Drawbridge Seminars -- Bringing Research to Practice





If determining the causes of TMJ Disorders was a relatively straight forward process, the myriad of scientific studies that have been done would have long ago spelled them out. How do we explain the interplay of a wide variety of factors that can influence whether a non-symptomatic individual may develop a temporomandibular disorder?

Okeson has proposed a model that considers all of the potential contributing factors to the development of TMDs:

• Dental Occlusal Factors
• Trauma (Macro and Micro)
• Emotional Stress
• Deep Pain Input
• Parafunction

[These are each considered individually on the "Contributing Factors" page.]

It is common for a patient with a TMD to display more than one of these potential contributing factors, referred to as a multi-factorial causation.

There are also possible factors that may weigh against the development of disorders and diseases, including TMDs. These are related to the individual’s “adaptability” or “physiologic tolerance” and may include:

• Genetic factors
• Biologic factors
• Hormonal factors
• Generally Robust Health and Immune System
• Possibly others?

One of the major difficulties in identifying a “cause” or “causes” of TMD in any individual patient is that neither the contributing factors nor the factors that constitute a person’s “adaptability” are easily quantifiable. This makes doing scientific studies especially difficult.

Therefore, in an individual with a robust “adaptability”, in spite of the presence of one or more significant potential contributing factors, the individual may not develop a TMD. In another individual, perhaps with a similar complex of potential contributing factors, but with a diminished “adaptability”, the development of a TMD may occur. Onset may occur acutely, in response to a triggering mechanism, or it may occur insidiously and appear without an apparent trigger.

In the patient in whom a triggering mechanism appears to have been present, it would be easy to attribute the development of the TMD to the triggering mechanism, alone. However, it is also possible that the patient had been predisposed to the onset. Although signs or symptoms may not have been apparent, the presence of any of the contributing factors listed above, prior to the onset of symptoms, might have played a role in predisposing the patient. The triggering mechanism may have simply pushed the patient beyond their individual “adaptability" threshold and may have been no more than the “straw that broke the camel’s back”. In considering treatment of such an individual, it is important to be aware of other possible factors that may have contributed to the onset, as predisposing factors. These may only become apparent with a thorough history and examination.

In this respect, as is apparently true with many other health issues, there appears to be an on-going dynamic relationship between contributing factors and adaptive factors.

Okeson further suggests how aTMD, which initially may developed as an acute problem, might progress into a true chronic pain condition. Two possible factors that can act separately or, in some instances in combination, may contribute to the evolution of acute pain to chronic pain.

The first possibility is that the patient’s “adaptability” is further lowered, perhaps by other systemic factors such as other chronic illness or an increase in stress levels. The second possibility is that, in the absence of appropriate or adequate treatment, an initially acute source of pain might persist and become a prolonged pain input to the CNS, leading to activation of what are known as “central mechanisms.” These include:

• Altered hypothalamic-pituitary-adrenal (HPA) axis function
• Increased central sensitization
• Decreased descending inhibition

It is also recognized that with the development of pain chronicity, there is often a change at the emotional or psychological level in response to the ongoing pain. In fact, this type of emotional change is recognized as one of the hallmarks of chronic pain.

A statement from Dr. Charles Greene is worth consideration: “this term (multi-factorial) often is a cover-up for the word ‘idiopathic’”. The largest challenge to finding a solidly scientific resolution to the quandary of the causation of TMDs is the fact that most, if not all, of the acknowledged contributing factors cannot easily be quantified. When factors involved in a scientific hypothesis cannot be measured, testing the hypothesis becomes, if not impossible, a true enigma.

The causation of TMDs is clearly not the result of a single factor but a complex and dynamic process that is almost certainly different in each patient. As clinicians, we should recognize that the clinical evidence for a significant occlusal component to this complex picture, in most patients, cannot be dismissed.





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