S4S sponsors this annual course – and each year we come we have helped improve the lives of dentists and their patients. 

Don’t miss this opportunity!

 HAVE YOU EVER THOUGHT IF YOU JUST KNEW AS MUCH AS THOSE TMJ OR RESTORATIVE GURUS YOU COULD HELP THAT PATIENT WHO HAS JOINT PAIN OR CLICKS? HAVE YOU EVER TRIED TO DO WHAT THEY DO ... EQUILLIBRATE PERFECTLY?   AND FIND THAT THE PATIENT JUST DIDN'T RESPOND THE WAY THEY WOULD IF THE GURU DID IT? Can you say "The Emperor's New Clothes? Come learn that you are smarter than you think you are. -  and that occlusion and bruxism aren't as difficult as they make it! Learn about when occlusion matters -- and when it doesn't! Learn how to help your patients in conservative, reversible ways so that you can protect them from the forces that threaten them and the dentistry you do for them. Are you across the pond? Come to Sheffield or London in JUNE.


No, it won't take a series of mini courses. Just two days. The way you think of occlusion on EVERY patient will change.... and your life will be easier and less frustrating. Just sayin

On an online forum, a college professor in the UK wrote to me:

I would suggest that someone at the start of their journey, studies the established protocols of Dawson Pankey AES first and once they are proficient with them can evaluate the merits of other treatment modalities (as I assume you did?)

I responded: 

Yes, I did start what I term my “treacherous” journey studying with Niles Guichet and the Society for Occlusal Studies, which led me to work with Harold Gelb for seven years or so, and then with BioRESEARCH and ICCMO and neuromuscular concepts.  These all led to some increased conflict and confusion, and eventuality I learned that so much that was being taught was indeed empirically derived.  And thus,  each practitioner was left with their choice to pick and choose – whatever worked best in their hands(Donoff, 2000) – which is in itself problematic. 

Yes, along the way I met Peter Dawson, and yes, I was asked to lecture to his inner sanctum. This led to several of his instructors spending time in my office, a discussion of my moving my pain practice to join his.  I introduced what they named the “B splnt” to them, and then they took it back to Florida and bastaridzed the concepts to fit their agenda.  We actually use their videos in our course to demonstrate how the concepts are totally manipulated incorrectly.

 Most of the restorative agendas (as the one’s you have mentioned) are based on Travell’s Vicious Cycle Theory(Travell, 1960) which essentially suggests that interferences of some type cause hyperactivity (lateral pterygoid “spasms” which rarely if ever actually occur) leading to pain and dysfunction.  Many years ago, Lund refuted the theory showing that the “interferences” suggested to cause hyperactivity actually cause hypo-activity and proposed the Pain Adaptation theory(Lund et al., 1991).  Unfortunately, this mechanism doesn’t fit the existing agendas from the major restorative camps, which by the way, can be traced back to Ramfjord and Ash’s 1961 book which suggests that interferences “cause” bruxism, a concept that continues to be taught with zero evidence(Ramfjord, 1961).

These restorative “pioneers” created the way for us to move forward, but like with any pioneers, the maps change.  They are to be respected and yes, revered, for what they have done.  It is my impression that what they teach restoratively is nothing short of brilliant. But the connection to pain and dysfunction needs to be re-evaluated(Campbell, 1957).  But if they continue to hold onto principles and prevent science from moving us forward, this would be like not revamping a pioneer’s old map(Glassman and Malizia, 2017). 

So no.  I would NOT suggest that a dentist start down this path of essential understanding by learning a non-evidenced based agenda – a cook book of sorts teaching mechanisms as fact that are in fact not totally understood, and in some cases being taught “facts” that are in fact already demonstrated as incorrect. 

A few points:

1.      I totally understand the problem of “one size fits all” diagnosis and treatment.  I have been on a campaign to eliminate the term “TMD” from our vernacular. I have spoken to nearly every well-known lecturer and researcher in our field and while they all agree with the concept, they pronounce that it is far too embedded at this point and that it is a way to “communicate.”  I submit that it is responsible for much miscommunication(Nitzan, 2008).

2.     Therefore, we teach diagnostically driven therapy. Those diagnoses include various types of internal derangements, degenerative disease states, neuropathies, neurovascular disorders, cervicogenic disorders, ligament insertion injuries, etc.  Each of these disorders does in fact have their own specific recommended treatment considerations(Manfredini et al., 2011).

3.      That being said these treatment procedures are not necessarily “dental” as the teeth and the “occlusion” are not necessarily the key factor – and shouldn’t be considered that just because we are dentists and that is where our attention lies. 

4.     How do “splints” work?  What is the intended mechanism?  When do they work?  Clearly muscle health is not at the forefront of most of the disorders we listed, and the preponderance of the evidence suggests that the “occlusion” is not related directly to these disorders, including the intracapsular disorders.  This, Paul, is the reason for the oversite suggestion that occlusion is not related and that it shouldn’t be changed in treatment.  I would argue that we have evidence (not confirmation bias) that there could be a relationship, but the mechanisms are not what we are being taught by our restorative gurus who have for some reason become the leaders in treatment recommendations for pain and dysfunction. This helps understand the governmental regulations – and while I understand them, I would fight for your right to treat as you feel appropriate.   That being said, what we teach is that we do not suggest that restorative treatment is required to help our patients with their pain and dysfunction, but we treat their pain and dysfunction so that they can have the restorative treatment they need or want and that we would like to give them!   The goal, then, is to provide conservative, reversible therapy when possible(Reid and Greene, 2013).  We call this the pain/dysfunction restorative “disconnect.”  This is not to suggest that occlusion can’t play a role in pain or dysfunction, but to suggest understanding what that role is and WHEN it is a factor will help explain the majority of patients who have malocclusions with no pain or dysfunction.

5.     Since it has been demonstrated that mandibular re-positional therapy is not in itself a key factor, and the preponderance of evidence suggests no direct link between occlusion and “TMD”  (Zonnenberg and Mulder, 2013, TÜRP and Schindler, 2012)(for example… many others could be listed here) and that therefore the goal of any nocturnal or diurnal appliance is to protect the patient from destructive parafunctional forces, no matter what the diagnosis, our appliance design became essentially simplified and consistent.  This was a conflict internally for me as well. There I was preaching diagnostically driven therapy, but in the end, many of the conditions could be aided by efficient parafunctional control which of course doesn’t stop parafunction but decreases destructive force vectors hopefully allowing for heading and adaptation(May and Garabadian, 2000). 


Whatever has been taught about splints and occlusion – I have been taught –believed – and in some cases taught myself. The biggest lesson to be learned is that our teeth are only in contact about 20 minutes a day – and that is ANY form of contact, not necessarily MIP.  And since MIP is almost never reached during function (we can have a discussion at a later time about the swallow but I think you’d find the literature interesting in this regard) occlusion itself only becomes a factor when we are “occluding” –  and that factor can be destructive forces based on force vectors magnitude, direction and duration. 

 I in no way mean to be offensive when I question what is being taught.   But the truth is much of what is taught creates “hoops” for our general dentists to jump through and teaches mechanisms that are just flat out wrong, but in many cases reinforced through confirmation bias.  Yes, we palpate muscle, but have found that most injuries are not in the muscle itself but at the enthesis, the real weak point of the musculo-skeletal system.  We as dentists tend to “stipulate” occlusion.  We tend to think of the teeth as together, and understanding rest, function and parafunction and the potential forces involved to negatively affect the components of the cervicomandibular cranial system is critically important. 

 It is my firm belief that so many of our general dentists could help so many people if they weren’t turned off by all the unnecessary controversy as our legends hold on to agendas to protect their legacy ignoring the science we need to help guide our art. 


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DONOFF, B. 2000. It works in my hands. Evidence-Based Dentistry, 2, 1-2.

GLASSMAN, B. H. & MALIZIA, D. L. 2017. The Curious History of Occlusion in Dentistry. DentalTown Magazine, 55-62.

LUND, J. P., DONGA, R., WIDMER, C. G. & STOHLER, C. S. 1991. The pain-adaptation model: a discussion of the relationship between chronic musculoskeletal pain and motor activity. Can J Physiol Pharmacol, 69, 683-94.

MANFREDINI, D., BUCCI, M. B., MONTAGNA, F. & GUARDA-NARDINI, L. 2011. Temporomandibular disorders assessment: medicolegal considerations in the evidence-based era. J Oral Rehabil, 38, 101-119.

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RAMFJORD, S. P. 1961. Bruxism, a clinical and electromyographic study. J Am Dent Assoc, 62, 21-44.

REID, K. I. & GREENE, C. S. 2013. Diagnosis and treatment of temporomandibular disorders: an ethical analysis of current practices. Journal of Oral Rehabilitation, 40, 546-561.

TRAVELL, J. 1960. Temporomandibular joint pain referred from muscles of the head and neck,. The Journal of Prosthetic Dentistry, 10, 745-763.

TÜRP, J. C. & SCHINDLER, H. 2012. The dental occlusion as a suspected cause for TMDs: epidemiological and etiological considerations. J Oral Rehabil, online early.

ZONNENBERG, A. J. & MULDER, J. 2013. The incidence of centric slides in healthy individuals and TMD patients. Eur J Prosthodont Restor Dent, 21, 109-13.