There can yet be another cause of facial and mandibular asymmetry and this patient is an example of that condition.

      This is Katelyn and she is age 16.  At age 10-11, Katelyn began to complain of constant ear ache symptoms

and was treated for chronic ear ache (otitis media) for assumed ear infections.  Despite multiple trials of anti-

biotics, she did not improve .  Soon after, she began to have jaw popping and locking of her right jaw joint

(left side of photo).  She did not experience any issues with her left jaw joint.  Her condition deteriorated

and she began to have difficulty with mouth opening due to chronic locking of the right joint.  It soon became

very painful to chew, she lost weight, and could consume a restricted diet only due to pain of chewing, joint locking  and difficulty with mouth opening.

She was referred for orthodontic treatment at age 13, which was at the beginning of her accelerated skeletal growth period.  Her facial asymmetry worsened and she continued to have difficulty with mouth opening, loading the right joint with chewing forces, and joint locking was becoming more frequent.  At age 16, Kately was finally imaged.  The following are her MRI images.

This is the left TM joint. There is barely any discernable joint space for protection of the disc/capsule but no discernable Wilkes derangement or detachment of the disc/capsule from its adaptation to the condyle. Space does not allow the coronal view, but it confirms a condyle with normal morphology.  Not the shallow slope  of the eminence with the steepness of the eminence below.  There is no reported pain or complaints of joint dyfunction now, or historically.

This is the right TM joint.  There is a Wilkes III derangement .  Also note that the size and volume of the condyle is much smaller than the one on the left.  Note also the mass of the articular eminence and its steepness compared to that of the left.  The disc of the joint has been sheared off of the condyle and the patient functions only on herniated posterior ligament tissue which is normally designed to limit forward translation of the joint complex.  The dark  oval structure is the ear.  One can see that any potential painful process in the TMJ can often be mis-interpreted as ear ache pain just due to structure proximity.

A previous blog discussed the timing of growth between the two boney structures of the TMJ, the fossa (socket) and the condyle.  The fossa forms as does the base of the skull, which finishes its growth around age 6.  The condyle will grow until skeletal maturity is completed in the teen age years.  Hence, there is a potential decade of growth differential between the two structures.  When the condyle grows wider than the fossa, lateral impingements can develop and impact orthopedic joint function.  Another differential growth pattern impacting the TMJ can be the vertical depth and slope of what is called the articular eminence which is the boney structure the condyle and disc/capsule articulate with and glide forward against during mouth opening.   If there is a significant difference in the size, architecture or mass of these structures relative to one another, co-ordinated biomechanical function between the two joints is impossible and one may become loaded excessively, creating derangement at a young age.

It is becoming clear in this field that altered growth and facial form, particularly children developing deviations in facial form due to mandibular growth problems is associated with a high degree of penetration of joint derangements.  Often the growth problem is minor, but sometimes it can be impressive as in this case.  Condyle growth and hence jaw growth can be impacted by a derangement that develops in childhood.  In this case, it appears an abnormal and asymmetric base of skull developmental issue occured as part of base of skull growth. (significant eminence developmental deformity of base of the right temporal bone versus the left  ).  This enlarged eminence created problems with joint function particularly with mouth opening as Katelyn grew.  This was biomechanical in nature as the deeper, steeper eminence impacted smooth and co ordinated  bilateral joint function.  

There is a school of thought in healthcare that patients this age do not develop significant derangement issues that are painful, dysfunctional, and also capable of significantly impacting growth and development.  This is unfortunate.    To be sure, timing of treatment of these cases is quite important.  There is little known about interceptive treatment of such cases, even if the diagnosis were known, say around age 13.  Nevertheless,  pediatric joint derangements should be acknowledged to exist by the clinical world. Imaging is the fundamental paradigm of diagnosis.

The Previous blogs will supplement this discussion:

1. TMJ Growth and Development: A Natural Cause for Problems ?

2. The Disc/Capsule Complex

3. The Wilkes/Schellhas/Piper Stages of TMJ Derangement.

 What is seen at the bottom of this blog is a coronal image of a 35 year old patient with a vertical stress fracture of her mandibular condyle and a greater than 20 year history of pain and joint dysfunction.  She had never been imaged before but had spent years in dental treatment management, pain medication, psychological counseling etc. etc. 

 Not that this approach was necessarily faulty in relation to common practice .  The  previous providers applied  their treatment paradigms and followed those proposed in current dental education on the subject (1,2).  This should not be considered as a heterogeneous disorder any more than a stress fracture of the tibia bone of the leg be considered in the same light.

In my clinical experience, this condition is seen in patients with complaints that have been  longstanding.  It occurs in a much younger age group of patients than patient populations that have compression stress fractures of the spine, bones of feet, or lower leg (except athletes) and hip (older patients with osteoporosis.  In this field, it appears as though the stress fracture is associated with a significant and impingement where with mouth opening, there is point contacts with osteophytes (bone spurs) or a heavy ledge of bone in the lateral most aspect of the joint socket that loads the moveable  joint structures excessively. 

The TMJ has two joint spaces, a superior and inferior space.  Biomechanical engineers have shown conclusively that loading is greatest in the lower compartment and maximizes with mouth opening.  These loads increase significantly when derangement exists . If there is bone to bone contact during the sequence of mouth opening, this increases the load on the mandibular condyle significantly  ( 3-6 ). Advanced derangement can lead to or be associated with significant arthrosis, which is when stress fractures will most commonly be seen.  Coronal MRI  scans of the TMJ must be employed to reveal them.

  In this coronal image, one can see a vertical stress fracture of the condyle.  This is associated with a very large fossa impingement.  This image was taken with a mouth splint in place and still one can see near bone to bone contact in the lateral most aspect of the joint.  Such a phenomenon has significantly increased point loading of the condyle of the jaw as it moves during mouth opening and side to side during chewing function. The stress fracture has also impacted the blood supply flow to the condyle.  The left side of the image is the medial and the image to the left of the stress fracture is healthier bone marrow tissue than that seen to the right of the stress fracture.  The patient is 35 years old.  This was her first image ever taken of the joint during over 15 years of on and off treatment for pain and joint dysfunction.

References

1. Maixner WL et al:  Orofacial pain prospective evaluation and risk assessment study_ the OPPERA study.  Jnl of Pain. Vol 12, No 11, Supplement 3, 2011.  PP…T4-T11.

2. Greene, CS (editorial) “Managing patients with temporomandibular disorders: a “new” standard of care”  Am Journal of Orthodontics and Dentofacial Orthopedics.  2010, 138:3-4.

3.  del Perez palomar, A and M Doblare.  3D finite element simulation of the opening movement of the mandible in healthy and pathologic situations. Jnl Biomech Engineering.  128:242-249. 2006.

4.  Koolstra JH and TM van Eijden.  Prediction of volumetric strain in the human temporomandibular joint cartilage during jaw movement. J Anat.  209: 369-380.  2006.

5. Gallo LM:  Modeling of temporomandibular joint function using MRI and jaw tracking technologies.  Cells Tissues Organs.  180: 54-68. 2005

6. Kirk W and B Kirk. A biomechanical basis for primary arthroplasty of the temporomandibular joint.  OMS Clinics of North America, 18: 345-368.  2006.

1. A Picture of Pain

2. Long term consequences of mis-diagnosis

3. A patient’s perspective

4. Development of derangement in adolescents, Part I and II.  (There are 2 additional postings discussing the development of this orthopedic condition in pre and adolescent patients)

5. The face of trauma

6. The Wilkes/Schellhas/Piper MRI staging of TMJ derangements.

7.  TMJ and chronic headache

One fact of life relative to the majority of dental providers is that they almost always (exception orthodontia and  current emphasis on cosmetics) dealing with people in acute pain due to varying degrees of oral disease.  This mindset and emphasis has also influenced much of the direction of dental university research that is performed in the area of “TMJ” research.

Many US dental schools are associated with and house  centers of dental research who produce government and corporate  funded   research on varying topics from dental reconstruction materials to research relative to understanding the various neurological aspects of oral-facial pain.  Most of this research in “TMJ”  and its emphasis has not changed much in the last 30-40 years in that the emphasis has been on the human pain response mechanism. That is to say that various central nervous system and peripheral nervous nervous system responses and individual groups of patients and their collective psychological responses to chronic pain are the emphasis of study.  In the world of TM joint orthopedic dysfunction and potential impairment, all other mechanisms are emphasized over the mechanism that may have created physical pathology that triggers the human pain response in the first place.

Presently, the National Institutes of Health (NIH) and a branch of this organization, the National Institutes of Dental and Craniofacial Research (NIDCR) have funded a 7 year study with the objective to describe who is a “TMJ” patient and what the various factors of development of the condition might be. For short it is called the OPPERA Study. (1)

  The strength of such projects is that they add much to the understanding of the human physical and psychological response to chronic pain.  The weakness is that for a condition labeled with such a broad description as “TMJ” ( and with a name that incorporates in its core a condition that involes a joint of the body); what is glaringly absent from this research is any cause and effect relationship to the development of pain mechanisms coming from consequences of orthopedic injury or disease creating  poor function of the joint itself…the orthopedic model that impacts many individuals that this web site is dedicated to.  

Review of the emphasis of such a project always is preceeded by an excellent review of how such a condition impacts humanity.  Some of the more interesting aspects of the first report of this 7 year project are as follows:

1.  Such a project describes “TMJ” as a “heterogeneous family” of musculoskeletal disorders.  Calls have come from the clinical and research literature to be more specific and focus on “homogeneous” cause and effects, particularly relative to patients who have significant orthopedic joint  dysfunction and problems  of jaw use and eating function.  This distinction is unique to a dental research model compared  to an orthopedic/ medical research model.  That is to say, in orthopedics, one does not hear of TFD (Tibeo-femoral disorder) as a heterogeneous group of muscular, skeletal, neurological and psychological parameters that discuss everything under the sun other than ligament tears and arthritic disease processes (regardless of age) .  The emphasis is on what makes the joint hurt and not work well relative to physical necessity.  Not so with the “heterogeneous” paradigm.

2.  Collections of such research over the past several decades reveals that 51- 67% of patients diagnosed intitially with “TMJ” continue to have problems 5 years after initial diagnosis and likely get worse.  In this light,  chronic “TMJ” mimicks chronic low back pain relative to percentages of those who spontaneously get better and those that get worse.  Both groups have interesting data relative to psychological profile of patients with chronic problems.

3.  85% of the overall costs of treating “TMJ” from a macro-economic standpoint involves the treatment of a small group of patients who develop persistent pain and dysfunction.

4.  Females outnumber males anywhere from a 2:1 (overall incidence) to 8:1 (clinical treatment) ratio.   In the US, caucasian females predominate the statistics and outnumber other races in well done epidemiologic studies.

5. The estimate of penetration of TMJ in the US population where pain and dysfunction is consistent and relatively impairing is estimated at any one time to be about 12.1%.  This is a very large number of impacted people.  True, some spontaneously get better and leave the impacted “pool” of  individulals , but a core group of impaired people is high.  Higher than many other human diseases (HIV for instance) and many forms of cancer that get all the media and health funding attention from government.

6. Onset of TMJ impacts a younger group of people than low back pain…often beginning in teen years and peaking in the late 20s to 30s for many impaired individuals.

7.  For every 100 million workers in the US, 17.8 million work days are lost due to this condition.

Such statistics have been appearing in the literature for years and the profile of individuals has not changed.  What also has not changed is the emphasis of describing everything but the orthopedic model of joint disease and impairment.

This web-site has offered visual examples of orthopedic disease,the destruction of joint tissues, and pictures of painful conditions. Trauma mechanisms and dysfunctional biomechanical mechanisms and the suggestion that the initiation of many painful and progressively impairing conditions are similar in mechanism to rotator cuff tears that occur in the human shoulder joint.  Unfortunately, this paradigm is not part of the discussion in such reports as this one sponsored by the NIDCR.

To wit, this report states:

1.  The primary clincal factor with TMD pain onset is the presence of other pain conditions.  Never mind the concept of traumatic or functional joint injury.  A true “TMD” patient is someone who has pain elsewhere and this creates the onset.

2.  TMD patients have lower overall physical  pain thresholds when tested.

3.  TMD patient have significant and  similar penetration of chronic depression from chronic pain as do patients with low back pain.

4.  Patients who have chronic pain are genetically predisposed to chronic pain.

5. TMJ patients have higher levels of somatic awareness.  This is a nice way of saying they are obcessed with their body and particular functions, and may  overstate potential pain problems.

How does this relate to the training of health care providers?   Unfortunately, many of these researchers predominate the lectures and course content  given to medical and dental students during their initial didactic exposure to the field.  It is estimated that medical students receive less than 9 hours of exposure to pathology of the head and neck region, and in particular the maxillofacial region.  Many dental educators lecture on pain management in this field to dental students and present a muscular and psychosomatic model of the average “TMJ” patient.  In the United States, little , if any, exposure is given to the orthopedic model of TMJ pain and dysfunction.

  The predominant perception that both medical and dental students take away from their education in this arena is that this condition is associated with high levels of depression in people, is due to unique ability of different ways pain is managed, and that patients are perhaps genetically predisposed to the condition because of pain elsewhere.  Much medical or dental management is based on the psychological paradigm rather than an organic disease paradigm.  This makes this a “unique” area of study only because the central focus of what is actually might be orthopedically  wrong in the joint in the first place  is never discussed.

So, any given patient who has a true dysfunction or arthrosis of the joint itself will often be told there is nothing to do other than medication to treat depression or pain medications.  Yes, it is in your head, but not in the way such providers think it is.  Unfortunately, their opinion and biased is totally based on their training model which reflects the current research model reflected by the OPPERA NIH funded study.  

The objective of this web site and that of the American Society of TMJ Surgeons (ASTMJS.org) is to educate the public on the orthopedic nature of certain problems of the human jaw joint that create impairment.  Our position is that if a joint is painful and dysfunctional, it must be understood in the nature of internal orthopedic paradigms and not those of the psychological, genetic, or central neuro-biochemical models.  Sure, these can be an  impact in chronic patients.  Keeping an individual who may develop such a condition as a teenager ( as the OPPERA study acknowledges) from getting to this level and becoming a statistic is what is necessary in today’s world.  The research emphasis and educational model must change and at least incorporate this information for there to be any significant advance in this field.

1.  Maixner,W, L Diatchenko, R Dubner et al : “Orofacial Pain Prospective Evaluation and Risk Assessment Study – The OPPERA Study”,

Jnl of Pain, Vol 12, No. 11 (November), Suppl. 3, 2011: PP T4-T11.

1.  Open Arthroplasty relief of Lateral impingement.

2. Clashes of paradigms

3.  A “new” orthodontic standard of care

4. The oral orthotic or bite splint

5. A picture of TMJ pain   6.   Bruxism and TMJ

The above picture is a CT Scan of a patient of the TMJs  taken with mouth in the full open position.  Review of the scan reveals the relationships between both fossa (sockets of the TM joint) at the base of the skull, and the forward fully translated (glided open) positions of both condyles (ball components of the joint system)  of the mandible (lower jaw).  Examination reveals a significant difference in the width and curvature of each fossa and a significant narrowing and near bone to bone contact of the most lateral aspects of the joint system. These structures are not congruent during function.   This is another patient who has had longstanding joint dysfunction consisting of both closed and open mouth locking problems and pain “for as long as I can remember”.

This CT is an an example of what is very important to diagnose in younger symptomatic patients.  Unfortunately, it will not happen if a “TMJ therapist/provider” is more focused on other treatment paradigms (dental related modalities, psychologic counseling medications and pain management ) rather than starting a treatment paradigm with 3-dimensional  imaging and an appropriate diagnosis of potential orthpedic pathology or functional problems caused from issues within the joint itself. (3)  In this CT example, one sees  that in this patient that both condyles of the mandible are much wider than the fossas at the base of the skull at this point in the mouth opening  functional sequence..

This is an individual who had been managed without imaging or radiographic diagnosis in this dimension for years by a provider, who with good intentions, treated the patient with various dental related modalities and multiple bite splint appliances. (4)  This was to manage a significant orthopedic problems with both joints  but with the mindset the patient’s problems were due to chronic “muscle spasm” as the etiology.  Changing the way the teeth fit among themselves was the therapeutic goal costing the patient significantly.

Not only is the TMJ unique in its biomechanical function and make up, it is unique in its growth and development.  The fossa or “socket” of the TMJ develops as does the base of the skull which is a membranous bone formation.  The unique aspect of human skull growth is that the base of the skull completes its growth and development around age 5-6. (See bibliography references below).  Multiple studies using CT and MRI analysis have supported this developmental fact.  This is basicallly due to the fact that during our first 5-6 years of human existance, the brain and central nervous system are the most rapidly and developing system.  The growth and accomodation of the encasing protective skull is an interesting and unique phenomenon.  However, this may impact significantly the functional development of the TMJ, particularly in adolescents.

Most joints of the body have similar time-clocks to their sequential development.  Not so the TMJ.  The condyles of the mandible are the growth centers of the lower jaw.  The lower jaw originates as a cartilagenous structure when we are embryos…to be replaced by bone as we grow and develop thereafter. So “programmed growth differences” or other potential developmental issues exist in this natural mismatch of the growth and development of the boney components of the joint system.  After age 6, the mandible is just beginning its path to final adult growth and morphologic development is very different from the very beginning.  The lower jaw will continue to grow, vertically and horizontally away from the upper jaw and base of skull until about the mid to late teen years.  Consequently, there is a potential of continued growth and development of the condyles of the jaw for greater than a decade than that of their boney  articulation partner, the fossa.  This is a significant mismatch in developmental sequence that is not found similarly in other skeletal regions or joints of the body.   It is a critical issue relative to TMJ function, particularly if the mismatch is that which is similar to the degree seen in the above CT scan.

The reason:  The real scientists in today’s TMJ orthopedic research field are the boimechanical engineers who have employed computer studies to recognize that the human jaw joint is loaded the most when the mouth opens.  Dental education has taught students for over 100 years that the reverse is true….that the jaw is loaded the most when the teeth are together and therefore, dental positioning is paramount to good jaw joint function.  About the only time when joint loading with the teeth together remotely approaches mouth opening is likely to be during pathologic bruxism. (6)

Biomechanically, the mismatch in the width of the sockets versus the intercondylar width of the mandible creates mouth opening functional problems due to point contact loading when a condyle that is too wide for its corresponding fossa.  This in turn will increase loading in the disc/capsule of the joint system during mouth opening that, if severe enough, will create progressive lateral collateral ligament damage due to normal attempted mouth opening function.   Joint instability (jaw popping, pain and joint locking, open or closed) gives rise to increased problems with dysfunctional loading and causes bone spurring (1) to develop.  A similar mechanism of development occurs in the shoulder with rotator cuff impingement or tearing of that joint cartilage.  This orthopecic paradigm is visually obvious with appropriate MRI or CT imaging as well as numerous surgical observational examples. (5)

Studies of human base of skull and skull morphologic development also tell us there is a significant difference in the growth and development of the female skull versus the male skull.  These observations were noted to be statistically significant.  Males grow in greater dimension anterior-posteriorlly which may impact the anterior-posterior length of the jaw joint fossa.  Females have an earlier and more rapid rate of development of the body of the sphenoid bone and middle fossa in the region of the developing ear structures.  This too is in the region of the Developing TMJ fossa.  Though the rate is faster earlier on, males continue to develop a little longer.  These differences could explain all sorts of possibilities relative to differences in the development of the TMJ fosssa in females…and consequently explain why more women, who may never have been imaged or diagnosed when first becoming symptomatic in their adolescent or growth and development years seem to statistically have more issues with TMJ orthopedic dysfuncton than do men.

This is an area of research that is ripe for enterprising PhD students to investigate.  Growth and development mapping of the developing TMJ fossa relative to that of the condyle is an important issue to better understand. Following the lead and methodology of investigators using MRI imaging in growing individuals is science that is greatly needed.

BIBLIOGRAPHY

1. Myer, CM: Growth of the pediatric skull base: assessment using Magnetic resonance imaging.  Laryngoscope (1995) 105: (Supplement 75) PP. 1-11.

2. Sgouros s, K Natarajan, AD Hockley, JH Goldin, and M Wake:  Skull base growth in childhood.  Pediatric Neurosurgery (1999) 31:259-268.

3. Farkas, LG and JC Posnick:  Growth and development of regional units in the head and face based on anthropometric measurements.  Cleft Palate and Crniofac Jnl (1992) 29: 301-308.

4.  Relethford, JH:  Craniometric variation among modern human populations.  Am Jnl Phys Anthropol (1994) 95: 53-62.

5. Sekiguche, T, BS Savara, and BS AryaL Norms of size and annual increments of six anatomical measures of the cranium on boys and girls from four to fifteen years of age.  Am Jnl Phys Anthropol (1979) 39:49-56.

JT was seen for second opinion related to “My TMJ”.   Her history was that she had problems “since about 10 years old”.  It had impacted her jaw growth (crooked or asymmetric mandible) and because her joint disease was likely to have been present during her growth and development years, she now had significant malocclusion and facial deformity.  Traditional orthodontic treatment and orthognathic surgery was recommended and carried out  as the philosophy of both the treating orthodontist and surgeon was that such treatment would correct the problem. .

When JT would open her mouth, it would make a loud popping and grinding noise that was easily audible by anyone.  Mechanical locking and significant pain had been present for many years.

Below are Coronal MRI images of JT’s joints.

A

Image A is the patients symptomatic joint.  B is the normal joint.  In the lateral most compartment of the symptomatic joint (A), an image that is much darker than the remaining disc/capsule is seen.  This represents a calcified stone or often what is referred to as “loose bodies” by radiologists when commenting on atypical calcium deposits in cartilage tissues of joints.  This “loose body” in this TMJ image is embedded in the lateral attachment of the  disc/capsule of the joint complex.  Fortunately, frictional wear and tear had  not yet destroyed the joint boney surfaces at JTs young age.    It is not quite the character of bone, but nevertheless is partially calcified which will impair joint function significantly.  Compare with the homogeneous signal from the joint space in B.  

The clinical  term for this is “synovial chondromatosis”.  Another term is “pseudogout”.  The mechanisms for development of these calcified bodies in synovial joints is due to biochemical abnormalities in synovial tissues and  with normal joint fluid production and/or a combination this and cartilage growth and development. In younger patients there may be genetic issues in play. This condition can also  occur in severe and longstanding  osteoarthritic disease of synovial joint as an end stage pathology.  The condition is more prevalent in larger joints such as the knee, but can be seen in the TMJ nevertheless.

B

  Space does not allow inclusion of sagittal images in this case.  The absolute size or volume the patient’s symptomatic right joint A, is approximately 50% that of the left.  These growth differences are likely to have contributed to the crooked jaw that has developed as JT and her parents relate joint symptoms present well before puberty and skeletal growth advanced.  Though orthognathic surgery would be required to correct this consequence, the primary joint disease  would have to be addressed as well.  Many “TMJ” patients are simply evaluated imaging wise with a traditional dental “panorex/panoramic” film.  These films are generally of little value compared to tomography, CT or MRI.  

Conditions such as synovial cysts, tumors, ankylosis or joint fusion, avascular necrosis (AVN), stress fractures, and joint impingements occur in the TMJ as in other joints of the body. MRI is the appropriate examination for these conditions.  Most of all, “TMJ”  is not always “TMJ” .  Contrary to published editorials in dental professional journals, imaging is of upmost importance in diagnosis, particularly in younger patients with facial growth anomalies and provide much more insight than just talking to the patient, taking their history, and providing dental related or stress management therapy. ( 1 ) 

See Blog (this website), published 8/20/2010. “A Response to a “New” orthodontic standard of care.

1.  Greene, CS, editorial: “Managing patient with temporomandibular disorders: A new “standard of care”. American Journal of Orthodontics and Dentofacial Orthopedics, 2010, 138;  3-4.

To supplement this blog, review of the following  previously posted blogs on this site may help the viewer to better visualize the complex orthopedic biomechanics of TMJ function.  Please refer to the archives section for reference prior to viewing:

1. The disc/capsule complex
2. The Wilkes/Schellhas/Piper stages of TMJ derangement
3. A Picture of TMJ Pain

NORMAL JOINT RANGE OF MOTION AND FUNCTION.

As addressed in previous discussion of biomechanics of the TMJ, this is perhaps the most complex orthopedic system in the body.  It has both rotation and displacing gliding function (translation) where the condyle/disc/capsule leave the fossa (socket) in front of the ear and glide together as a unit with mouth opening.  Computer finite element studies have shown that physical loading of this joint system is greatest during mouth opening, as this is this orthopedic system’s most dynamic, viable, and stressful function.

In this video, notice how the disc/capsule functions with  the condyle during this  translation function.  The basic nature of the “cartilage” of this joint system is that it naturally has highly flexible and elastic properties that allow the shape of the disc/capsule to actually change its entire shape to adapt to the curvature of the boney structures of the joint structure during function.  Note in this video how this particular joint  functions  as the disc/capsule is  functionally adapted  to the condyle of the jaw during the gliding sequence of mouth opening.

Click Here for Video

A WILKES III  DERANGEMENT IN ATTEMPTED MOUTH OPENING FUNCTION

This video shows complete detachment of the disc/capsule from the condyle of the jaw.  (Wilkes III derangement { “non reducing disc”} ).  Movement is painful and guarded.  From the beginning of the mouth opening sequence, the disc /capsule never re-locates or adapts  to the gliding function.  Painful mouth opening is due to progressive tearing and detachment of ligaments that are designed to maintain the functional integrity of the  moveable parts.  Progressing  distributed shear throughout the soft tissue cartilage portions of the joint create progressive tissue destruction.  Such long term destruction is shown in surgical examples in other blogs of this website.

Click Here for Video

Final Comments:

Increased levels of shear and other damaging physical forces distributed throughout the disc/capsule in abnormal TMJ orthopedic function are responsible for progressive destruction of this orthopedic mechanism.  To that degree, orthopedic dysfunction of the TMJ and its consequences mimic progressive destruction of tearing seen in the rotator cuff of the shoulder, progressive destruction and evolution of arthritic processes in unstable knees etc.

It is a principle that cannot be ignored, but unfortunately is in much traditional clinical management of “TMJ Syndrome”, or “ TMD” patients or any convenient catch all categorization that often leads to tangential treatment of this clinical problem.  Often, the orthopedic problem within the joint is the last thing that is addressed after years of misdiagnosis, no imaging, or other forms of investigational neglect in long term symptomatic patients.  This can eventually lead to progressive development of chronic  pain mechanisms that are difficult to manage and are eventually the overwhelming  impairing issue.    In the end,  continuous  dysfunctional instability of this joint system can lead to progressive tissue destruction and worsening of derangement states (Wilkes III –V) and development of destructive arthritic processes in select patients.

In the late 60′s and into the 70′s,  dental and medical education did place much attention on the associated psychological state of the  “TMJ” patient.  This was because of large studies which showed positive subjective improvement to experimental treatment “placebo” therapies.  This suggested then and is true today that many early pain issues are transient and self limiting.  As a consequence then and now, many people who consulted providers were counseled that if they could just eliminate stress from their lives and not succumb to depression of chronic pain,  and perhaps go on antidepressants, that their “TMJ”  issue would magically disappear .  Unfortunately, there were many people who found that not to be true in their own experience.  That type of  professional “management” still goes on today.  It has also introduced a specific bias toward understanding a cause and effect relationship that a majority of health care providers were “brought up” with in their education process. This website is dedicated to education relative to true orthopedic pathologies of the human jaw joint and impairing conditions.

Much of the “psychological stress” component of this complicated clinical issue is serendipitously connected to the real physical  phenomenon of bruxism, or jaw/teeth  clenching.   If this were the total story of cause and effect relative to  pain and orthopedic dysfunction of the jaw,….well…..all of us would have a problem to deal with because a reality is that probably  all of us brux from time to time.

Bruxism is mentioned many times in Biblical writings.  It was observed and commented on by ancient Egyptian, Greek, and Roman empire physicians.  Most of us will brux during sleep.  It particularly occurs in specific levels of sleep when an individual can be quite physically active, yet in a deep sleep state and is totally unaware and unable to control such.  Jaw clenching does occur when humans are stressed.   It is so common in a human population as acknowledged by simple visualization that it ranks up there as something that is truly “nothing new under the sun” as it reflects the history of mankind.

The problem with psycho/physical ailments   are that there are cases when this truely is the real problem behind the “clinical condition”.  For providers, this phenomenon is a real frustration to deal with because there are people out there who enjoy going to doctors with complaints that are imagined.    These encounters, make it easy to label groups of patients with  a perceived condition as a “stress ailment”.  This is very common in the “TMJ” population and daily  patient encounters. Unfortunately, many individuals with true orthopedic disease of the jaw joint are often lumped into this category and suggested to seek treatment with stress counselors, biofeedback therapists, general dental providers (who will then turn this into a malocclusion/bite alignment problem) and a muscle spasm disorder due to stress from clenching again assumed to be dental or tooth related phenomenon.

BRUXISM PARADOX

True and isolated muscular pain ailments must be separated from true joint orthopedic problems. Also, bruxism can accelerate with oral and dental pain conditions.  Classic controlled studies in earlier eras showed conclusively that if a simple dental filling in a tooth was “too high” and contacted before other teeth contacted, bruxism was seen to increase.  It is nature’s way of trying to self adjust the fit of the teeth. Consequently, this type of bruxism is an acute exacerbation, totally related to an abrupt and  recent change in oral physiology or the status quo if you will.   This reality is why your dentist must be and can be  so obsessed with “getting the bite right”.

Bruxism can indeed be increased during stress.  There are certain human personality types that do physically target stress reactions in this way and end up with sore and painful jaw and neck  muscles do to this issue.  So it can not be completely dismissed as a relative  and significant issue requiring periodic management.

The most severe types of bruxism are seen in individuals with history of brain injury,stroke, or other central nervous system pathologies.  Here, true and constant jaw  closing muscle spasm  and no ability to separate the teeth can be seen. The same conditions can sometimes be seen in individuals receiving medication for certain  psychiatric conditions.  Various neurologic conditions associated with physical dyskinesias or involuntary uncontrolable  muscular movements are common in this subset and are difficult to manage.

Finally, bruxism can be a significant modifying factor in long term success for people who have true orthopedic problems of the jaw joint and it must be accounted for.  When bruxism occurs, individuals can load an injured or deranged jaw joint with longer periods of time and with forces that are greater than when we eat a meal.  It is this group of patient that can truely benefit from the constructed oral orthotic or bite splint.  The splint will accomplish two main objectives.  It can be constructed to an xray confirmation that the disc/capsule is not under physical loading to the degree that when the teeth are in contact.  Also, it will decrease the ability of muscle groups to generate their maximum amount of isometric muscle contraction force during involuntary jaw clenching maneuvers.  For this reason, I advise all surgical patients to have a custom orthotic constructed for night time  and indefinite use.

Bruxism tendencies can never be totally eliminated, only attempts at decreasing intensity, frequency,  and duration of the phenomenon can ever be attempted or accomplished in my clinical experience and that of others.

This author was the first to publish in the oral and maxillofacial surgical literature, a clinical evaluation of patients undergoing physical therapy for “TMJ” problems.  In that paper, our practice analyzed  68 consecutive patients with 87 collective joint derangements. We analyzed two separate clinical responses…joint function and pain response.  An overall improvement in joint function (improved or eliminated joint locking, joint instability etc) of 86% was achieved with this group .  Pain response improved in 82% of patients. Bite splints or orthotics were also used in many patients to help reduce joint loads during treatment.  All therapy was completed with two sessions per week for 3 to 6 weeks at which time they were subjectively re-evaluated.  No medications other than external applications of anti-inflammatory medications used with ultrasound muscle massage therapy were used with these patients as part of pain management.  (4)

Patients who responded well, were basically a group of patients with joint instability that occured very early in the mouth opening maneuver and had experienced symptoms for a year or less.  Physical therapy was not successful in patients who showed joint instability much later in the mouth opening sequence or with side to side jaw movements.  Many of these patients had subjective symptoms for greater than 2 years and included cases of Wilkes II and III derangement (“reducing and non reducing disc displacements”  as they were once referred to.)  Physical therapy functional and pain management is not very effective in Wilkes III derangements or greater for a significant period of time.  This is due to many of the inherent joint pathologies that impact orthopedic joint function as presented elsewhere in this blog.  In general, patients with significant lateral impingements will not respond well to physical therapy.

ADVANTAGES OF PHYSICAL THERAPY MANAGEMENT

1.  The biggest advantage is its obvious non invasive qualities.  It also uses hands on manipulation and patient jaw opening exercises to attempt to educate patients in biomechanics aimed at limiting  joint loading, hypermobility etc. and other potential damaging functional movements.

2.  Avoidance of long term use of anti inflammatory medications which can cause stomach irritation and risk other organ toxicity.

3.  Improvement in removal of various biochemical pain mediators in both the joint capsule and associated musculature, reducing reflexive muscular spasm of  muscles that are part of  jaw opening  and  closing.  Since neck musculature can also be impacted and neck therapy can be employed simultaneously. Physical therapy directed to muscle spasticity can avoid use of various medications used to combat muscle pain that often create sedation and are not compatable with work etc.

4.  It is non invasive and often rapid response to treatment with a skilled therapist with interest in TM joint dysfunction is achieved.  It is very cost effective.  This applies not only to the concept of surgical invasiveness, but also expensive and sometimes irreversible dental reconstruction procedures that are costly and often take significant time to assess efficacy.

A WORD ON BOTOX

In recent years, Botox injections into the muscles of mastication (jaw muscles) has become used frequently.  Botox is a powerful paralytic agent that is injected directly into musles to reduce spacticity.  It is very effective in true rigid muscle spasticity conditions such as conditions similar to spastic torticollis and other musculoskeletal muscle rigidity conditions.  Its problem is that the medication wears off in a couple of months with need to re administer.  It is a very expensive treatment and many patients can find themselves “on retainer” in various pain management centers and medical/dental offices.

A recent controlled, double blinded study evaluating Botox in the management of myofascial TMD pain showed it to be no more effective than injection of normal saline into muscular tissues.  There was a slight improvement in pain response with Botox, but  not significantly.  The authors concluded the costs of Botox outweighed any predictable and consistent clinical outcome and that much of the positive response was felt to be placebo, as similar scoring by patients occured when saline was injected.  (5)

1.  Rocabado M:  Diagnosis and Treatment of Abnormal Craniocervical and Craniomandibular Mechanics, Tacoma,WA, Rocabado Institute, 1981

2. Rocabado, M: Arthrokinematics of the temporomandibular joint.  Dent Clin North Am 27:586, 1983.

3. Wing ML Phonophoresis with hydrocortisone in the treatment of temporomandibular joint dysfunction. Phys Ther 62:32, 1982.

4. Kirk, WS and Calabrese, DK:  Clinical evaluation of physical therapy in the management of internal derangement of the temporomandibular joint. J Oral and Maxillofac Surg. 47: 113-119, 1989.

5.  Ernberg M, Hedenberg-Magnusson B, List T, Svensson P:  Efficacy of botulinum toxin type A for treatment of persistent myofascial TMD painL  a randomized, controlled, double-blind multicenter study,  PAIN  (2011) ,  doi:10.1016/j.pain. 2011.03.036.

Previous blogs have discussed orthopedic injury and other intrinsic mechanisms which create orthopedic impairment of the human jaw joint.  Systemic degenerative disease or arthritic processes can attack the TMJ as they do other joints of the body.  The above photographs are clinical occlusion example above and a panoramic radiograph below of a patient with bilateral rheumatoid arthritic destruction of both TM joints.  The resultant bite relationship pattern is called an open bite.  It is caused by collapse of the vertical height of the posterior supporting aspect of the jaw called the ramus.  The ramus becomes shortened due to destruction of the boney mass of the condyles of the jaw.  The same destructive pattern is seen in other joint systems where the entire boney architecture of joint structures is lost due to destruction of the joint.  The jaw is uniquely designed but its tell tale dysfunctional state is the collapse of the jaw vertically and horizontally and the bite limited to dental contacts only of the very back molar teeth.  This patients has 28 teeth available for chewing and eating function.  Unfortunately,dental contacts available for function are limited to only 6 teeth.  In the radiograph (x ray), note how the condyles are resorbed and now resemble little sticks.  They are roughly 5-10%  of what would be expected of normal bone size and mass for a mature adult.

Many rheumatologists underestimate damage to the TMjoint caused by autoimmune arthritic diseases such as rheumatoid arthritis, psoriatic arthritis, and other connective tissue diseases of the body.  The most important diagnosis to make is jeuvenile rheumatoid arthritis as it can impact facial growth significantly.

There are two important clinical parameters with rheumatoid arthritis of the TMjoints…pain management and correction of the malocclusion component.  The treatment can differ significantly between adults and adolescents who develop jeuvenile rheumatoid arthritis. 

In adults, a total joint replacement can be a viable option in that the malocclusion and joint destruction can be managed with joint replacement and reconstructive jaw (orthognathic) surgery which realigns bone and tooth segments back into alignment for chewing function.  In the past, before the development of reliable prosthetic joint replacements such as the TMJ Concepts and Biomet prostheses, ribs were often transplanted with the same objective of joint replacement.  Unfortunately, the disease process can continue on and attack the transplanted rib causing a relapse of the malocclusion.  So, in the adult patient, total joint replacement has to be an option.

Below is a before and after result of a patient with jeuvenile rheumatoid arthritis.  In this particular case, the patient had excellent range of motion of the jaw and very little joint pain.  Her disease destroyed the joints of her hands and feet and TM joints….all smaller joints of the body.  The disease struck quickly and was active for 3-4 years and then subsided.  Since she had little joint pain or range of motion difficulties, no surgery of the joints were performed, rather she had orthodontic and  orthognathic surgery alone with no relapse of her condition 20 years after surgery.  In the case of rheumatoid arthritis, development of malocclusion is very rapid.  Both joints are not always involved to the same degree and asymmetries of the lower jaw can develop rapidly.  Most rheumatoid arthritic joints are quite painful in their active states. Orthotic appliances (bite plates) applied to the lower jaw in order to decompress the painful joint(s) can be used in pain management until definitive joint replacement takes place.   The development of malocclusion with generalized osteoarthritis  is generally much slower and insidious with varying degrees of adaptation.  The worst case scenario for any arthritic joint is fusion or ankylosis of the joint which will always require surgery to restore movement of the jaw.

This syndicated photograph details issues that are not for the faint of heart….but it is the reality of what happens during all kinds of jaw and facial trauma at the point of impact whether it be sustained in an auto accident, fall, playground accident in the case of children, domestic trauma, industrial/work related accidents etc. Past blogs published in this series also serve as a basis for further discussion of injuries that occur to the temporomandibular joint (TMJ) soft tissues during jaw trauma. The consequences of facial/jaw trauma or long term consequences of any TMJ hyperextension injury (sprain) are poorly understood by most physicians and dentists….through no fault of their own, it rarely if ever is part of their formal educational curriculum….but unfortunately the following realities and consequences are rarely considered by most healthcare providers….particularly after acute injury. Some homework is necessary. Please refer to the following as a background for the science that follows with this discussion :

TMJ and Whiplash Injuries (12/8/09)
The Disc/Capsule Complex ((9/2/10)
A “new” orthodontic standard of care (7/9/10)
A Response to an orthodontic standard (8/10)
Wilkes/Schellhas/Piper Staging of TMJ Derangement (11/14/10)
A Picture of TMJ Pain (2/15/11)
A Patient’s Perspective (3/10/11)
Genetic Factors Not Likely (5/31/11)

THE BIOMECHANICS OF ACUTE TMJ HYPEREXTENSION INJURY

We have all viewed sporting events on television and likely seen the unfortunate consequence of an athlete who has sustained a knee injury…sooner or later the announcers inform the viewing fans that immediate and preliminary examination and MRI have revealed a cruciate ligament or other ligament tear or injury to the joint. To repair the injury, that athelete will undergo repair as soon as possible to repair and protect the integrity of the supporting ligament injury and the function of the joint itself. This is the orthopedic standard of care or paradigm and is well accepted based on evidence based experimental and practical clinical research. Unfortunately it is not an accepted parameter of care in significant ligamentous injury to the jaw joint that remains dysfunctional after a similar event.

Refer to the photograph above and look right in front of the ear of the boxer receiving the blow. Through the distortion of the face and the kinetic injury causing such concussive distortion, one can see the condyle of the jaw dislocating laterally. This lateral hyperextension occurs to the opposite joint to the side of the jaw to which the blow is delivered. If the blow is severe enough, the jaw will fracture, generally in two places because of the design and distributed forces throughout the curvature of the mandible. One of the most common places of the jaw to fracture is in the region of the condyle and these statistically make up the most common site of fracture.

There is one significant difference between a professional boxer and the average child or adult….the boxer wears a large, rigid, mouth piece that the upper and lower teeth both fit in and from the time he begins to learn his craft… it is his most important piece of equipment……he knows how important it is to keep the jaw closed tightly into this mouthpiece….if he doesn’t, he will have a short career as there is a neurophysiologic mechanism referred to as the trigeminal/vagus reflex….that is, there is a nervous system interconnection between the 5th Cranial nerve which supplies the brain information that when the jaw (basically a floating bone with two joints ) is displaced violently from this area… another cranial nerve called the vagus nerve….immediately activates and rapidly slows the heart rate among other things. (immediate nausea for instance). This and other concussive kinetic energy force waves through the brain create the famous “knockout punch” . The more stability the boxer provides to the jaw while receiving the blow, the better trained he is to prevent this from happening. You can see the amount of displacement that occurs in this trained professional who is still engaged with his mouthpiece. Imagine the potential of displacement that will occur in any human being with no such device stabilizing the jaw and TMJs at the moment of impact.

Biomechanical data tells us that it takes an average of 620 Newtons of force to break the jaw at the condyle. (1) An important contribution (though unfortunately ignored by many “TMJ” clinicians) from Ben Amor and associates in Paris (2) has documented that it takes roughly 10% of the force delivered to the jaw required to fracture the condyle to cause lateral detachment or rupture of the disc/capsule of the human TMJ from its attachments to the condyle. There are other mechanisms of hyperextension injury other than lateral dislocation of the condyle. An anterior subluxation or hyperextension sprain or injury can occur when the disc/capsule and condyle transtlate or glide forward too far forward during mouth opening. This mechanism exceeds the capabilities of another ligament attachment system posteriorly in the joint between the ear and the condyle of the joint. Regardless, ligament detachment, tearing or rupture can occur in this joint as in any other of the body.

Children can sustain significant jaw impact during falls and not sustain a fracture. This is because their developing bone tissues have more inherent elasticity or resistance to fracture than mature adults. The tale tell sign of a playground or bike accident creating a deep laceration to the chin is not too uncommon. The amount of energy created during impact of the chin directly on a hard surface and capable of cutting or tearing the soft tissues of the chin are above those in terms of Newtons of force that can cause detachment of the disc/capsule from a developing child’s mandibular condyle. The paradigm is to go to the ER, sew up the injury. It is not necessarily the present paradigm or standard to image to determine potential for injury or bleeding of the joint…..this is a project necessary to be studied in OMS academic centers before the paradigm becomes standard of care. However, Dr. Schellhas in Minneapolis and Dr. Piper in St. Petersburg have shown this to be a significant finding in published data in the medical radiology literature. They and others have also shown that those children who do sustain significant joint injury to one or both joints are at potential risk to have significant disturbances in jaw and facial development growth (short lower jaw) as a consequence. (3,4,5 )

Fortunately, many of these occurances may not lead to immediate progression of problems and impairment…in children, favorable growth and development adaptations (often referred to as remodeling…especially after fracture) can provide remarkable functional recovery. However for those pediatric and adolescent patients who are referred by the medical community to the dental community to the orthodontic community to correct a worsening “TMJ” problem….it is necessary to first inquire about potential for early injury….and to at least image these patients if they are becoming impaired with chronic pain and joint dysfunction. (See Wilkes/Schellhas/Piper staging of joint derangement). Unfortunately, this parameter has been slow to catch on inspite of MRI technology availbility for the past quarter of a century (Blogs of July and August 2010). In place of this approach, often the problem is described as a “neuromuscular disorder, stress, tooth clenching or grinding, or a malocclusion or the way the teeth fit…naturally requiring orthodontic or bite changing intervention”.

Biomechanic research also tells us that the jaw joint is loaded most during attempted mouth opening. After injury, the natural forces distributed throughout the disc/capsule are shearing and damaging to the integrity of the joint…just like that athlete who has the knee injury….the joint function can not support the demands of routine normal function, not to mention athletic competition. A focus on the way the teeth fit together as the cause of the problem ignores the science of pathologic biomechanics of an injured joint. It is an area in healthcare that must undergo significant change in perspective. (6,7 )

The unfortunate consequence of much of all this is that it has been ignored as a fundamental cause of “TMJ”….that nebulous diagnostic term that is too much of an expansive diagnosis to provide any meaning of cause and effect…after all that athlete who is injured is not reported to now have “knee syndrome” or “knee”….heck, even the average sports fan is astute enough to understand his or her favorite athlete’s past cruciate ligament knee or rotator cuff shoulder repair and long term consequences to his or her career if the injury is severe enough. The fundamental question has to be asked as to why medicine and dentistry have not provided didactic information during educational training of providers to mirror these accepted paradigms.

In people with chronic conditions, pain researchers, clinicians, and patient advocacy groups are steering research to all corners of the “research” paradigm to explain what “TMJ Pain” might be. There is almost no funding of important studies that are needed to document actual degrees of injury sustained to the joint itself soon after hyperextension injury. This is a research paradigm that is 40 years behind the research which describes consequences of other orthopedic joint injuries scientifically. To the credit of pain researchers, they have done a masterful job of describing the complex biochemical and neurological activities in the body and nervous system that create chronic pain….and this research helps produce drugs for chronic pain managment and other modalities. But the paradigm of what initiates the TMJ injury and tissue destruction in the first place has been ignored….it is an approach of collective negligence that needs to be adapted relative to the known science presented by orthopedic biomechanics and the consequences of injury damage potential in any age patient.

BIBLIOGRAPHY

1. Hylander, WL: The human mandible, lever or link? Am J Phys Anthropol 1975; 43: 227-42.
2 Ben Amor F, Carpentier P , et al: Anatomic and mechanical properties of the lateral disc attachment of the temporomandibular joint. J Oral Maxillofoc Surg 1998; 56: 1164-7.
3. Schellhas KP, Pollei SR, Wilkes CH: Pediatric internal derangements of the temporomandibular joint : Effect on facial development. Am J Orthod Dentofacial Orthop , 1993, 104:51-9.
4. Defabianis P: Post-traumatic TMJ internal derangement: impact on facial growth (findings in a pediatric age group), J Clin Pediatr Dent 2003, 27(4): 297-303.
5. Sanroman J, et al: Relationship between condylar position, dentofacial deformity and temporomandibular joint dysfunction: an MRI and CT prospective study. Jnl Cranio Maxillofac Surgery (1997) 26: 35-42.
6. Tuijt M, Koolstra JH et al: Differences in loading of the temporomandibular joint during opening and closing of the jaw. Jnl of Biomechanics, 43(2010)1048-54.
7. Gallo LM: Modeling of Temporomandibular Joint Fuinction Using MRI and jaw-tracking technologies-mechanics. Cells Tissues Organs (2005); 180:54-68.