdotal in its presentation” and relies on Newton’s laws, is puzzling. The analysis of a physical process using the laws of physics can hardly be termed anecdotal. Dr Kirk alludes to the triad of etiologies, malocclusion, bruxism, and stress, as a legal mechanism for claim refutation. In fact, these conditions are cited broadly in the medical and dental literature as components in the multifactorial etiology of temporomandibular joint disorders. Dr Kirk suggests that experimental testing should be conducted to study the phenomenon of extension-flexion effects on the mandible and temporomandibular joint. If the purpose of the testing is simply to determine whether significant tensile forces can be generated at the temporo-
427
