Internal Derangement of the Temporomandibular Joint

Internal derangement of the temporomandibular joint is defined as a disruption within the internal aspects of the TMJ in which there is a displacement of the disc from its normal functional relationship with the mandibular condyle and the articular portion of the temporal bone¹. The prevalence of TMJ internal derangement has been well documented. Dulcic et al. examined 96 elderly subjects and verified that the symptoms in internal derangement of the temporomandibular joint were found in 9.3% or subjects and tissue specific diagnosis were established in 52.1% or the subjects².

Guler examined patients with known bruxism and was able to correlated via MRI that 64 or 102 joints exhibited evidence of disk displacement³. Studies by Farrar show that as much as 25% of the entire population has an internal derangement⁴. Internal derangement can be divided into four separate stages.

In the first stage of internal derangement clicking begins suddenly and spontaneously or after an injury. This reciprocal clicking is considered to be pathognomic for the first stage of disc displacement. The noise is often loud and can sometime be heard by others. The patient may be aware of an obstructive feeling within the joint during movement until the click occurs. The mandible frequently deviates toward the affected side until the click occurs and then returns to the midline. It has been stated that the later the opening click occurs the more advanced the disc displacement, however this point has been under debate. The fifth World Congress on Pain determined that "Clinic cases cannot be distinguished from controls on the basis of clinically detectable joint sounds."⁵ This concept is further emphasized by Rohlin and others, who showed in an arthorgraphic study that anterior displacement with reduction can exist without joint noises⁶.

The second stage of disc displacement is reciprocal clicking with intermittent locking. Symptoms include locked jaw and usually, but not always, severe pain over the affected joint. Patients may describe an obstructive feeling to opening within the joint. Patients may be able to use manipulation in order to reposition the joint and restore function. In some cases, the jaw may unlock spontaneously. In most cases, a previous history of joint clicking exists.

The third stage of disc derangement is associated with limited opening and has been termed closed lock. A limited opening of < 27mm will exists as well as preauricular tenderness and deviation of the mandible to the affected side with mouth opening and protrusive movements. Again, the patient will often describe a feeling of fullness or obstruction. In chronic closed lock episodes, if the condition progresses, the condyle may steadily push the disc forward to achieve almost normal ranges of mouth opening, in spite of the presence of a non-reducing disc.

The fourth stage shows continued mandibular function as the stretched posterior attachment slowly loses its elasticity. The patient begins to regain some of the lost range of motion. As retrodiscal tissue continues to be stretched and loaded, it becomes subject to thinning and perforation. Anatomic studies have shown that this tissue may remodel before it succumbs, ill-adapted to the functional load and perforates⁷. Although it is often classified as a characteristic of a separate final stage, hard tissue remodeling probably occurs throughout all stages.

Many patients undergo the progressive changes that have been previously described. However, it is still not clear as to whether or not this progression happens in all cases. Numerous studies show that this progression does not exist. For instance, in a 10 year study performed by Magnusson et al. 293 subjects with clicking exhibited no progression of clicking into locking⁸. At the 10 year follow up, only one of the 293 subjects reported intermittent locking⁹. In addition, the authors state that half the patients who exhibited clicking at age 15 no longer did so at age 20, and about half of those who did not exhibit clicking at age 15 went on to develop clicking. This lack of progression of internal derangement from a reducing disc to a non-reducing disc condition has also been confirmed in studies by Greene and Laskin, Lundh and others.

Other studies have been performed examining the natural course of anterior disc displacement without reduction. Sato et al observed 44 patients with anterior disc displacement. At 18 months, 68% of the study population exhibited successful resolution¹⁰. Although this finding suggests that the symptoms of an anterior displaced disc without reduction can resolve without intervention, the authors fail to mention what happened to the disc. It is possible that there was some stretching and remodeling of the retrodiscal tissues enabling the disc to be displaced more anteriorly by translating the condyle. These findings are similar to another study performed by Kurita et al¹¹. In their study they examined 40 patients over a period of 2.5 year. After 2.5 years, 43% of the patients were asymptomatic, 33% had decreased symptoms, and 25% of the patients showed no improvement or had required treatment. The result of this prospective cohort study indicated that approximately 40% of patients with symptomatic disc displacement without reduction will be free of symptoms within 2.5 years, one-third will improve, whereas one-quarter will continue to be symptomatic.

Although studies have accurately shown that internal derangements can be treated conservatively or simply monitored, there still exists a small proportion of patients that will require therapy. Internal derangement is normally treated with non-surgical methods initially. Should these methods prove unsuccessful, they are often followed by surgical methods such as meniscectomy, disc repositioning procedures and condylotomy. The use of invasive surgical means has decreased in recent years as the introduction of more conservative surgical procedures has become more popular. TMJ arthroscopy is an example of minimally invasive surgical therapy.

Works Cited:

1. Dolwick MF, Katzberg RW, Helms CA. Internal derangements of the temporomandibular join: fact or fiction? J Prosthet Dent 1983; 49: 415-8.

1. Dulcic N, Panduric J, Kraljevic S, Badel T, Celic P. Frequency o finternal derangement of the temporomandibular joint inelderlhy individuals. Eur J Med Res 2003 Oct 22; 8(10): 465-71.

1. Guler N, Yatmaz PI, Ataoglu H, Emlik D, Uckan S. Temporomandibular intgernal derangement: correlation of MRI findings with clinical symptoms of pain and joint sounds in patients with bruxing behaviour.

1. Farrar WB. Myofascial pain dysfunction syndrome [letter]. J Am Dent Assoc 1981; 102: 10-1.

1. Stohler C. Disk-interference disorders. In: Zarb G, Carlsson G, Sessle B, Mohl N, editors. Temporomandibular joint and masticatory muscle disorders. Copenhagen: Munksgaard; 1992. p271-6.

1. Rohlin M, Westesson PL, Eriksson L. The correlation of Temporomandibular joint sounds with joint morphology in fifty-five autopsy specimens. J Oral Maxillofac Surg 1985; 43: 194-200.

1. Heffez L, Blaustein D. Pathologic anatomy of internal derangements. In : Heffez L, Blaustein D, editors. Arthroscopic atlas of the Temporomandibular joint. Philadelphia: Lea & Febiger, 1990.

1. Magnusson T, Egermark-Eriksson I, Carlsson GE. Fiver year longitudinal study of signs and symptoms of mandibular dysfunction in adolescents. J Craniomandib Pract 1986; 4:338-44.

1. Magnusson T, Carlsson GE, Egermark I. Changes in subjective symptoms of crainiomandibular disorders in children and adolescents during a 10 year period. J Orofacial Pain 1993; 7:76-82.

1. Sato S, Takahashi K, Kawamura H, Motegi K. The natural course of nonreducing disc displacement of the temporomandibular joint: changes in condylar mobility and radiographic alterations at one-year follow-up. Int J Oral Maxillofacial Surg 1998; 27: p173-7.

1. Kurita K, Westesson PL, Yuasa H, Toyama M, Machida J, Ogi N. Natural course of untreated symptomatic temporomandibular joint disc displacement without reduction. J Dent Res. 1998 Feb;77(2):361-5.