Coronoid impingement syndrome: literature review and clinical management

Clinical presentation

The condition typically presents as painless progressive reduction in mouth opening due to contact interference between the elongated coronoid process and the medial surface of the zygomatic arch or the temporal aspect of zygomatic bone [2]. It can occur in unilateral and bilateral forms [9]. Facial asymmetry may occur if the hyperplasia is unilateral [11]. The condition is alternatively termed ‘coronoid impingement syndrome’ (CIS) [3]. Where pathological elongation of the coronoid process results in the formation of a new joint with the zygomatic process, this is also referred to as Jacob’s disease—named after Oscar Jacob in 1899 [11]. Symptoms can present as young as almost 7 years of age [2] and typically affect young patients with an average age of 25 years [7, 11]. A case of Jacob’s disease has been reported in a 39-year-old [10] and 52-year-old woman [11]. Male individuals are more commonly affected with a reported male to female ratio of 5:1 [12].

The aetiology of coronoid hyperplasia is as yet unclear [4, 10]. Possible causative factors include previous trauma to the temporomandibular joint, temporal muscle hyperactivity, chronic disc displacement, endocrine anomalies, and genetic alterations [7, 9, 11, 13]. Individuals with idiopathic short stature (ISS) who underwent treatment with growth hormone therapy have been found to develop trismus caused by bilateral coronoid process hyperplasia [7]. Familial inheritance patterns have been postulated [9]. Syndromic associations include trismus pseudocamptodactyly syndrome—affected individuals are unable to extend their fingers at the interphalangeal joints with their wrists in dorso-flexion and have severely limited mouth opening due to shortening of the temporalis muscle’s flexor muscle-tendon unit with possible coronoid process elongation. This syndrome is autosomal dominant, with variable expression [9].

Diagnosis can be made with panoramic radiographs [9, 10] and three-dimensional computerized tomography (CT) scans [5, 10, 14, 15]. Open mouth CT scans are useful for demonstrating direct impingement of the coronoid process on the zygoma [15]. Where limited mouth opening ability is observed, coronoid process elongation should always be considered as a possible aetiological factor [8].

Histopathology

Histopathological examination is required to confirm a definitive diagnosis and reveals normal bone. The presence of cartilage and a synovial capsule indicates a new joint has formed, as in the case of Jacob’s disease [11].

Differential diagnosis

Unilateral coronoid osteomas and osteochondromas are often mistaken for unilateral coronoid hyperplasia [16]. Histopathological examinations of surgical coronoidectomy specimens of cases with Jacob’s disease have revealed an osteochondroma of the affected coronoid process [10]. A rare case of bilateral coronoid process hyperplasia associated with nevoid basal cell carcinoma syndrome (also known as Gorlin-Goltz syndrome) has been reported [17].

Management

Initial case management should always include a thorough history and clinical examination. Basic dental radiography including dental panoramic tomographs (DPTs) will reveal the outline of the mandible and relative size of the coronoid processes in relation to the condyles.

Where mouth opening is restricted to the extent that normal function is compromised, surgical treatment is often indicated [2, 3]. Surgery involves a coronoidectomy via an intraoral approach [6, 10], followed by early post-operative physiotherapy to prevent post-surgical fibrosis and re-establish muscular activity and maximum opening [1, 3, 6, 7, 10]. The use of dynamic laser physiotherapy post-surgery has also been suggested [10]. In the long term, patients should be monitored for possible regrowth of the coronoid process [7]. One case series report showed stable long-term results at 5 years post-surgery [6].