The TMJ condyle is covered with a layer of fibrocartilage. During ICR/PCR this tissue breaks down, and then the outer osseous cortex of the condyle starts to resorb [8, 9]. This is seen on imaging as resorption lacunae, with the disappearance of the dense outer cortical layer. Other changes include narrowing as well as shortening of the condylar process and ultimately there are changes in the length of the ramus [8]. There is demineralization of the bone below the cortex of the condyle. This may result in the collapse of articular surface bone, which is clinically manifested by a rapid opening of the bite and opening rotation of the mandible [9]. Although the disease is described as condylar resorption, there may also be resorptive changes occurring in the articular eminence which tends to flatten [3, 9]. ICR/PCR can affect either one or both condyles; if unilateral, the result is significant facial asymmetry. However, in most cases both condyles are involved, although one joint may demonstrate more advanced pathology than the other. This more common bilateral pattern may indicate a genetic predisposition as well as the humoral nature of the etiology. Hatcher has illustrated both the resorptive stages and the eventual healing stages of condylar resorption visualized on CBCT imaging (Fig. 7.2) [26].

The TMJ disc acts as a shock absorber during load bearing mandibular movements, while also providing lubricated surfaces over which translation and rotation movements occur [11, 27]. The role of the disc in the etiology of ICR/PCR is controversial in terms of “chicken-and-egg” explanations. The functional surfaces of both the condyle and the articular eminence can demonstrate degenerative changes when the disc is perforated or displaced without reduction [28, 29]. Link and Nickerson studied patients referred for orthognathic surgery and reported that all their open bite cases and 88 % of their Class II malocclusions had bilateral disc displacement [30]. On the other hand, the condyles undergoing resorption simply may not be able to maintain normal disc position, so the discs may become displaced. Wolford and Cardenas recommend joint surgery to attach the displaced disc to the head of the condyle prior to or during orthognathic surgery for ICR/PCR to prevent reoccurrence of disc displacement or changes in disc morphology [31]. Other surgeons do not agree that disc surgery is necessary. They do not enter the joint when performing orthognathic surgery on ICR/PCR patients, especially if the joint is functional – even if the condyle and ramus are severely affected by the disease (Figs. 7.1 and 7.3) [3, 13]. It should be remembered that TMJ disc displacement occurs in about 1/3 of asymptomatic individuals in the random population, while ICR/PCR is a relatively rare occurrence [2, 32]. Also, patients with degenerative joint disease of the TMJ do not necessarily have abnormally positioned discs [32].

Author CH mailed a questionnaire in 1998 regarding ICR/PCR experience to a group of orthodontists who were members of the Midwest component of the Edward H. Angle Society and faculty of the orthodontic department at the University of Illinois, Chicago [2]. From a total of 69 mailings there were 57 responses, and these practitioners reported seeing only 56 cases of ICR/PCR during their years in practice. An incidence of ICR/PCR of approximately 1 per 5,000 patients was derived by estimating the number of new patients examined over the years in each practice. Another way of looking at the rarity of the incidence was that each provider saw an average of 1.3 ICR cases in his/her career up to the point of the survey. This incidence may be low due to failure to recognize the disease, and small sample size, but it does demonstrate the infrequency of ICR/PCR seen in an orthodontic practice. Surgery centers that perform a large number of orthognathic procedures have reported an incidence of 2–5 %, which is still infrequent, but more common than reported by the orthodontists [15–19].

Of the 56 cases of ICR/PCR recorded in this survey, 35 (62.5 %) were spontaneous with no history of surgery, while 21 (37.5 %) developed the problem following surgery. The following data were derived from 40 of the questionnaires where there was adequate reporting:

From the responses, it is clear that these were patients that the orthodontist remembered well. This survey should be repeated with a greater number of orthodontic offices participating. However, even these limited findings confirm the anecdotal reports in the literature that ICR/PCR is a disease affecting young females of Caucasian or Asian descent, less than half presenting with TMJ pain, and with variable occlusions prior to developing this problem, and when ICR/PCR does occur it presents as a severe management problem.

The role of the orthodontist prior to orthognathic surgery is to prepare upper and lower teeth to an ideal arch form that will maximize occlusal contact in a normal Class I occlusion following surgery. This is true no matter which surgical approach is taken. A limited number of ICR/PCR cases can be successfully treated following remission of the disease by orthodontic means, without performing surgery. This is especially true when the resorption starts in the 20s rather than in the early teens (Fig. 7.5). These patients may have acceptable aesthetics, but this is not the situation in many cases. The tremendous loss of condylar mass and the resulting facial deformity in most cases requires comprehensive surgical management (Fig. 7.1).

ICR/PCR typically first appears in young adolescents, although Dibbets et al. has shown deformed condyles and growth disturbances in a younger age group [37]. The period from the teen years to the early 20s appears to be the most active time for ICR/PCR. Optimistically, the disease goes into remission and eventually “burns out” by the mid 20s. However, some patients continue to have active ICR/PCR into their 30s (Fig. 7.3). As a result, teenagers diagnosed with ICR/PCR should be advised to postpone orthognathic surgery, young girls with severe facial deformity and/or their parents often insist on correction earlier due to social and peer related pressures.

Another option available is to advance the mandible slowly by distraction osteogenesis, thereby allowing the soft tissue and musculature to adapt to the large mandibular advancements often required in such cases. Schendel et al. reported a case of 15.6 mm vertical elongation and 13.4 mm horizontal advancement using a curved distractor [40].

Gunson and Arnett have taken a more biomedical and pharmacologic approach in the management of patients with ICR/PCR or who might be at risk of postsurgical ICR/PCR [36]. They prescribe an occlusal splint employed for 6 months prior to as well as following orthognathic surgery to reduce the mechanical loads on the joint. Also, before and after surgery they place the patient on a comprehensive series of drugs to relax the musculature, decrease bruxism, decrease inflammation and reduce the patient’s inherent bone resorption capacity [10, 36, 41]. They reported stable postorthognathic surgery results at 24-month follow-up in 24 ICR/PCR patients (American Society of TMJ Surgeons, May 2,3, 2014, Chicago, IL).

The approach to the management of ICR/PCR cases should be individualized and based on the extent of the disease process. Arnett’s and Gunson’s approach appears appropriate for most early cases of ICR/PCR requiring orthognathic surgical management. For cases requiring extreme mandibular advancements, distraction osteogenesis might be considered [38].

If condylar resorption is still active, replacement of the joint with an autologous costochondral graft or total alloplastic temporomandibular joint replacement prosthesis is possible [25, 40–45]. There are a number of ICR/PCR patients who present with one of the following problems, who are best treated with synthetic total joint replacement (TJR). They are individuals with:

Patients with active ICR/PCR may also be candidates for total joint replacement as the artificial joint cannot resorb. The next section will discuss this option in detail.

End-stage disease is the most pernicious condition of an organ or disease state; in this state the organ can barely function. Examples include end-stage renal disease where the kidneys have shut down and the patient requires dialysis, or end-stage cardiac disease where the heart is functioning so poorly that it requires mechanical support or transplantation for the patient to survive [45].

End-stage joint disease portends a joint so architecturally devastated by disease or injury that it results in a severe functional impairment for the patient. In the ICR/PCR patient, the local adaptive capacity of the TMJ condyle has been mechanically and biologically tested in vivo by the disease process and it has failed. This failure is demonstrated by the load-compromised bony architecture having end-stage pathological changes as seen on imaging. Clinically, the articular end-stage pathology is manifested by the patient’s signs and symptoms [41–45].