There have been few reports of mouth closing disturbances in the final phase of occlusion caused by the posterior thickness of the retrodiscal tissue. Two such cases are described here. The first was a 70-year-old female suffering from a painless mouth closing disturbance on the right side of the temporomandibular joint (TMJ). She complained of a feeling like there was an air cushion. The second case was a 51-year-old male with a painless mouth closing disturbance on the left side of the TMJ. In both cases, magnetic resonance imaging (MRI) revealed enlargement of the posterior joint space on the affected side. The conditions of these two cases were improved by local injection of steroid preparations; however further additional treatments were required, including mandible traction in one case and dental prosthetics in the other. Consequently, we consider that the local injection of steroid preparations is useful as an initial treatment, while the use of local injection of steroid preparations alone is not sufficient for the treatment of posterior thickness of the retrodiscal tissue.
Generally, the concept of internal derangements of the temporomandibular joint (TMJ) is based on a spatial relationship between the disc and the condyle. The anatomy of the TMJ including the disc, connective tissue, and ligaments are described well by Rees.
Mouth closing disturbances can be classified into two groups, those that occur just after maximum mouth opening and those that occur just before complete mouth closing. It has been demonstrated that a mouth closing disturbance affecting the phase just after maximum mouth opening is caused by either luxation or open locking of the TMJ, while a mouth closing disturbance just before complete mouth closure is generally caused by inflammatory conditions, a pseudotumour or tumour, or posterior disc displacement. The inflammatory conditions are symptomatic and include pain, swelling, redness, and fever. Tumours show typical outgrowths on the condyle or in the glenoid fossa. Posterior disc displacement is described as a painful, sudden inability to close the mouth to maximum intercuspation.
Steinhardt was the first to discuss cases with posterior disc displacement of the TMJ. Theoretically, a disc displacement can occur in four directions: anterior, posterior, medial, and lateral. Among these, anterior disc displacement is found most frequently, whereas it is rare to see cases with posterior disc displacement. In posterior disc displacement cases, once the mandibular condyle slips over the front rim of the disc during mouth opening, there is difficulty in returning to a normal disc position spontaneously. The sensation resulting from a mouth closing disturbance of posterior disc displacement is described as the feeling that an elastic material is present in the joint. An arthrotomographic examination of posterior disc displacement revealed that the affected condyle was located in front of the anterior band of the disc; the affected condyle was thereby disturbed mechanically in the posterior movement into the articular fossa.
A mouth closing disturbance just before complete mouth closing may also be caused by the posterior thickness of the retrodiscal tissue (PTRT). However, only a few reported cases of PTRT have been published, and the aetiology and therapy of PTRT have not yet been identified. We describe two cases of posterior open bite caused by PTRT. Both cases experienced a certain degree of improvement following local injection of steroid preparations. However they both required additional treatments, including mandible traction in one case and dental prosthetics in the other.
A 70-year-old female visited our clinic because of a painless mouth closing disturbance occurring in the final phase of occlusion on the right side of the TMJ. About 1 month prior to the first visit, she had experienced this mouth closing disturbance suddenly, without any apparent cause. At the first visit, the patient was able to open her mouth smoothly without pain. There was no trismus. She complained of a feeling like there was an air cushion on the right side of the TMJ. An oral examination revealed a posterior open bite and a mandibular midline deviation towards the left side. A repositioning manoeuvre did not change this condition. With regard to the TMJ, there was no snapping or crepitation. On magnetic resonance imaging (MRI), enlargement of the posterior joint space on the right side could be seen ( Fig. 1 A) , but no arthritic changes of the condyle were found ( Fig. 1 A). Accordingly, the mouth closing disturbance in the final phase of occlusion and the mandibular deviation were considered to be affected by PTRT.
The patient was then treated, under 2% lidocaine local anaesthesia, with a steroid preparation (0.5% betamethasone), which was injected locally into the upper joint space on the right side. In addition, the mandible was retracted on the right side using a screw and class III elastics just after the injection. The elastics were initially used during the whole day for a few weeks. After that, the patient was able to bite completely, therefore the elastics were used intermittently for the next 2 months. Following treatment, the patient was able to open her mouth without any problems and MRI showed a narrowing of the right posterior joint space and no degenerative arthritic changes ( Fig. 1 B).
A 51-year-old male visited our clinic because of a painless mouth closing disturbance in the final phase of occlusion on the left side of the TMJ. He had first experienced the mouth closing disturbance 10 days earlier, and it had occurred without any apparent cause. At the first visit, the patient complained of a posterior open bite, while there was no snapping or crepitation. There was no trismus. On MRI, a widened joint space posterior to the left condyle could be seen ( Fig. 2 A) . Accordingly, we considered PTRT to be the cause of the mouth closing disturbance. Local injection of a steroid preparation (0.5% betamethasone) in the upper joint space on the left side was performed under local anaesthesia with 2% lidocaine, three times over the course of 5 months. After that, the condition improved gradually, although he could not occlude completely. We therefore replaced his old dental prosthesis of the left lower molar with a new prosthesis to provide the maximal occlusion. At the end of treatment, the patient was able to open his mouth without any problems, and MRI showed a narrowing of the right posterior joint space ( Fig. 2 B).
There are a number of TMJ lesions that are characterized by a mouth closing disturbance in the final phase of occlusion. Posterior disc displacement is one of these lesions. Blankestijn and Boering reported posterior disc displacement to be characterized by the following: (1) a sudden inability to bring the upper and lower dentition together in maximal occlusion, where it feels like there is elastic material between the molar teeth; (2) pain in the affected joint, especially when trying to close the teeth firmly together; (3) on the affected side, the mandible is shifted in an anterior direction about 4 mm, or half the width of a bicuspid, which results in a chin-point deviation to the non-affected side; (4) lateral movement of the mandible to the affected side is restricted and/or painful; and (5) there is no or only slight restriction of mouth opening. Pseudotumours and tumours of the TMJ are relatively uncommon, but can also lead to such a mouth closing disturbance. Tumours with typical outgrowths on the condyle or in the glenoid fossa show many clinical findings, some of which can help distinguish a TMJ tumour from other diseases. These findings include trigeminal nerve palsy, continuous pain without any change in jaw movements, and occlusion alterations with the presence of swelling. These symptoms increase with the growth of the tumour. On the other hand, some TMJ pseudotumours and tumours manifest clinically in ways very similar to a TMJ disorder (TMD). For example, the clinical findings of synovial chondromatosis of the TMJ are reported to include pain, pre-auricular swelling, restricted mandibular movement, deviation of the mandible to the affected side upon jaw opening, and the inability to close the jaw, and this bears some resemblance to the findings of posterior disc displacement.
In the two cases presented, there were no clinical findings except for the mouth opening disturbance. We first diagnosed these cases as posterior disc displacement, however neither patient had pain in the affected joint, which is inconsistent with the features of posterior disc displacement. Furthermore, we could find no evidence of posterior disc displacement or tumours in the MRI of both cases.
PTRT is a very rare condition. The posterior attachment consists of loose organized connective tissue. When the disc is displaced anteriorly, the posterior attachment is compressed between the condyle and the fossa, but it is not designed for loading. If the disc is recaptured correctly, the posterior band is at the 12 o’clock position of the condyle at mouth closing. This change results in an increased joint space between the condyle and the fossa, especially in the postero-superior portion of the joint. In other words, replacement of the posterior attachment with the posterior band should reposition the mandible antero-inferiorly. Kai et al. reported the development of a posterior open bite after anterior repositioning splint therapy. They also reported that continuous anterior positioning of the condyle might surpass the volumetric expansion capacity of the posterior disc attachment, which increases the volume of joint fluid in the upper joint cavity.
The treatments used for posterior disc displacement reported previously include lavage of the upper joint component, local injection of steroid preparations into the TMJ, and surgical repositioning of the disc. Sumiyoshi et al. reported surgical repositioning of the disc by arthroscopic surgery. In contrast, there have been only a few reports on the surgical treatment of PTRT. Kaneyama et al. demonstrated a case of PTRT in which an open arthrotomy was performed. It was stated in their report that the aim of the open arthrotomy was to check for the existence of a TMJ tumour and to eliminate the obstruction against the reduction of the condyle to the fossa. However, the case reported by Kaneyama et al. was unusual because the involuntary movement of the mandible with TMJ dislocation was caused by an extrapyramidal disorder that developed as a side effect of antipsychotic drugs.
Corticosteroids modify the vascular response, and inhibit enzymes and inflammatory cells during the inflammatory response. Huddleston Slater et al. demonstrated that intra-articular injection of dexamethasone following an arthrocentesis did not improve the effect of the arthrocentesis in cases with TMJ arthralgia. In contrast, it has been shown that the injection of corticosteroid and local anaesthesia is suitable for patients with disc displacement without reduction. In the present two cases, local injection of steroid preparations was performed to resolve the oedema in the connective tissue, which improved the condition of both patients to some degree. Accordingly, we suspected that one of the aetiologies of PTRT might be oedema of the posterior attachment connective tissue. However, both cases eventually required additional treatments, including mandible traction in one case and a dental prosthesis in the other. Consequently, it is suggested that PTRT might be caused by both oedema and hyperplasia of the posterior attachment connective tissue, and that the local injection of a steroid preparation alone is not sufficient for the treatment of PTRT. Because local side effects of steroid injections, such as destruction of the articular cartilage, infections, and progression of a pre-existing joint disease, are well-documented, we consider that posterior traction of the mandible should have been applied at an earlier stage, instead of repeated steroid injections, in case 2.
In conclusion, this report describes two rare cases of posterior open bite caused by PTRT. This is a phenomenon that is poorly understood and requires further study to elucidate the mechanism underlying the disorder.