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TO THE EDITOR:Director of Orofacial Pain Studies College of Dentistry University of Illinois at Chicago The issues raised in the guest editorial by Dr. Pentii Alanen are disturbing, but not for the reasons that he states (Alanen, 2002). Yes, he is correct when he says that occlusal comparisons between non-selected populations leave some doubt about whether there is enough difference between ’normals’ and TMD patients to reach valid conclusions. However, his proposed solution to that problem is much worse than not being certain, because he suggests we can produce a ’pure normal’ group through occlusal adjustment! He also is right in saying that occlusion will never rise to the level of being a sufficient causal factor all by itself, but he insists that we leave it on the menu of possible causal factors until it is absolutely disproved. Since that kind of negative final proof can never be attained, it will remain on the menu forever. And finally, he may be correct in saying that healthy people will react to experimental interferences differently than TMD patients, but the same also has been demonstrated for a large variety of other physical and psychological stressors. So what is missing? I submit that Dr. Alanen and other defenders of occlusal concepts of etiology have overlooked an important practical question: What difference will it make in the care of TMD patients if occlusion is dismissed or included as an etiologic factor? Excluding the small subgroup with obvious traumatic or post-dental restoration sequelae of jaw pain and dysfunction, most TMD patients report mysterious onset of their troubles. This leaves the field open for all sorts of speculation about possible etiologies, and indeed all sorts have been proposed over the years, each leading to a different treatment strategy (Greene, 2001). Meanwhile, during the same time period, there have been a great number of reasonably controlled TMD treatment studies conducted, most of which are NOT directed at etiologies of any kind. Instead, they are directed at common pathophysiologic mechanisms (e.g., joint inflammation, disc interference, myofascial pain), and the outcomes for various treatment modalities are compared and reported. The literature on these TMD treatment studies rather consistently shows good results, both short- and long-term, using a variety of conservative and reversible modalities. This is especially true for non-chronic cases, while chronic patients remain a serious challenge for all clinicians. If occlusal variables were as important as their advocates believe, we should have seen significant outcome differences by now when comparing treatments that either do or do not ’correct’ the occlusion. Since occlusal modification carries with it increased risk/benefit ratios, advocates also must show that these higher risks are worth taking. Therefore, the question of whether occlusion still belongs on the large menu of possible TMD etiologic factors has become truly of academic interest only. Such menus are often described as multifactorial; but as I pointed out in a recent article (Greene, 2001), this term often is a cover-up for the word ’idiopathic’. While treating etiologic factors directly is generally superior to symptomatic treatment, many morphologic, functional, and behavioral variables cannot be manipulated therapeutically. It is for these reasons that Christian Stohler and George Zarb have written their excellent article on TMD treatment (Stohler and Zarb, 1999), and I join them in advocating a conservative approach to these conditions (Greene, 1992). In doing so, I am willing to leave occlusal imperfections on the menu of possible etiologic factors, but I also am willing to leave occlusal modification out of my treatment plan for most of my patients. REFERENCES
Journal of Dental Research, Vol. 81, No. 11,
732 (2002)
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