Seldom in the health care sciences is the acrimonious rift between clinical practice and academia greater than that observed in the theater of the diagnosis and treatment of temporomandibular joint pain/ dysfunction problems. The February JADA article by Drs. Gary Klasser and Charles Greene, "Predoctoral Teaching of Temporomandibular Disorders: A Survey of U.S. and Canadian Dental Schools" (
JADA 2007;138[2]:231–7
), clearly exposes this rift.
The authors have taken great pains to expose the status of undergraduate dental training in temporomandibular disorders (TMDs) for what it is, and for that I applaud them. Things really need to change in this regard, and in a hurry. But the authors then go on to list certain TMD concepts that some dental schools are, in fact, teaching that are totally appropriate and proceed to imply that they are not. One of their more contentious comments in this regard, concerning the role of maxillomandibular skeletal relationships and retruded condylar position during function, states that such concepts represent a "relatively small role" in the etiology of most TMD cases. However, there are those in clinical practice who feel such things play a major role in TMD. There is sound scientific literature that does, in fact, reflect this.1–5
Many experienced practitioners, possessing both advanced clinical skills and irreproachable professional integrity, observe that classic garden-variety, dysfunctionally induced TMD is a matter of an overly posteriorly dislocated condyle that, to accommodate the existing occlusion, has migrated chronically and steadily so far up and back in the confines of its own fossa that it has shredded or torn itself loose from its more anteriorly tethered intra-articular disk.
In so doing, it can create not only an orthopedic internal derangement–type model but also a neurogenic inflammation–enhanced, chronic compression nerve damage–type model in the bilaminar zone. This occurs at an important retrocondylar arborization of the auriculotemporal branch of the mandibular division of the trigeminal nerve, a cranial nerve known for its penchant for sensitization and its potent "trigeminovascular reflex" (a complex chronic pain–processing neurological reflex that is intimately related to vascular headaches).
It also has been observed that, when the repetitive nociceptive input and associated intracapsular damage reach a certain threshold level sufficient to propel their physiological status beyond the subclinical level to the chronically overt clinical level, treatments that are less aggressive, structurally reversible, temporary or indirect often prove inadequate. Rather, the treatment of choice often proves to be full-scale mandibular (condylar) relocation (advancement) and stabilization of the temporomandibular joints for the long term (often nine to 12 months), in concert with permanent alteration (correction) of the occlusion, by any means, to maintain that corrected structural relationship.
For example, Simmons and Gibbs,1 in a university-based study, found that 66 percent of patients with TMD reported themselves completely free of temporomandibular joint–related headaches, and 33 percent reported being "vastly improved," after mandibular anterior repositioning therapy. Gaudet and Brown2 examined 2,104 patients with treated TMD and 250 patients with untreated TMD by using scientifically validated methods and found that anterior repositioning splints worked better than mere flat-plane splints. If this doesn’t indicate a connection between maxillomandibular relationships, occlusion, condylar position and TMD, what does?
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