Teaching Case

A 31-year-old female patient with learning difficulties presented with progressive trismus. She reported no dental pain and was able to tolerate a soft diet. Clinically, maximum opening of the mouth was measured at 15 mm (normal >40 mm) and she had difficulty in performing lateral excursion of the mandible.

A dental panoramic demonstrates elongation of the coronoid processes (Fig. 1). The extent seen in the radiograph may be affected by positioning error (chin raised). As such, non-contrast CT of the mandible was acquired to assess for ankylosis of the temporomandibular joints (TMJs). Figure 2a and 3 shows elongation of the coronoid processes, especially on the left, extending superior to the zygomatic arch. The processes are bulbous, and may impinge on the arch on opening. There is no evidence of ankylosis in the TMJs (Fig. 2b).

Incidental findings of opacities of varying density are associated with the apices of the lower right premolars and second molar, and the lower left second molar (LL7). Hypercementosis is seen, most markedly affecting the right mandibular canine. Associated thinning of the mandibular buccal cortex and mild bucco-lingual expansion is seen in the LL7 region on CT. Appearances are consistent with florid cemento-osseous dysplasia.

Trismus is defined as mouth opening of less than 40 mm [1]. The causes of trismus are multiple, but include myofascial pain, trauma, joint ankylosis, deep space infection and tumour invasion into the masticator space.

Coronoid hyperplasia is a rare cause of trismus. Elongation of the coronoid process with normal bone formation causes impingement of the process against the posterior aspect of the zygomatic arch, restricting translational movement of the condyle along the articular eminence on opening. Men are more frequently affected than women (5:1). Presentation may be with endocrine stimulation, trauma and familial predisposition proposed [3].

Extension of the coronoid process above the superior border of the zygomatic arch is seen on imaging acquired with the mouth closed. Some authors suggest that extension greater than 1cm above the arch is pathognomonic [4]. Hyperplasia can usually be detected on a dental panoramic or Water’s view. CT in the open mouth position may demonstrate impingement of the coronoid on the arch, and remodelling of the posterior surface of the arch may be seen. Dynamic MRI of the TMJ should be performed with a field of view large enough to include the coronoid process.

Treatment is with coronoidectomy. Delay in diagnosis and treatment can result in secondary TMJ ankylosis [5]. Coronoid hyperplasia may result in the formation of a pseudojoint between the coronoid process and the zygomatic arch, termed Jacob’s disease [3].

Cemento-osseous dysplasia (COD) is an idiopathic process in which bone in the periapical regions of the jaws is replaced with fibrous tissue and metaplastic, amorphous bone. Poor vascularity within the affected bone increases susceptibility to infection [6]. A predilection for middle-aged, black women has been noted [7]. It is frequently asymptomatic and presents as an incidental finding on dental radiographs, although local expansion is occasionally seen. Variants of COD are determined by distribution of the lesions: periapical COD involves the apical bone of the mandibular anterior teeth; focal COD is associated with a single tooth; and florid COD, as in the presented case, is multifocal.

Radiographically, florid COD lesions are usually seen bilaterally and in both the maxilla and mandible, although the mandible is more commonly affected. Lesions have varying density, with a soft tissue capsule and central sclerotic areas [7]. Lesions can cause thinning of the mandibular cortices and mandibular expansion. Roots of associated teeth may demonstrate hypercementosis. No treatment is required, however, due to the susceptibility to infection, regular dental assessment is recommended.