TMJ Surgeon: The Wilkes/Schellhas/Piper stages of TMJ derangement
Science demands standardization of experimental models. This is one fact that has made TMJ “research” so difficult and why so many theories of etiology of “TMJ” end up either being mutually exclusive or too filled with multiple variables to be of any value. In studying specific orthopedic disease of the jaw joint, Drs. Wilkes and Piper (founding members of ASTMJS) along with Dr.Schellhas a prominent Minneapolis radiologist and ASTMJS member, developed a standardized model(s) of describing variable stages of TMJ orthopedic derangement. The Wilkes and Piper classifications are based on sagittal MRI scanning characteristics of dynamic motion. The differences between the two systems is slight. Piper has more subcategories in particular stages than the Wilkes staging and are based on degrees of lateral rupture of the disc/capsule from its lateral pole of the mandibular condyle. His model is a chronologic progressive/descriptive one which mirrors advancing biomechanical dysfunction .
What follows here is a synopsis of those classification systems. What is necessary going forward in all reporting of surgical data and clinical data reviews of success or failure of various treatment parameters is the required categorization of patient groups and what stage of derangement they exibit when part of a study group.
This is also a plea for clinicians (especially surgeons and orthodontists and dental reconstructive “TMJ SPECIALISTS” ) to communicate about patients with a true orthopedic TMJ disorders with a sound method of classification. (Rather than the outdated and non-specific generic terms “TMJ syndrome” or TMD etc. What needs to be separated are those patients with true orthopedic disease/dysfunctions and a ready way of distinguishing that from other conditions that can create facial pain conditions.)
These stages define both soft tissue degeneration and arthritic bone changes in the joint itself.
Stage I: Normal range of motion of the TM joint requires congruent adaptation of the disc/capsule to the condyles of the jaw.
Stage I is essentially a congruent relationship of this adaptation and the ability of the fibrous tissue disc to re-shape itself during mouth opening and during compression loading while chewing food.
Stage II. Biomechanical study of TM joint function is clear. The lateral aspect of the human jaw joint is vulnerable to early shear and torque forces, either sustained via injury or normal mouth opening translational force loads. In the Stage II derangement, the critical lateral supporting disc/capsule attachments to the lateral perimeter of the condyle can become loose (loose trampoline spring analogy offered by Athanasiou/Detamore), or in the case of trauma or hyperextension sprained, strained or torn/detached. This is initial TMJ orthopedic instability, experienced as a painful snapping noise, sometimes audible to others, during mouth opening. Prior to classification models, this phenomenon was referred to as “a reducing disc displacement”. However, this term invites a mental image of a two dimensional functional disorder while we have to think in 3 dimensions. Use of the term Stage II gives not only the structural abnormality a dysfunctional classification, it also should inform the provider that minimal destruction of critial articular tissue structures have yet to take place…except at the very lateral of the joint where surgical treament can be successfully employed. The stage II derangement has a high rate of success when non surgical treatment fails to correct orthopedic instability and pain with mouth opening and chewing of food is painful and refractory to non surgical methods.
Stage III There is little in the literature that provides insight relative to time progression between Stage II and III. However, the differentiation of II vs. III is very important especially if associated with complicated maxillofacial developmental deformity. Stage III derangement is associated with irreversible changes in the overall form of the disc/capsule and its adaptation to the curved surfaces of the condyle and fossa. The most dramatice tissue changes occur on the lower articulating surface or “cup” adaptation of the disc/capsule. In this stage, the integrity of the entire lateral ligament attachment has been lost and tearing of the posterior inferior disc/capsule attachment is present. Often this tear creates intense pain interpretetd to be a severe ear ache. Many patients are seen in physician offices for this problem and mis-diagnosed with variations of “earache”.
In Stage III, the important elastic tissue quality of the structure begins to be lost. Occasionally, the fibrous tissue undergoes a change in character or “metaplasia” by developing small islands of calcium deposits in the disc/capsule itself. This creates a very unstable and painful joint with tendencies for the joint to either exhibit a “closed lock” (inability to open the mouth beyond two finger widths) or the tendancy for “open Lock” or joint subluxation, where open mouth movement result in the mouth getting stuck open.
Surgical studies have shown that success rates between Stage II and III derangements can decrease, mostly due to the gross distortion of tissues and bone surface changes which impact the complicated movements of the TMJ. Impingements can develop rapidly or increase in size rapidly in this stage in my experience. This stage has also been associated with problems with certain orthognathic surgical procedures in susceptible patients when undiagnosed prior to implimentation of those surgeries.
Stage IV….In this stage, the disc/capsule is still in tact but deformation and bone changes are even greater. This stage generally develops after longstanding, incorrected derangement in susceptible patients. Type II and III impingements are frequent and joint locking increases to almost daily and mouth opening ability begins to decrease substantially. Pain is generally intense and refractory to all medications. Patients are becoming significantly impaired at this stage.
Stage V….Stage V is an osteoarthric joint, exibititng joint collapse, bone/bone contact during translation or mouth opening, bone spurring of the condyle and rupture of the disc/capsule. This rupture occurs when disc/capsule tissues no longer are strong enough to resist the dysfunctional shear and torque of joint loading.
FIGURE 1 Wilkes/Piper MRI scan classifications are a sagittal (lateral view scan) examining the adaptation of the disc/capsule to the condyle. The above is a normal adaptation of the disc/capsule to the condyle.

This is a normal adaptation of the disc/capsule in the lateral dimension. Note how the image mimics that of the normal specimen.
FIGURE 2
Normal or Wilkes I sagittal MRI image of TMjoint anatomy. Note relationship of central disc portion of disc/capsule complex to condyle of jaw. The ear canal is the dark oval structure behind the joint. The front of the face would be to the left of the image.
Compare with photo above.

FIGURE 3
This is a normal mouth open Sagittal MRI image of the human TMJ. Orientation is same as above. Note how the condyle of the jaw has glided forward while the fibro/elastic /cartilage disc capsule has maintained an adapted congruent relationship with the condyle of the jaw. Note the change in configuration of the disc to meet the demands of stress/strain forces placed as curved boney structures pass along their respective surfaces.

FIGURE 4
This is a Wilkes II sagittal derangement. This is a two dimensional lateral view. Compare to Figure 2. This image represents a disc/capsule that via shear forces has lost its primary congruent position and adaptation to the mandibular condyle. Such a joint would be considered orthopedically unstable, giving rise to jaw snapping or popping with mouth opening. Pain can range from moderate to severe and is reflected by degrees of ligment tearing or other forms of detachment of the disc/capsule from its normal adaptated relationship with the condyle (Figure 1) In general, if the mouth open MRI appears as in Figure 3, the integrity of the disc/capsule and severe destruction of tissue via shearing forces have not yet developed. If on mouth opening the disc/capsule does not normalize as in Figure 3, more extensive damage and bone changes (impingements) are likely to be present.
FIGURE 5
This is an advanced sagittal derangement (Wilkes III). In this image mouth opening is severely compromised due to a near total loss of congruency of the disc/capsule where it has now become completely sheared off of the jaw condyle. Pain is extreme due to ligament entrapment pain, progressive tearing of ligament attachments binding the disc to the condyle of the jaw. Often this leads to locking of the joint and marked diffiiculty with mouth opening . Bite splints may be no longer effeciive as the predominant issue is significant biomechanical dysfunction with mouth opening and ranges of motion required for chewing and other functions. Surgical specimens of similar cases are presented elsewhere in this website to show degrees of tissue destruction of the TMJ disc.
FIGURE 6

Figure 6 is a Wilkes III open mouth view (non-reducing) derangement. This is in a 15 year old female who has recessive jaw developing. Relative to figures 1 and 3, the disc/capsule is no longer congruent with the head of the condyle and remains detached from the condylar head in all ranges of jaw motion. The ligament attachment of the disc/capsule to the lateral aspects of the condyle have become excessively stretched or torn to the point the structure begins to fold upon itself or assume irreversible shape and loss of natural elasticity to absorb normal loads generated during mouth opening/jaw translating function. Stage III can be a very dysfunctional state associated with significant orthopedic instability (joint popping) and various states of locking in attempted mouth opening.
Tags: TMJ classifications, TMJ derangement classifications, TMJ MRI, TMJ MRI Anatomy, TMJ Surgery




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